Dissertations / Theses: 'Antioxidant defences'

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Rickett, Guy Masami Wilson. "Perinatal development of pulmonary antioxidant defences." Thesis, University of Southampton, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316750.

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Grundy, Jean Elizabeth Carleton University Dissertation Chemistry. "Antioxidant defences during estivation in the spadefoot toad Scaphiopus couchi." Ottawa, 1996.

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3

Nelson, Michelle Amy, and n/a. "Protein Bound 3,4-Dihydroxyphenylalanine as a Signal for Enhanced Antioxidant Defences." University of Canberra. n/a, 2008. http://erl.canberra.edu.au./public/adt-AUC20081209.125208.

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Protein-bound 3,4-dihydroxyphenylalanine (PB-DOPA), a long-lived, redox-active product of protein oxidation, is capable of functioning as both a pro- and anti-oxidant. A number of in vitro and in vivo studies have demonstrated a toxic, non-toxic or even beneficial effect of free DOPA, however little investigation has examined the physiological activity of PB-DOPA. Furthermore, as free DOPA is currently the major treatment available for Parkinson?s disease, most studies have focused on the effect of DOPA within neurological cells or tissues, although the presence of PB-DOPA in other locations, for example within atherosclerotic plaques, suggests that broader research is needed to fully understand the physiological effects of both free and PB-DOPA. The hypothesis presented in this thesis is that under physiological conditions, when little redox active transition metal is available, PB-DOPA can function as a redox signalling molecule, triggering an enhancement of cellular antioxidant defences, with a potentially specific role in the regulation of defences targeted against protein oxidation. Physiological levels of PB-DOPA are very low, however the level on individual proteins can change to a proportionally large degree during oxidative stress, an appropriate property for a signalling molecule. In addition, remarkably elevated levels occur in some pathologies, including atherosclerosis. As an initial and commonly formed product of protein oxidation, PB-DOPA is well placed for a signalling role, promoting a significant up-regulation of antioxidant defences in the early stages of oxidative stress, before extensive damage has occurred. As an initiator of antioxidant defences, PB-DOPA would be potentially useful as a therapeutic for the treatment of diseases involving oxidative stress or the accumulation of oxidative damage. The main objective of this thesis was, therefore, to examine the effect of PB-DOPA on the cellular antioxidant defence system using monocytic and macrophage-like cells, key cells involved in the formation of atherosclerotic plaques. The incorporation of free DOPA into protein during protein synthesis, a process previously shown to occur both in vitro and in vivo, was used to generate PB-DOPA. Neither free nor PB-DOPA were found to be toxic to monocytic or macrophage-like cells in culture, but rather were both capable of protecting these cells from oxidative stress. Free DOPA was shown to be capable of directly scavenging radicals, a process that was thought to be in part responsible for the protection induced during oxidative stress. The presence of free and PB-DOPA up-regulated the activity of catalase and NAD(P)H:quinone oxidoreductase, two enzymatic antioxidants, however the activity of superoxide dismutase and the concentration of oxidised and reduced glutathione were not affected. Whilst it was thought that PB-DOPA would have a specific effect on the activity of antioxidant defences targeted against protein oxidation, proteolysis and bulk chaperone activity were not affected by a combination of free and PB-DOPA. Oxidatively-induced protein aggregation, however, was inhibited by the presence of free and PB-DOPA, suggesting that a more specific chaperone regulation may be taking place. The regulation of gene and protein expression was thought to be one possible mechanism by which PB-DOPA could function as a signalling molecule. To test this hypothesis, the effect of free and PB-DOPA on transcription factor activation and protein expression were investigated. Free and PB-DOPA did not induce the expression or activation of Nrf2, AP-1 or NFJB, three transcription factors thought to be involved in the expressional regulation of genes involved in the antioxidant defence system. However, the expression of a number of proteins, including antioxidants, chaperones and proteins involved in cell cycle progression, were regulated in monocytic and macrophage-like cells following the administration of free DOPA under conditions that resulted in either a high or low level of PB-DOPA generation. The regulated proteins differed between the two conditions, suggesting that the level of PB-DOPA may be a key factor in determining the specific defences targeted. The results presented in this thesis support the hypothesis that PB-DOPA can function as a signalling molecule, triggering an enhancement of cellular antioxidant defences, with a specific role in the regulation of the chaperone system, a key defence targeted against protein oxidation. This thesis may provide the basis for the potential use of free or PB-DOPA as a therapeutic for diseases known to involve oxidative stress or oxidative damage, however more research will be required to determine if the effects demonstrated in this thesis are also capable of occurring in vivo.

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Nelson, Michelle Amy. "Protein bound 3,4 dihydroxyphenyalanine as a signal for enhanced antioxidant defences /." full text via ADT, 2008. http://erl.canberra.edu.au/public/adt-AUC20081209.125208/index.html.

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Mubarak, Bashayer Rashed A. "Control of anti-apoptotic and antioxidant pathways in neural cells." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8057.

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Oxidative stress is a feature of many chronic neurodegenerative diseases as well as a contributing factor in acute disorders including stroke. Fork head class of transcription factors (Foxos) play a key role in promoting oxidative stress-induced apoptosis in neurons through the upregulation of a number of pro-apoptotic genes. Here I demonstrate that synaptic NMDA receptor activity not only promotes Foxos nuclear exclusion but also suppresses the expression of Foxo1 in a PI3K-dependent fashion. I also found that Foxo1 is in fact, a Foxo target gene and that it is subject to a feed-forward inhibition by synaptic activity, which is thought to result in longerterm suppression of Foxo downstream gene expression than previously thought. The nuclear factor (erythroid 2-related) factor 2 (Nrf2) is another transcription factor involved in oxidative stress and the key regulator of many genes, whose products form important intrinsic antioxidant systems. In the CNS, artificial activation of Nrf2 in astrocytes has been shown to protect nearby neurons from oxidative insults. However, the extent to which Nrf2 in astrocytes could respond to endogenous signals such as mild oxidative stress is less clear. The data presented herein, demonstrate for the first time that endogenous Nrf2 could be activated by mild oxidative stress and that this activation is restricted to astrocytes. Contrary to the established dogma, I found that mild oxidative stress induces the astrocytic Nrf2 pathway in a manner distinct from the classical Keap1 antagonism employed by prototypical Nrf2 inducers. The mechanism was found to involve direct regulation of Nrf2's transactivation properties. Overall these results advance our knowledge of the molecular mechanism(s) associated with the control of endogenous antioxidant defences by physiological signals.

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Aucoin, Richard R. "Antioxidants and antioxidant enzymes as biochemical defenses against phototoxin ingestion by insect herbivores." Thesis, University of Ottawa (Canada), 1991. http://hdl.handle.net/10393/7679.

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Many secondary plant compounds are capable of photoactivation resulting in the production of toxic species of oxygen. One mechanism of defense for insects feeding on phototoxic plants may be the presence of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPOX), and glutathione reductase (GR). The activities of these enzymes were examined in larvae of three lepidoptera: Ostrinia nubilalis, Manduca sexta, and Anaitis plagiata. Highest levels of antioxidant enzyme activity were found in A. plagiata, a specialist feeder on Hypericum perforatum, which contains high levels of the phototoxin hypericin. Larvae of A. plagiata fed leaf discs treated with hypericin exhibited a short-term, concentration-dependent decline in enzyme activity. Longer term studies with A. plagiata fed either the phototoxic H. perforatum, or the closely related but non phototoxic H. calycinum, resulted in increased CAT and GR activity in larvae fed the phototoxic plant whereas superoxide dismutase activity was not significantly different. These results suggest that CAT and GR may be inducible defenses against phototoxins. Other insect defenses against phototoxins include specific biochemical defenses such as antioxidants. These antioxidant defenses eliminate or quench the deleterious singlet oxygen and free radicals formed by these phototoxins. We examined the role of dietary antioxidants in protecting the phototoxin-sensitive insect herbivore M. sexta. Elevated dietary levels of the lipid-soluble antioxidants beta-carotene and vitamin E resulted in a concentration-dependent reduction in the mortality associated with treatment of larvae with the phototoxic thiophene $\alpha$-T. Elevated levels of dietary ascorbic acid had no effect whereas reduced levels greatly increased the toxicity of $\alpha$-T. Tissue levels of antioxidants were shown to increase substantially in larvae fed antioxidant-supplemented diets. The results suggest that the ability to absorb and utilize plant-derived antioxidants could be an important defense against photo-activated plant secondary compounds and may have allowed some insects to exploit phototoxic plants. The effects of oxidative stress induced by $\alpha$-T at the biochemical level and the protective effect of antioxidants and antioxidant enzymes were also examined. The phototoxin $\alpha$-T strongly induced lipid peroxidation (LPO) in midgut tissues of the phototoxin-sensitive M. sexta in a UV-dependent manner, however this LPO was prevented when the compound was administered to larvae raised on high vitamin E diets. In the absence of UV, $\alpha$-T caused a significant increase in GPOX, GR, and non-GSH-dependent PER activity over 72 h. However in the presence of UV, $\alpha$-T strongly inhibited GPOX and GR and prevented the increase in PER. $\alpha$-T also affected cellular thiol status with approximately a 50% increase in total and GSH content in midgut tissue, although this was not UV-dependent. The effectiveness of antioxidant enzymes and the antioxidant GSH in providing protection against phototoxins were also examined. Neither the SOD inhibitor DEDC nor the CAT inhibitor 3AT affected the acute toxicity of topically applied $\alpha$-T to M. sexta larvae. The GSH-depleting agent BSO also had no effect on acute toxicity. In contrast, GSH depletion strongly enhanced the chronic (72 h) toxicity of $\alpha$-T when the phototoxin was incorporated into diets. GSH depletion also enhanced LPO in midgut tissue of $\alpha$-T-treated larvae. Implications of the results are discussed in terms of the role antioxidants and antioxidant enzymes may have played in the successful adaptation of some insect species to phototoxin-containing plants. The interrelationships of biochemical, physiological, physical, and behavioural mechanisms of defense are considered.

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Cardona, Emilie. "Influence de l'environnement trophique de l'élevage en biofloc sur les performances physiologiques de la crevette Litopenaeus stylirostris : Étude de paramètres de la nutrition, de l'immunité et de la reproduction." Thesis, Nouvelle Calédonie, 2015. http://www.theses.fr/2015NCAL0001/document.

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Le biofloc est un système d’élevage intensif avec un faible renouvellement d’eau ; ainsi se développe une population diversifiée de micro-organismes (micro-algues, zooplanctons et bactéries) associée à de la matière organique qui forme les floculats. Ces derniers jouent le double rôle de filtre biologique et de complément alimentaire. Cette thèse a pour objectif de mieux comprendre le fonctionnement de ce système d’élevage et ses interactions avec la crevette Litopenaeus stylirostris. Dans cet objectif général s’inscrit deux objectifs plus spécifiques : (i) mesurer les gains zootechniques apportés par l’élevage en biofloc (ii) étudier les interactions trophiques entre le milieu d’élevage et la crevette en lien avec les performances zootechniques. Nos résultats montrent des gains relatifs de l’élevage en biofloc aux niveaux de la survie, de la croissance, des performances de reproduction des femelles et de la qualité de leur progéniture. Ces meilleures performances s’expliquent par la contribution de la productivité naturelle, estimée entre 37 et 40%, dans l’alimentation de la crevette. Ce complément d’aliment, outre d’être toujours disponible dans le milieu d’élevage, apporte de l’énergie, des nutriments et des molécules bioactives. L’aliment naturel représente une source nutritive de lipides, particulièrement riche en phospholipides et en acides gras polyinsaturés, qui sont essentiels pour la reproduction et le développement des larves en phase de lécitotrophie ; ces lipides sont accumulés dans la glande digestive et les œufs des femelles élevées en biofloc. L’aliment naturel est également une source de glutathion, puissante molécule antioxydante, qui contribue au renforcement du système des défenses anti-radicalaires de la crevette et protège les lipides insaturés de la peroxydation, une cause du stress oxydant. Les bactéries sont prépondérantes dans la productivité naturelle d’un élevage en biofloc et contribuent donc à l’alimentation de la crevette. Aussi, dans le dernier volet de cette thèse, nous avons caractérisé la diversité taxonomique et l’abondance des bactéries du milieu d’élevage et montré son influence sur le microbiote intestinal des crevettes. De façon générale, nous observons une meilleure santé des animaux élevés en biofloc qui se traduit par une régulation positive des gènes impliqués dans l’immunité et les défenses anti-radicalaires après un stress au peroxyde d’hydrogène. Ainsi, les effets positifs de l’élevage en biofloc sur les survies, les croissances et la reproduction ont pour origine le complément d’aliment apporté par la productivité naturelle
Biofloc is an intensive rearing system with zero or minimal water exchange where a diverse population of microorganisms (microalgae, zooplankton and bacteria) develops in association with organic matter to form the floc particles. These particles play the double role of biological filter and dietary supplement. This dissertation aims to better understand the process of this rearing system and its interactions with the Litopenaeus stylirostris shrimp. Two specific objectives were integrated within the framework of this general objective: (i) to measure the production gain from biofloc rearing and (ii) to study the interaction between biofloc environment and shrimp and to assess its role on production performances of shrimps. Thus, our results show production gains of shrimp reared in biofloc in terms of survival, growth, reproductive performances and quality of larvae. This better performance can be explained by the contribution of natural productivity, estimated between 37 and 40%, in shrimp food. This food supplement, constantly available in the environment, provides energy, nutrients and bioactive molecules. The natural productivity represents a source of lipids, in particular of phospholipids and polyunsaturated fatty acids, which were essential for the reproduction and development of larvae during the lecitotrophic stage; these lipids were accumulated in digestive gland and eggs from females reared in biofloc. The natural food is also a glutathione source, a powerful antioxidant molecule, which contributes to strengthen antioxidant defense system of shrimps and protects lipids against peroxidation, a cause of oxidative stress. Bacteria were dominant in natural productivity of biofloc environment and contribute to shrimp food. Thus, in the last part of this dissertation, we characterized the taxonomic diversity and abundance of bacteria in biofloc environment and showed their influence on shrimp intestinal microbiota. Generally, we observed a better health of biofloc resulting in up-regulation of the studied genes involved in immunity and anti-radical defenses after oxidative stress with hydrogen peroxide. The positive effects of biofloc rearing on survival, growth and reproduction originate from food complement provided by natural productivity

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Dallaqua, Bruna [UNESP]. "Intervenção com Azadirachta indica (Neem) na prenhez de ratas diabéticas: repercussões materno-fetais." Universidade Estadual Paulista (UNESP), 2011. http://hdl.handle.net/11449/99186.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Diabetes mellitus (DM) é uma síndrome de etiologia múltipla caracterizada por hiperglicemia crônica. Esta hiperglicemia induz o aumento na produção de espécies reativas de oxigênio (ERO) e diminuição das defesas antioxidantes. Devido às complicações causadas pelo diabete, muitos indivíduos optam por terapias alternativas à base de plantas medicinais para amenizar seus efeitos. Sendo assim, nesta revisão de literatura, foram analisados e descritos diversos trabalhos experimentais com a utilização de animais diabéticos para comprovar os efeitos antioxidantes de algumas dessas plantas e verificar se os títulos e resumos disponibilizados nos artigos são compatíveis aos objetivos de nossa busca
Diabetes mellitus (DM) is a syndrome of multiple etiologies characterized by chronic hyperglycemia. This hyperglycemia induces increased production of reactive oxygen species (ROS) and decreased antioxidant defenses. Due to complications caused by diabetes, many people choose for alternative therapies and herbal medicine to alleviate its effects. Thus, in this literature review, several experimental studies with the use of diabetic animals were analyzed to demonstrate the antioxidant effects of some plants and to verify if the titles and abstracts provided in the articles are compatible to the aims of our search

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Bond, Jennifer M. "Investigations on antioxidant defence proteins and peptides." Thesis, Cranfield University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278723.

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10

Thornley, Andrew Charles. "Antioxidant defence and autoxidative damage in neoplastic disease." Thesis, University of Surrey, 1987. http://epubs.surrey.ac.uk/848118/.

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The principal factors governing antioxidant defence and lipid peroxidation in vitro have been determined for neoplastic and normal tissues, from mice, bearing Lewis lung carcinomas. These parameters were measured at varying intervals after the intramuscular transplantation of Lewis lung carcinoma cells in C57BL6 mice. The activities of glutathione peroxidase (EC 1.11.1.9), superoxide dismutase (EC. 1.15.1.1), gamma glutamylcysteine synthetase (EC 6.3.2.2), and catalase (EC. 1.11.1.6) were similar in tumour tissue to those of lung, the tissue of origin. Glutathione reductase (EC. 1.6.4.2) and glutathione-S-transferase (EC. 2.5.1.18) activities were considerably greater than those of lung. Gamma-glutamyltranspeptidase (EC 2.3.2.2) activity was about 25% of the corresponding value in murine lung. Lewis lung carcinoma tissue contained considerable quantities of lipid peroxide (as determined by the thiobarbituric acid test). The in vitro lipid peroxidation of tumour microsomes was less than that of pulmonary tissue. Tissue from the tumour "core" had significantly greater reduced glutathione concentration, lower mitochondrial superoxide dismutase, glutathione peroxidase and gamma-glutamyltranspeptidase activities, and lower lipoperoxide concentration than the periphery. Glutathione peroxidase, gamma glutamylcysteine synthetase and superoxide dismutase activities from Lewis lung carcinoma cells in monolayer culture (18% O[2] concentration) were greater than those of solid tumour. Histological sections of lung and liver from Lewis lung carcinoma- bearing mice were found to have many pathological changes. The livers of tumour-bearing mice had raised glutathione and DNA concentrations, and increased glutathione reductase, glutathione-S-transferase and gamma-glutamyltranspeptidase activities; hepatic catalase and mitochondrial glutathione peroxidase activities were decreased. Hepatic microsomes from carcinoma-bearing mice had increased thiobarbituric acid-reactivity and were more susceptible to iron/ascorbate lipid peroxidation. Storage, as a suspension in a glycerol-containing phosphate buffer at -80°C, conferred resistance to in vitro lipid peroxidation to liver microsomes from healthy animals, but not to those from tumour-bearing mice. Disturbances in Lewis lung carcinoma-bearing mice could generally only be determined at 9 or more days after tumour cell implantation, when the tumour was just palpable. The livers of genetically obese C57BL6 mice had some similar biochemical characteristics to those of tumour-bearing hosts. Kidney and erythrocytes of Lewis lung carcinoma-bearing mice, and tissues of mice, bearing B16 melanomas, also displayed perturbations of antioxidant defence and lipid peroxidation. The significance of the above observations is discussed. Further experiments are suggested to improve the understanding of the role of autoxidation and antioxidant defence in neoplastic disease.

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Budde, Heike. "Antioxidant defense in Trypanosoma brucei brucei." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968912192.

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Macedo, Giulianna Echeverria. "Ação de Senecio brasiliensis (spreng) Less sobre a taxa de eclosão e modulação de marcadores de toxicidade em larvas de Drosophila Melanogaster." Universidade Federal do Pampa, 2017. http://dspace.unipampa.edu.br:8080/xmlui/handle/riu/1451.

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Submitted by Ana Damasceno (ana.damasceno@unipampa.edu.br) on 2017-05-09T18:30:20Z No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Ação de Senecio brasiliensis (spreng) Less sobre a taxa de eclosão e modulação de marcadores de toxicidade em larvas de Drosophila Melanogaster.pdf: 2537151 bytes, checksum: c5213c1eaff7c1ecdeaf706e6ced1e1a (MD5)
Made available in DSpace on 2017-05-09T18:30:20Z (GMT). No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Ação de Senecio brasiliensis (spreng) Less sobre a taxa de eclosão e modulação de marcadores de toxicidade em larvas de Drosophila Melanogaster.pdf: 2537151 bytes, checksum: c5213c1eaff7c1ecdeaf706e6ced1e1a (MD5) Previous issue date: 2017-03-02
O Brasil apresenta uma rica biodiversidade, sendo que muitas das espécies aqui encontradas tem servido como fonte de compostos com propriedades únicas tanto na medicina como na área biotecnológica. Muitos destes compostos são sintetizados a partir do metabolismo secundário vegetal e nas plantas atuam como atrativos ou mecanismos de defesa. Pesquisas relacionadas com os potenciais das plantas são necessárias para um melhor entendimento das propriedades biológicas que apresentam. Senecio brasiliensis (Spreng) Less., é uma espécie vegetal conhecida popularmente como “maria mole”, presente em pastagens da região Sul do país, sendo suas folhas consumidas pelos animais e capaz de causar hepatotoxicidade. Tal toxicidade se deve ao seu metabolismo secundário, responsável pela síntese de metabólitos tóxicos, principalmente os alcaloides pirrolizidínicos. A espécie é utilizada popularmente para fins medicinais, e possui demonstrada ação tóxica em insetos. Em vista de sua toxicidade e potencial biotecnológico, um estudo mais completo de sua ação se faz necessário. Neste trabalho avaliou-se o efeito biológico da exposição do extrato hidroalcoólico das folhas de Senecio brasiliensis (EHSB) no modelo experimental de Drosophila melanogaster. A análise do perfil fitoquímico do EHSB demonstrou a presença de ácidos fenólicos e flavonoides, e atividade antioxidante in vitro através dos ensaios de ABTS, DPPH, fenóis totais e FRAP. Em ensaios in vivo, EHSB não causou mortalidade de moscas na fase adulta, entretanto a taxa de eclosão foi significativamente diminuída quando as moscas desenvolveram-se em meio de cultura contendo 1 mg/mL de EHSB. Nas larvas do terceiro ínstar observaram-se diminuição da viabilidade celular, aumento da atividade das enzimas antioxidantes GST e SOD, EROs, e diminuição da CAT e aumento da razão GSH/GSSG. Houve aumento na expressão dos genes Nrf2, TrxR, CAT, Drice e Dilp6, e diminuição da fosforilação de proteínas quinases JNK1/2, ERK2 e p38MAPK e AKT, além de um aumento na clivagem de PARP, em paralelo com aumento da atividade de caspase 3/7. Também observou-se uma diminuição nos níveis de glicose, glicogênio e triglicerídeos. O aumento da expressão gênica de Nrf2, da atividade das enzimas GST e SOD e razão GSH/GSSG servem como um indicativo de um estado de estresse oxidativo ocasionado pelo EHSB e atuação da defesa antioxidante das larvas. A diminuição nos níveis de glicose, glicogênio e triglicerídeos pode indicar uma diminuição na reserva energética necessária para fases posteriores ao desenvolvimento larval, como para a eclosão em indivíduo alado, podendo isto ser ocasionado pela inibição da fosforilação de proteínas de transdução de sinal envolvidas neste processo pela diminuição do ATP. Dessa forma, nossos resultados demonstram a toxicidade do HESB e sua capacidade em induzir marcadores de estresse oxidativo e apoptose celular, prejudicando o desenvolvimento de larvas de D. melanogaster e processo de eclosão de moscas adultas.
Brazil has a high biodiversity, and many species found here are source of compounds with unique medicinal and biotechnological properties. These compounds are synthetized by plants secondary metabolism and can act as attractive or defensive to other species. Thus, studies with plant species are necessary to knowledge about their biologial properties. Senecio brasiliensis (Spreng) Less., is a native species popularly known as “maria mole” and is found in pastures of the south region of the country, its leaves serving as food to animals and are able to cause hepatotoxicity due to its secondary metabolism, responsible for the synthesis of toxic metabolites, such as pirrolizidinic alkaloids. In spite of its documented toxicity, this plant is used by Brazilian folk with medicinal purposes. In this study, we have evaluated the biological effects to hydroalcoholic extract of leaves of S. brasiliensis (HESB) exposure in Drosophila melanogaster experimental model. The fruit fly D. melanogaster is an advantageous alternative model useful for the screening of natural substances. Phytochemical constitution of HESB showed the presence of phenolic acids and flavonoids but when comparing with other species, it presented a lower in vitro antioxidant activity by ABTS, DPPH, FRAP assays. Survival and locomotor activity of adult flies was unaltered by extract. Nevertheless, we have observed a significant decreasing in eclosion rate of flies, since its embryonic period at 1 mg/mL concentration of HESB. Biochemical and molecular parameters revealed significant changes in third instar larvae of D. melanogaster exposed to 1 mg/mL of HESB such as decreased cell viability, stimulation of the activity of antioxidant enzymes SOD and GST, decreasing of CAT, and increasing in GSH/GSSG ratio. The mRNA expression of Nrf2, TrxR, CAT, Drice and Dilp6 were also significantly up-regulated. Decreasing in the phosphorylation of JNK1/2, ERK2, p38MAPK and AKT protein kinases were verified. Apoptotic cell death was inducted by extract. This fact was attested PARP cleavage, in parallel with increasing of caspases 3/7 activity. The increased expression of Nrf2, augmented activity of GST and SOD enzymes activities, and GSH/GSSG ratio in parallel with induction of ROS formation, is an indicative of a state of oxidative stress caused by the HESB and the action of the antioxidant defense of the larvae. It was also observed a decreasing in glucose, glycogen and triglycerides levels indicating a diminution in the energetic reserve required for later stages of larval development, such as for eclosion of winged individuals. Therefore, our results demonstrated of the HESB toxicity and its capacity to induce of cell stress markers and of apoptotic cell death impairing thus the development of D. melanogaster larvae and eclosion process of adult flies.

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Dallaqua, Bruna. "Intervenção com Azadirachta indica (Neem) na prenhez de ratas diabéticas : repercussões materno-fetais /." Botucatu : [s.n.], 2011. http://hdl.handle.net/11449/99186.

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Orientador: Débora Cristina Damasceno
Coorientador: Tiago Rodrigues
Banca: Kleber Eduardo de Campos
Banca: Emilio Herrera
Resumo: Diabetes mellitus (DM) é uma síndrome de etiologia múltipla caracterizada por hiperglicemia crônica. Esta hiperglicemia induz o aumento na produção de espécies reativas de oxigênio (ERO) e diminuição das defesas antioxidantes. Devido às complicações causadas pelo diabete, muitos indivíduos optam por terapias alternativas à base de plantas medicinais para amenizar seus efeitos. Sendo assim, nesta revisão de literatura, foram analisados e descritos diversos trabalhos experimentais com a utilização de animais diabéticos para comprovar os efeitos antioxidantes de algumas dessas plantas e verificar se os títulos e resumos disponibilizados nos artigos são compatíveis aos objetivos de nossa busca
Abstract: Diabetes mellitus (DM) is a syndrome of multiple etiologies characterized by chronic hyperglycemia. This hyperglycemia induces increased production of reactive oxygen species (ROS) and decreased antioxidant defenses. Due to complications caused by diabetes, many people choose for alternative therapies and herbal medicine to alleviate its effects. Thus, in this literature review, several experimental studies with the use of diabetic animals were analyzed to demonstrate the antioxidant effects of some plants and to verify if the titles and abstracts provided in the articles are compatible to the aims of our search
Mestre

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Xia, Ling. "Regeneration of the antioxidant ubiquinol by flavoenzymes and the role of antioxidant defence in experimental hepatocarcinogenesis /." Stockholm : [Karolinska institutets bibl.], 2002. http://diss.kib.ki.se/2002/91-7349-244-2.

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Gunnarsson, Thomas. "The role of antioxidant defence in models of vascular function." Thesis, Queen Mary, University of London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404338.

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Carville, David Gerald Michael. "The effect of copper status on blood antioxidant defence enzymes." Thesis, University of Ulster, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328211.

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MOREIRA, Vanessa Ribeiro. "ANTIMONIATO DE MEGLUMINA (GLUCANTIME®) CAUSA DANOS AO DNA POR ESTRESSE OXIDATIVO E INDUZ SUPEREXPRESSÃO DE GENES ENVOLVIDOS NA DEFESA ANTIOXIDANTE E REPARO DO DNA." Universidade Federal do Maranhão, 2017. http://tedebc.ufma.br:8080/jspui/handle/tede/1767.

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FAPEMA, CAPES
Leishmaniasis is a neglected disease caused by more than 20 species of parasites of the Leishmania genus. Pentavalent antimonials are the drugs commonly used for the treatment of leishmaniasi and among then Glucantime® is the first choice drug recommended by the World Health Organization. Its toxic effects are well known, including as genetic damage inducing. However, the mechanism of its genotoxic effect has not been elucidated yet. Given this, we investigated the mechanism by which Glucantime® causes damage to DNA in BALB/c mice infected with Leishmania (Leishmania) infantum, treated with 20mg/kg/day during 20 days. Damage to DNA have been assessed by the comet assay using peripheral blood leukocytes and for assessment of oxidative damage, the comet assay was followed by treatment with the enzymes formamidopyrimidine-DNA-glycosylase (Fpg) and endonuclease III (ENDO III), which recognize and remove oxidized purines and pyrimidines of DNA. The mutagenic potential of the drug was investigated by the micronucleus test in bone marrow cells. The consequences of the oxidative process were measured by the activity of the enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). In addition, we evaluated the expression of genes related to antioxidante defense (GSS, GSTP1, GPx1, SOD1, SOD2 and CAT) and to the DNA repair system (OGG1 and MTH1). Our data demonstrated that Glucantime® causes damage to DNA in mammalian cells by oxidating the nitrogenous bases. The increased frequency of micronucleated cells in animals treated with antileishmanial revealed that the genomic instability was fixed in mutations. In addition, Glucantime® induced overexpression of genes related to the antioxidant defense, as well as the genes OGG1 and MTH1, that work in the DNA repair mechanism of damage caused by oxidation of nitrogen bases. Our data also revealed that infection by L. infantum and the treatment with antimonial significantly increased the enzymatic activity in the SOD-CAT axis, while the SOD-GPx axis was inhibited, probably by the depletion of glutathione. Thus, our data suggests that the antimonial pledges to GPx leading to saturation of the antioxidant system and causes damage to DNA through oxidative stress. These findings were supported by the reduction of genetic damage thought a treatment combined with ascorbic acid, a potent antioxidant. At last, we demonstrated that the stressfull effect of Glucantime® triggers a molecular response in mammalian cells, positively modulating the expression. Of genes related to DNA repair and antioxidant defense.
Leishmaniose é uma doença negligenciada causada por mais de 20 espécies de parasitas do gênero Leishmania. Antimoniais pentavalentes são os fármacos normalmente utilizados para o tratamento das leishmanioses e, dentre estes, o Glucantime® é a droga de primeira escolha recomendada pela Organização Mundial de Saúde. São bastante conhecidos seus efeitos tóxicos, inclusive como indutor de danos genéticos. Entretanto, o mecanismo pelo qual o fármaco exerce seu efeito genotóxico ainda não está elucidado. Nesse sentido, investigamos o mecanismo pelo qual o Glucantime® causa danos ao DNA em camundongos BALB/c infectados com Leishmania (Leishmania) infantum, com regime de tratamento de 20mg/kg/dia durante 20 dias. Danos ao DNA foram avaliados pelo ensaio do cometa usando leucócitos de sangue periférico e, para avaliação de danos oxidativos, o ensaio do cometa foi seguido pelo tratamento com as enzimas formamidopirimidina-DNA-glicosilase (Fpg) e endonuclease III (ENDO III), que reconhecem e retiram bases púricas e pirimídicas oxidadas do DNA. O potencial mutagênico da droga foi investigado pelo teste do micronúcleo em células de medula óssea. As consequências do processo oxidativo foram medidas pela atividade das enzimas superóxido dismutase (SOD), catalase (CAT) e glutationa peroxidase (GPx). Além disso, avaliamos a expressão de genes relacionados à defesa antioxidante (GSS, GSTP1, GPx1, SOD1, SOD2 e CAT) e ao sistema de reparo do DNA (OGG1 e MTH1). Nossos dados demonstraram que o Glucantime® causa danos ao DNA em células de mamíferos pela oxidação das suas bases nitrogenadas. O aumento da frequência de células micronucleadas nos animais sob tratamento com o antileishmanial revelou que a instabilidade genômica foi fixada em mutações. Além disso, o Glucantime® induziu a superexpressão de genes relacionados a defesa antioxidante, bem como dos genes OGG1 e MTH1, que atuam no mecanismo de reparo de danos ao DNA ocasionados por oxidação de bases nitrogenadas. Os nossos dados revelaram também que a infecção por L. infantum e o tratamento com o antimonial aumentou significativamente a atividade enzimática no eixo SOD-CAT, enquanto que o eixo SOD-GPx foi inibido, provavelmente, pela depleção de glutationa. Assim, nossos dados sugerem que o antimonial Glucantime® compromete a atividade da GPx levando a saturação do sistema antioxidante e causa danos ao DNA por estresse oxidativo. Esses achados foram corroborados pela redução dos danos genéticos pelo co-tratamento com o ácido ascórbico, um potente antioxidante. Finalmente, demonstramos que o efeito estressante do Glucantime® dispara uma resposta molecular nas células de mamíferos, modulando positivamente a expressão de genes relacionados ao reparo do DNA e à defesa antioxidante.

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Arc-Chagnaud, Coralie. "Regulation of antioxidant defenses in the prevention of skeletal muscle deconditioning." Thesis, Montpellier, 2019. http://www.theses.fr/2019MONT4005.

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Le système musculaire joue un rôle primordial dans l’homéostasie de l’organisme. Il est impliqué dans différentes fonctions indispensables aux activités de la vie quotidienne telles que la production de mouvement, la locomotion, le maintien postural et l’équilibre. La qualité du tissu musculaire est donc primordiale dans le maintien de la qualité de vie et, à long terme, à la longévité. L'hypoactivité et le vieillissement sont deux situations qui entraînent le déconditionnement musculaire, et qui partagent une caractéristique commune: une perte de force musculaire, une atrophie et la modification du typage musculaire, ainsi que l'accumulation de tissu adipeux intramusculaire. Aujourd'hui, il existe de nombreuses données dans la littérature indiquant un lien entre le stress oxydant et le déconditionnement musculaire. Le but de cette thèse était d'évaluer l'impact de la modulation des défenses antioxydantes sur la prévention du déconditionnement musculaire. Cela a été étudié sous deux angles, l'un dans le contexte du vieillissement, et le second dans un contexte d'hypoactivité. La première étude avait pour but d'évaluer la fragilité chez un modèle souris âgées, utilisant un groupe de souris WT et un groupe de souris transgéniques sur-exprimant l'enzyme G6PD. Nous avons évalué des paramètres de qualité musculaire et de stress oxydant et avons réalisé une analyse transcriptomique à partir d'échantillons musculaires des souris de chacun des deux groupes. La seconde étude a été conduite dans le but d'évaluer les effets d'un cocktail enrichi en composés anti-oxydants et anti-inflammatoires, durant deux mois d'hypoactivité (modèle Bedrest). Nos résultats ont démontré l’inefficacité de cette supplémentation sur la prévention de la perte de masse et de force musculaire. De plus, les données concernant les mécanismes moléculaires ont démontré une altération des processus de récupération chez les sujets supplémentés.Les conclusions de nos études donnent des pistes sur les stratégies anti-oxydantes les plus appropriées contre le déconditionnement musculaire. Il semble préférable de intéresser à la stimulation des systèmes de défenses endogènes, plutôt que de se centrer sur une supplémentation nutritionnelle exogène. Néanmoins, la complexité des voies de signalisation redox requièrent une meilleure compréhension pour optimiser les mesures de prévention afin de limiter la perte de fonction musculaire
Musculoskeletal system plays a key role in organism’s well-functioning and is responsible for a large variety of functions such as posture, locomotion, balance, and activities of daily life. The quality of the skeletal muscle is therefore capital to maintain quality of life and, in the long term, survival. Hypoactivity and aging are two situations that cause skeletal muscle deconditioning, therefore sharing common characteristics: loss of muscle strength, muscular atrophy and MyHC redistribution, as well as IMAT accumulation. To date, there is plenty of evidence supporting a causative link between oxidative stress phenomenon and muscle deconditioning.The general aim of this PhD thesis was to evaluate the impact of the modulation of the antioxidant defenses on the prevention of muscle deconditioning. It has been studied from two perspectives, the first one in the context of aging and the second in the context of hypoactivity.The first study aimed to evaluate frailty in old female animals, using WT and G6PD-overexpressing mice. We evaluated muscle quality parameters and oxidative stress markers. Finally, we performed a transcriptomic analysis of muscle samples and highlighted differentially expressed genes in both groups of mice.The second study was conducted to evaluate the effects of a cocktail enriched in antioxidant/anti-inflammatory molecules in a 2-month hypoactivity experiment (Bedrest model). Our results clearly demonstrate the ineffectiveness of this type of supplementation in the prevention of muscle mass and strength loss. Moreover, data regarding muscle molecular mechanisms highlight an alteration of recovery processes in the supplemented subjects.Finally, the conclusions of our two studies gave clues on the suitable antioxidant modulation strategy for the prevention of skeletal muscle deconditioning. It seems preferable to focus on the stimulation of endogenous defense system whether than towards exogenous supply of nutritional antioxidants. Nevertheless, the complexity of redox signaling requires better understanding to optimize countermeasures in muscle wasting situations

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Zhang, Zhi Jun. "Investigation into membrane lipid peroxidation and antioxidant defence enzymes in schizophrenia." Thesis, University of Sheffield, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310764.

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Zitouni, Karima. "Ethnic differences in antioxidant defence in patients with type 2 diabetes." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1446823/.

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Objective: Throughout the Western World, the incidence of end-stage renal disease (ESRD) due to diabetes mellitus is 4-6 times greater in patients of Afro-Caribbean origin compared with Caucasians. The mechanism of increased susceptibility to renal failure in patients of Afro-Caribbean origin is poorly understood. Even after adjusting for the higher prevalence of diabetes and hypertension. An increase in oxidative stress is considered to promote the development of long-term complications in diabetes mellitus. This may be a factor in the increased susceptibility to nephropathy in patients of Afro-Caribbean compared with Caucasians in the United Kingdom. The objective of this study was to examine the plasma antioxidant defence system in relation to the presence or absence of microalbuminuria and smoking habits in Afro-Caribbean patients and Caucasians. Studied population: Type 2 diabetic patients (n=80; Afro-Caribbean: n=35 and Caucasian: n= 45) with mean age of 65 years and mean duration of diabetes of 14.2 years, were recruited. Of these patients, 46 patients had normoalbuminuria and 34 patients had microalbuminuria. Results: Afro-Caribbean patients exhibited lower vitamin E, glutathione and total thiols Compared to Caucasian patients. Afro-Caribbean patients also showed higher superoxide dismutase and lower glutathione peroxidase activities compared to Caucasian patients. Plasma dehydroascorbate was elevated in the Afro-Caribbean patients when compared to Caucasians. Total antioxidant capacity as assessed by HOCl and O2- quenching of pholasin chemilumenescence was elevated in the Afro-Caribbean patients compared to Caucasians. Conclusions: Overall this study has revealed that African descent is a determinant of impaired antioxidant defence systems. Lower vitamin E, glutathione and total thiol levels that simultaneously coincided with elevated dehydroascorbate levels and increased SOD and lower GPx activities suggests that Africans experience enhanced oxidative stress compared with Caucasians. These findings may partially explain the increased susceptibility of Afro-Caribbean diabetic patients to kidney failure compared to Caucasians.

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Botelho, Marina Tenorio. "Biomarcadores na avaliação do estado fisiológico de juvenis de beijupirás, Rachycentron canadum (Linnaeus, 1766), de cultivo." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/21/21134/tde-11102017-104906/.

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A aquicultura é uma indústria em franco desenvolvimento no mundo todo, apesar de a criação de peixes marinhos no Brasil ainda estar aquém do seu potencial. O beijupirá (Rachycentron canadum) é uma espécie que vem despertando interesse dos criadores, devido às suas altas taxas de crescimento, adaptabilidade ao cultivo e aceitação no mercado. As condições de cultura intensiva podem gerar fatores de estresse aos organismos que afetam seu estado fisiológico. Neste trabalho, beijupirás foram cultivados em dois sistemas de criação diferentes, um tanque indoor com sistema de circulação de água aberto e um tanque-rede costeiro, e parâmetros genotóxicos, morfométricos e a atividade de enzimas da defesa antioxidante foram comparados ao final de um período de 11 semanas de criação. Não houve diferenças significativas nas taxas de crescimento dos dois tanques, porém o ensaio cometa e o de micronúcleo e demais anormalidades nucleares detectaram um maior dano ao DNA e uma maior frequência de anormalidades nucleares nos peixes mantidos no tanque indoor. Esses ensaios mostraram-se muito sensíveis para observar o estado fisiológico de beijupirás em cativeiro. A expressão da proteína p53, que é relacionada a integridade do DNA, foi detectada por imuno-histoquímica e não apresentou diferenças significativas entre os dois tanques, porém o valor da sua expressão foi alto, podendo indicar que a p53 estava ativada para regular os danos ao DNA já existentes e detectados pelo ensaio cometa. A atividade das enzimas superóxido dismutase (SOD), glutationa peroxidase (GPx) e catalase também não apresentaram diferenças significativas entre os peixes dos dois tanques. A atividade destas enzimas precisa ser melhor estudada, pois não há um padrão de respostas conhecido para as diversas espécies de peixes já estudadas. Também foi realizada uma exposição de beijupirás à β-naftoflavona (BNF) nas concentrações 2mg/kg e 10mg/kg em condições controladas de laboratório para compreender melhor os mecanismos de resposta desta espécie a um composto reconhecidamente tóxico. Foram avaliados parâmetros genotóxicos e enzimas relacionadas à defesa antioxidante. O ensaio cometa não detectou diferenças significativas no dano ao DNA entre os beijupirás dos controles e expostos à BNF, porém o ensaio de micronúcleo e demais anormalidades nucleares apresentou diferenças significativas entre os peixes expostos às duas concentrações em relação aos controles. Os danos detectados pelo ensaio cometa são quebras reparáveis que acontecem na fita de DNA, enquanto as anormalidades nucleares são danos permanentes, portanto, durante o período de exposição à BNF é possível que o tempo tenha sido suficiente para o reparo das quebras no DNA. Com relação às enzimas, apenas a catalase apresentou diferenças significativas de atividade, com uma inibição de atividade causada pela BNF em maior concentração em relação ao controle. Analisando-se os dois experimentos, as técnicas de ensaio cometa e micronúcleo e demais anormalidades nucleares indicaram serem as mais sensíveis para um monitoramento de beijupirás de cultivo, com a vantagem de não haver necessidade de sacrifício dos organismos. Ainda são necessários mais estudos com as enzimas da defesa antioxidante, em busca de um padrão na sua resposta a substâncias tóxicas.
The aquaculture production is continuously growing in the world, even though the marine fish cultures in Brazil are still smaller than its potential. The intention of rearing the cobia (Rachycentron canadum) species is currently increasing due to its high growth rates, adaptability to captivity and acceptance on the market. The intensive culturing conditions may cause stress to the organism, even affecting its physiological state. In this work, cobia has been reared in two different kinds of tanks: the first one was an indoor tank with open water circulation system and the other one was a near shore cage tank. Genotoxic and morphometric parameters and the activity of antioxidant defense enzymes were measured and compared at the end of 11 weeks of culturing. There weren\'t any significant differences between both tanks on the growth rate, but both the comet assay and the micronuclei and others nuclear abnormalities assay detected higher DNA damage and nuclear abnormalities frequency on the fish that were kept at the indoor tank. The comet and the nuclear abnormalities assays seem to be more sensitive to monitoring the physiological state of cobia during the culture. The protein p53, related to DNA integrity, expression was detected by immunohistochemical and didn\'t show significant differences, but the value of the expression was high, so it could indicate that p53 was activated to regulate the DNA damage that was detected by the comet assay. The activity of the enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase also didn\'t demonstrate any significant differences between the fish at any of the tanks. As there isn\'t any known response pattern for the several species of fish that have already been studied, more studies are necessary concerning these enzymes. In addition to the experiment already mentioned, cobia were exposed to β-naphthoflavone (BNF) at concentrations of 2mg/kg and 10mg/kg on laboratory controlled conditions to better understand the response mechanisms of this species to a toxic substance. The genotoxic parameters and the antioxidant defense enzymes activity were measured. The comet assay didn\'t detect any significant differences between the exposed to BNF and the control groups, however the nuclear abnormalities assay showed significant differences between the two exposed concentrations and the control groups. The DNA damages identified by the comet assay are breaks on the DNA strands, meanwhile, nuclear abnormalities are permanent damages. Therefore, during the exposed period it was possible that the time had been sufficient to repair the breaks on DNA. Catalase activity had significant differences with inhibition of the activity in cobia exposed to BNF of higher concentration, the others enzymes didn\'t demonstrate results with significant differences. Looking at both experiments, the comet assay and nuclear abnormalities assay seem to be the most sensitive to cobia\'s monitoring and they also have the advantage that there is no need to sacrifice the fish. Further studies on the antioxidant defense enzymes are needed in order to find a pattern on its response to toxic compounds.

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Silva, Maria Isabel Afonso da [UNESP]. "Alterações hematológicas e bioquímicas em uma população de Phrynops geoffroanus (Schweigger, 1812) em reposta a estressores ambientes." Universidade Estadual Paulista (UNESP), 2011. http://hdl.handle.net/11449/92533.

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Os quelônios estão entre os grupos de vertebrados com maior risco de extinção, sendo as principais ameaças para as populações, a degradação e poluição ambiental. A espécie Phrynops geoffroanus, popularmente conhecida como “Cágado-de-Barbelas”, tem se proliferado em ambiente poluído, sujeita a condições adversas que podem influenciar nos seus hábitos de vida e condições fisiológicas. Estudos que monitorem os efeitos da contaminação ambiental são fundamentais para o conhecimento da biologia da espécie e delineamento de estratégias de conservação efetivas. Deste modo, as análises dos parâmetros hematológicos e bioquímicos mostram-se importantes na avaliação da saúde de animais silvestres e riscos para o animal e ecossistema. O objetivo do trabalho foi verificar a influência do ambiente na fisiologia de uma população de Phrynops geoffroanus por meio da avaliação da capacidade antioxidante e respostas aos estressores ambientais, em comparação com espécimes de local sob condições controladas. Foram avaliadas, por meio do hemograma completo, dosagem de espécies reativas ao ácido tiobarbitúrico (TBARS), ensaio da capacidade antioxidante em equivalência ao Trolox (TEAC) e atividades das enzimas antioxidantes catalase e glicose-6-fosfato desidrogenase (G6PDH), amostras sanguíneas de sessenta espécimes, sendo trinta provenientes do córrego Felicidade, ambiente poluído, no perímetro urbano de São José do Rio Preto-SP; e trinta do criatório “Reginaldo Uvo Leone”, Tabapuã-SP, local sob condições controladas, cujas amostras constituem o grupo controle dos experimentos. Houve grande variação nos parâmetros hematológicos de Phrynops geoffroanus de ambiente urbano. Os valores de glóbulos vermelhos e hemoglobina foram significantemente menores que os observados em animais do criatório (p = 0,0004; p = 0,0371, respectivamente)...
The turtles are among the most endangered vertebrates groups, and the main threats to populations are the environmental pollution and degradation. The species Phrynops geoffroanus, popularly known as Geoffroy's side-necked turtle, has proliferated in polluted environments, subject to adverse conditions that could influence their living habits and physiological conditions. Studies that monitor the effects of environmental pollution are the key to understand the species biology and design effective conservation strategies. Thus, the analysis of hematological and biochemical parameters showed to be important in assessing the health of wild animals and for the animal and ecosystem risks. This work aimed to assess the environmental influence on the physiology of a Phrynops geoffroanus population through the evaluation of antioxidant status and responses to environmental stressors, compared to specimens from a place under controlled conditions. They were evaluated by hemogram, measuring thiobarbituric acid reactive species assay (TBARS), Trolox-equivalent antioxidant capacity evaluation (TEAC) and the activities of antioxidant enzymes, catalase and glucose-6-phosphate dehydrogenase (G6PDH), blood samples of sixty specimens, thirty from the Felicidade stream, polluted environment, within the São José do Rio Preto city, and thirty from the Reginaldo Uvo Leone breeding farm, Tabapuã-SP, place under controlled conditions, whose samples constitute the control group of the experiments. There was a wide variation in hematological parameters of Phrynops geoffroanus from the urban environment. The red blood cells and hemoglobin values were significantly less than those observed in animals from breeding farm (p = 0.0004; p = 0.0371, respectively). There was significant increase of thrombocytes (p < 0.0001) and leukocytes (p < 0.0001) to the animals from the Felicidade stream... (Complete abstract click electronic access below)

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Fisher, Gordon Pascoe David D. "Oxidative stress and antioxidant defenses in lymphocytes following high intensity interval training." Auburn, Ala., 2009. http://hdl.handle.net/10415/2003.

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Pês, Tanise da Silva. "EFEITO DA DIETA ENRIQUECIDA COM RUTINA SOBRE OS PARÂMETROS SANGUÍNEOS E BIOMARCADORES OXIDATIVOS EM JUNDIÁS (Rhamdia quelen)." Universidade Federal de Santa Maria, 2014. http://repositorio.ufsm.br/handle/1/9010.

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Silver catfish, Rhamdia quelen, is one of the most cultivated fish species in southern Brazil. Products destined for improving rearing and production of this species are required due to its importance for aquaculture. Oxidative stress (OS) is one of the main challenges in fish culture, so the use of compounds with antioxidant capacity may be valuable. The flavonoid rutin has several beneficial effects and represents an important alternative to reduce the physiological changes that arise from rearing-related stress. This study evaluated the influence of three diets containing rutin (0, 0.15 and 0.30 % rutin) on blood parameters and the antioxidant response of silver catfish. After a 21-day feeding period, blood was withdrawn for biochemical analysis and determination of plasma cortisol levels. The fish were then euthanized for sampling of the brain, gills, liver, kidney and muscle. Biomarkers of OS, thiobarbituric reactive substances (TBARS), lipid hydroperoxides (LOOH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), content of non-protein thiol groups (NPSH), content of ascorbic acid (AA) and total antioxidant capacity (TRAP) were determined. Fish fed the diet having 0.15 % rutin had lower cortisol levels compared to control. Nonetheless, the diet with rutin did not affect the hematological parameters. The levels of lipid peroxidation measured by determination of TBARS and LOOH in the brain, gills, liver and muscle decreased in the fish fed the diet containing rutin; in the kidney, however, only the levels of LOOH were reduced in these fish. When compared to control, the rutin-enriched diet increased the activity of SOD, CAT, NPSH content, AA and TRAP in the brain, GST and TRAP in the gills, SOD, CAT, GST, NPSH content, AA and TRAP in the liver, CAT, GST and TRAP in the kidney, and GPx, NPSH content, AA and TRAP in the muscle. In conclusion, these results suggest that rutin supplementation in silver catfish diet is recommended because it increases the tissue antioxidant response, thus preventing oxidative damage.
O jundiá, Rhamdia quelen, é uma das espécies mais cultivadas no sul do Brasil. Produtos destinados a melhorar o cultivo e produção do jundiá são necessários devido à importância desta espécie para a aquicultura. O estresse oxidativo (OS, do inglês oxidative stress) é um dos principais desafios no domínio da piscicultura, portanto a utilização de compostos com capacidade antioxidante pode ser útil. O flavonoide rutina tem vários efeitos benéficos e torna-se uma alternativa importante a fim de reduzir as alterações fisiológicas resultantes do estresse atrelado ao cultivo. Este estudo avaliou a influência de três dietas contendo a rutina (0, 0,15 e 0,30 % rutina) sobre os parâmetros sanguíneos e resposta antioxidante em jundiás. Após um período de 21 dias de alimentação, o sangue foi coletado para a análise sanguínea. Os peixes foram então eutanasiados para amostragem do encéfalo, brânquias, fígado, rim e músculo. Uma alíquota de sangue foi amostrada para a análise bioquímica e do cortisol plasmático. Os biomarcadores de OS, substâncias que reagem ao ácido tiobarbitúrico (TBARS), hidroperóxidos lipídicos (LOOH), superóxido dismutase (SOD), catalase (CAT), glutationa peroxidase (GPx), glutationa S-transferase (GST), o conteúdo dos grupos tióis não proteicos (NPSH), conteúdo de ácido ascórbico (AA) e a capacidade antioxidante total (TRAP) foram determinados. Os peixes que receberam a dieta contendo 0,15 % rutina apresentaram níveis de cortisol mais baixos do que o controle. No entanto, a dieta contendo rutina não influenciou os parâmetros hematológicos. Os níveis de lipoperoxidação medidos por determinação de TBARS e LOOH no encéfalo, brânquias, fígado e músculo diminuíram nos peixes que receberam a dieta contendo rutina; exceto no rim onde houve apenas a redução dos níveis de LOOH em todas as dietas. Quando comparado ao controle, a dieta enriquecida com rutina aumentou a atividade da SOD, CAT, o conteúdo de NPSH, AA e TRAP no encéfalo, GST e TRAP nas brânquias, SOD, CAT e GST, o conteúdo de NPSH, AA e TRAP no fígado, CAT, GST e TRAP no rim, GPx, conteúdo de NPSH, AA e TRAP no músculo. Em conclusão, estes resultados sugerem que a suplementação contendo rutina na dieta do jundiá é recomendada pois aumenta a resposta antioxidante no tecido, evitando o dano oxidativo.

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Kunikowska, Grazyna Maria. "Alterations of antioxidant enzymes following manipulations of basal ganglia : relevance to the pathogenesis of Parkinson's disease." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313737.

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Lichten, Louis A. "The roles of zinc and metallothionein in hepatocyte antioxidant defense." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0007024.

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Clement, Amy Marie. "The Antioxidant Defense Network: Synergistic Combinations to Prevent Oxidative Damage." BYU ScholarsArchive, 2008. https://scholarsarchive.byu.edu/etd/1549.

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One of the matchless ironies of the human body is its requirement for the highly reactive oxygen molecule, which has been clearly implicated in many diseases and the aging processes. Oxidants produced by metabolic processes damage cells by starting chemical chain reactions including oxidation of DNA and proteins as well as lipid peroxidation. Damage to DNA can cause mutations and lead to cancer if not reversed by DNA repair mechanisms. Damage to proteins causes enzyme inhibition, denaturation and protein degradation. Lipid peroxidation can cause cell lysis as well as creating mutagenic and carcinogenic by-products. The human body contains antioxidants and enzymes that together work to prevent oxidative damage to cellular components. By and large antioxidants either prevent these reactive oxygen species from being formed or remove them before they cause damage. There are many theories currently that tout the superior nature of diverse antioxidant combinations. One such theory is by Dr. Lester Packer of The University of California at Berkley. Dr. Packer puts forth the hypothesis that there is a superlative combination of five antioxidants that have the ability to "recharge" one another both in the blood plasma and intracellularly. This would result in a greater quality of antioxidant protection for an extended time. The current study evaluates Dr. Packer's theory of antioxidant combination from his book The Antioxidant Miracle. The decay rate of the antioxidants vitamin E, vitamin C, lipoic acid, glutathione, and coenzyme Q10 alone and in combination were determined using the ORAC (Oxygen Radical Absorbance Capacity) assay. The majority of the antioxidants retained activity for longer periods of time when tested alone, rather than in combination as Dr. Packer's theory would suggest. The assay was also preformed (using the same antioxidants and combinations) on oxidatively damaged Raji cancer cells. Cell viability and uptake of antioxidants into the cytoplasm were monitored. Finally, a variety of multivitamins were subjected to the ORAC assay and their antioxidant capacity compared to that of the "Packer Combination". The results suggest that multivitamins are superior antioxidants than the Packer ratio listed in The Antioxidant Miracle.

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Bender, Holly S. "The actions of gossypol on the physiologic antioxidant defense system." Diss., Virginia Polytechnic Institute and State University, 1987. http://hdl.handle.net/10919/82901.

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Gossypol , a yellow polyphenolic pigment found in cottonseeds, is known to promote the production of reactive species of oxygen in vitro, and has toxic actions on spermatogenic epithelium, hepatocytes and cardiac myocytes in vivo. Species vary in tissue sensitivity to the toxic effects of gossypol. The spermatogenic epithelium is the most sensitive tissue to gossypol in rats, followed by the liver. Toxic effects to the rat heart are found only after prolonged administration of gossypol. The antioxidant defense system that protects cells from injury by reactive species of oxygen was examined in the present study to determine a possible pathogenesis for gossypol associated tissue damage. The concentrations of several hepatic antioxidants including catalase, glutathione peroxidase, ascorbate and copper-zinc superoxide dismutase were decreased in gossypol treated rats. Catalase, glutathione peroxidase, ascorbate and glucose-6-phosphate dehydrogenase were decreased in the testis. In contrast, antioxidants including catalase and glutathione reductase were increased in the hearts of gossypol treated rats. The selective inhibition of testis and hepatic antioxidants may account for the greater sensitivity of these organs to reactive oxygen species generated by gossypol. The rat heart may adapt to oxidative insult by inducing the production of antioxidants. Glucose-6-phosphate dehydrogenase activity was decreased in the testis but not liver or heart of gossypol treated rats. This important enzyme is known to produce NADPH reducing equivalents for testosterone biosynthesis and the glutathione antioxidant system. In the present study, micromolar concentrations of gossypol inhibited glucose-6-phosphate dehydrogenase in a competitive manner with respect to glucose-6-phosphate. This may explain the degeneration of spermatogenic epithelium as well as decreases in serum testosterone concentrations in gossypol treated rats. Gossypol is known to cause infertility in women and female rats. The present study found irregularities in the estrous cycles and ultrastructural changes in endometrial macula adherentes of gossypol treated female rats.
Ph. D.

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SILVA, Juliana Scanoni. "HPAs biliares e biomarcadores bioquímicos na carapeba Eugerres brasilianus em quatro estuários tropicais do Nordeste brasileiro." Universidade Federal de Pernambuco, 2015. https://repositorio.ufpe.br/handle/123456789/16475.

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CAPEs
Hidrocarbonetos policíclicos aromáticos (HPAs) são compostos derivados de petróleo conhecidos por seu potencial de toxicidade a organismos aquáticos. Regiões estuarinas são frequentemente contaminadas por HPAs em decorrência de processos de urbanização e atividades industriais, incluindo a cadeia produtiva do petróleo. O trabalho teve o objetivo de avaliar a bioconcentração e efeitos bioquímicos de HPAs em Eugerres brasilianus coletados em quatro estuários no litoral sul de Pernambuco, a fim de obter um diagnóstico da poluição por estes contaminantes nestas regiões. As coletas foram realizadas no rio Ariquindá, sistema estuarino do rio Formoso (AR-SERF), no rio Massangana, no complexo estuarino de Suape (MA-CES), no sistema estuarino de Barra de Jangada (SEBJ), e no complexo estuarino da bacia do Pina (CEBP). A bile dos peixes foi analisada por Fluorescência Fixa para estimar a concentração em equivalentes dos HPAs naftaleno, fenantreno e criseno. Amostras de fígado foram utilizadas para análise de biomarcadores enzimáticos de fase I (etoxiresorufina orto-deetilase, EROD), fase II (glutationa S-transferase, GST), e defesa antioxidante (catalase, CAT, e glutationa redutase, GR). A análise de HPAs na bile e atividades enzimáticas em peixes coletados num ciclo anual em MA-CES e AR-SERF indicou uma semelhança na contaminação por HPAs na bile e nos níveis de atividades enzimáticas dos biomarcadores avaliados entre estes estuários, apesar da diferença do padrão de atividades antrópicas destas regiões. O CES comporta um complexo portuário com alta atividade industrial enquanto o SERF possui baixa densidade populacional e atividades turísticas. Os peixes coletados em SEBJ e CEBP apresentaram bile com concentrações do HPA criseno entre 13 x e 19 x maiores que AR-SERF, respectivamente. Foi detectado aumento das atividades da EROD, GST e CAT das regiões do SEBJ e CEBP, chegando a 30 x para a EROD, e aproximadamente 2 x para GST e CAT em comparação com AR-SERF. A maior bioconcentração de HPAs na bile e maior indução enzimática nos peixes E. brasilianus do SEBJ e CEBP indicam que estes estão dispendendo energia para tentar se adaptar a esta contaminação, o que pode ter consequências para o seu crescimento e sobrevivência nestas regiões. Os resultados indicam que SEBJ e CEBP recebem um maior aporte de HPAs, associado a maior densidade populacional e atividades antrópicas nas bacias desses rios. Os parâmetros utilizados serão úteis para o monitoramento destes sistemas estuarinos, em especial do CES, em franco processo de urbanização e industrialização.
Polycyclic aromatic hydrocarbons (PAHs) are oil derived compounds known for their toxicity potential towards aquatic organisms. Estuarine regions are frequently contaminated with PAHs as a result of urbanization processes and industrial activities, including the oil productive chain. The work aimed to evaluate the bioconcentration and the biochemical effects of PAHs in Eugerres brasilianus sampled from four estuaries in the south coast of Pernambuco, in order to obtain a pollution diagnosis by these contaminants in such regions. The data collection was made in the Aquirindá river, Rio Formoso estuarine system (AR-RFES), in the Massangana river, in the Suape’s estuarine complex (MA-SEC), in the Barra de Jangada estuarine system (BJES) and in the Bacia do Pina estuarine complex (BPEC). The fish’s bile were analyzed using fixed fluorescence to estimate the equivalent concentrations of the PAHs naphthalene, phenanthrene and chrysene. Liver samples were used for phase 1 enzymatic biomarkers analysis (Ethoxyresorufin-O-deethylase, EROD), phase II (glutathione S-transferase, GST) and antioxidant defense (catalase, CAT, and glutathione reductase, GR). The analyzes of PAHs in bile and enzymatic activity in fish that were sampled in an annual cycle in MA-SEC and AR-RFES indicated a similarity between PAHs contamination in bile and the enzymatic activity levels of the biomarkers evaluated among these estuaries, despite the different anthropogenic activity patterns. The SEC comprises a port complex with high industrial activity, while the RFES has low population density and touristic activities. The bile of the fish sampled in BJES and BPEC showed chrysene concentration between 13 x and 19 x higher than AR-RFEC, respectively. An increase in EROD, GST and CAT activities was detected in the regions of BJES and BPEC, reaching 30 x for EROD, and approximately 2 x for GST and CAT. The high PAHs bioconcentration in the bile and the high enzymatic induction in E. brasilianus fish from BJES and BPEC indicate that these fish are wasting energy to try to become adapted to this contamination, which may have consequences to their growth and survival in such regions. The results indicate that BJES and BPEC receive a greater input of PAHs, associated with the higher population density and anthropogenic activities in these rivers’ basins. The parameters used will be useful for the monitoring of these estuarine systems, especially in SEC, which suffers with a rapid urbanization and industrialization process.

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30

Pietarinen-Runtti, Petra. "Regulation of antioxidant defense in cells derived from the human lung." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/pietarinen-runtti/.

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31

Freitas, Robson Borba de. "AVALIAÇÃO DA TOXICIDADE DO EXTRATO AQUOSO DE Scutia buxifolia EM RATOS." Universidade Federal de Santa Maria, 2013. http://repositorio.ufsm.br/handle/1/5958.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico
Medicinal plants were and are very important for healing various diseases. However, improper use of plants for therapeutic purposes can cause a number of side effects. There are in the literature various reports about plants induced-toxicity and, in some cases patients have hepatic disorders. The knowledge about toxicity of vegetable materials is insipient because there are few scientific studies related to pharmacokinetics and pharmacodynamics. Plants containing pyrrolizidine alkaloids show hepatotoxic effects well documented. Scutia buxifolia Reiss is a Rhamnaceae. This plant occurred in Uruguay, Argentina and Brazil. It is used for hypertension treatment. Extracts and fractions obtained from S. buxfolia have antimicrobial and antioxidants effects. Nevertheless, S. buxifolia toxic effects are unknown. The present study was aimed to evaluate the acute and sub-chronic toxicity of S. buxifolia aqueous extract (SBSB). The flavonoids, condensed tannins, and flavonoids were measured in SBSB. The antioxidant scavenger capacity of SBSB was determined by DPPH assay. Antioxidant power of SBSB was comparable with the antioxidant ascorbic acid. The single dose of SBSB at concentrations 100, 200, 400 mg/ kg body weight administered to Wistar rats did not cause mortality and, behavioral changes. Then, we speculate that the lethal dose of SBSB is greater than 400 mg / kg body weight. In the sub-chronic assay, thirty-two animals are divides in 4 groups: the control group which receive distilled water by gavage and, the experimental groups which received the same doses used in the acute toxicity assay. The animals received water or SBSB once a day, during 30 days. The serum alanine aminotransferase (ALT) and asparate aminotransferase (AST) activities and, serum albumin levels were measured on 15º and 30º day of treatment. The malondialdehyde (MDA) and non-protein thiol groups (NPSH) contents and, the antioxidant activities of superoxide dismutase (SOD) and catalase (CAT) were quantified in the liver. Treatment with SBSB did not elevate the activity of AST and ALT, and did not alter the level of serum albumin in the doses of 100 and 400 mg / kg body weight. In animals treated with 200 mg / kg an increased activity of the enzyme AST was observed. This fact can occurred due, probably, to hemolysis. Treatment with SBSB preserves antioxidant defenses and does not increase the lipid peroxidation in liver tissue. These findings along with histopathological analysis show that the SBSB is safe.
As plantas medicinais foram e são de suma importância para a cura de diversas doenças. No entanto, o uso indiscriminado de plantas para fins terapêuticos pode provocar uma série de efeitos colaterais. Existem na literatura, vários relatos de intoxicação por plantas mundialmente usadas e em alguns casos, pacientes apresentaram falência hepática. O conhecimento dos efeitos tóxicos de matérias vegetais ainda é bastante insipiente, pois, há poucos trabalhos científicos sobre farmacocinética e farmacodinâmica. Plantas que contêm alcalóides pirrolizidínicos apresentam efeitos tóxicos para o fígado e já foram bem documentadas. Scutia buxifolia é uma Rhamnaceae que ocorre no Uruguai, Argentina e Brasil. Esta planta é popularmente usada no tratamento da hipertensão. Extratos e frações das folhas e cascas de S. buxifolia já tiveram suas atividades antimicrobianas e antioxidantes investigadas. Porém, os efeitos tóxicos do extrato de S. buxifolia são pouco conhecidos. O presente estudo teve como objetivo principal avaliar a toxicidade aguda e sub-crônica do extrato aquoso de S. buxifolia (SBSB). Neste extrato quantificou-se o conteúdo total de compostos fenólicos, taninos condensados, e flavonóides. A atividade antioxidante do SBSB determinada pelo método do DPPH é comparável á do ácido ascórbico. A dose única do SBSB nas concentrações de 100, 200 e 400 mg / kg de peso corporal administrada a ratos da raça Wistar, não causou mortalidade nos grupos e nem alterações comportamentais. Então, especula-se que a dose letal do SBSB seja maior que 400 mg/ kg de peso corporal. No ensaio sub-crônico, trinta e dois animais foram divididos em quatro grupos: o controle que recebeu água e, os experimentais que receberam o extrato nas mesmas doses que as utilizadas no ensaio da toxicidade aguda. Os animais receberam água ou extrato uma vez ao dia via gavagem, durante 30 dias. A atividade sérica das enzimas alanina aminotransferase (ALT) e asparato aminotransferase (AST) e o nível de albumina foram mensurados no 15º de 30º dia de tratamento. O conteúdo de malondialdeído (MDA), de tióis não-protéicos e atividade antioxidante das enzimas catalase (CAT) e superóxido dismutase (SOD) foram quantificadas no fígado dos animais. O tratamento com o SBSB não eleva a atividade da AST e da ALT e, não alterara o nível sérico de albumina nas doses de 100 e 400 mg/ kg de peso corporal. Os animais tratados com a dose de 200 mg/kg tiveram um aumento na atividade da enzima AST. O tratamento com SBSB preserva as defesas antioxidantes e não aumenta a peroxidação lipídica no tecido hepático. Esses achados juntamente com análise histopalógica mostram que o SBSB é seguro.

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32

Hamlin, Scott A. "Effects of resistance exercise on markers of inflammation and antioxidant defenses in heart transplant recipients." [Gainesville, Fla.] : University of Florida, 2005. http://purl.fcla.edu/fcla/etd/UFE0010509.

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33

Borçari, Nathalia Ruder. "Efeito da progesterona na expressão de genes envolvidos no estresse oxidativo e defesa antioxidante em células beta pancreáticas: uma abordagem in vitro para o estudo do diabetes gestacional." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/100/100142/tde-21052018-223214/.

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O diabetes gestacional (DG) é uma condição definida como intolerância a carboidratos e hiperglicemia, com início no segundo trimestre da gravidez. Trabalhos desenvolvidos por nosso grupo mostraram que a progesterona (PG) é capaz de causar a morte de células pancreáticas, por um mecanismo dependente da geração de radicais livres, o que poderia contribuir para o desenvolvimento do DG. O objetivo desse trabalho foi estudar o efeito da PG, na presença ou não de antioxidantes, na expressão de genes relacionados ao estresse oxidativo e na defesa oxidante em células pancreáticas da linhagem RINm5F. As células foram incubadas com PG 0,1, 1,0 e 100 µM por 6 ou 24 h, na presença ou não dos antioxidantes vitamina E e C. Após a incubação, foram realizados ensaios de viabilidade celular e fragmentação do DNA. A PG, não causou perda da integridade da membrana das células RINm5F, porém, ela promoveu fragmentação do DNA em, aproximadamente, 40% das células RINm5F e MCF-7 (controle positivo), enquanto que os antioxidantes vitamina E e C reduziram tal fragmentação. A partir da extração do RNA e síntese de cDNA foi investigada a expressão de 84 genes envolvidos no estresse oxidativo e defesa antioxidante. Dos 84 genes, cinco deles tiveram sua expressão aumentada em no mínimo, duas vezes em, pelo menos, duas concentrações diferentes, independentemente do tempo de incubação, ou nas mesmas concentrações em tempos diferentes, como os que codificam para a proteína de choque térmico a1a (Hspa1a), glutationa peroxidase 6 (Gpx6), dual oxidase 1 (Duox1), heme oxigenase 1(Hmox1) e estearoil-CoA desaturase 1 (Scd1). Esses genes, juntamente com a peroxirredoxina 4 (Prdx4), desempenham importante papel na fisiologia da célula pancreática e/ou DG. A expressão desses genes também foi estudada na pré-incubação das células RINm5F com as vitaminas E e C. Tais antioxidantes, de forma geral, foram capazes de aumentar a expressão de Hmox1 e Prdx4, genes com funções antioxidantes, e de diminuir de Scd1, um gene com função pró- oxidante. Ao nível citoplasmático, verificou-se que as quantidades das proteínas Hmox1 e Prdx4 também foram moduladas pela da PG e/ou vitamina E e C. Os resultados sugerem que esses antioxidantes apresentam importante papel na proteção da células RINm5F contra o dano oxidativo induzido pela PG. Desta forma, os resultados obtidos nesse projeto, em conjunto, devem colaborar para melhor compreensão da patogênese do DG, abrindo novas perspectivas não só para elucidação do mecanismo molecular envolvido na ação da PG sobre células pancreáticas e sua relação com o DG, mas para o desenvolvimento de estratégias de prevenção e tratamento dessa doença baseadas na terapia com antioxidantes
Gestational diabetes (GD) is a condition defined as carbohydrate intolerance and hyperglycemia, beginning in the second trimester of pregnancy. Studies developed by our group have shown that progesterone (PG) is able to cause pancreatic cells death, by a mechanism dependent on the generation of free radicals, which could contribute to the development of GD. The aim of this work was to study the effect of PG, in the presence or absence of antioxidants, on the expression of genes related to oxidative stress and oxidant defense in pancreatic cells of the RINm5F lineage. Cells were incubated with 0.1, 1.0 and 100 µM PG for 6 or 24 h, in the presence or absence of vitamin E and C antioxidants. PG did not cause loss of membrane integrity of RINm5F cells, however, it promoted DNA fragmentation in approximately 40% of the RINm5F and MCF-7 cells (positive control), whereas vitamin E and C antioxidants reduced such fragmentation. From the RNA extraction and cDNA synthesis was investigated the expression of 84 genes involved in oxidative stress and antioxidant defense. Among of 84 investigated genes, five of them had their expression increased, in the minimum 2-fold in, at least, two different concentrations independent of incubation time (6 or 24 h), or at the same concentrations at different times, such as those that encoding for heat shock protein a1a (Hspa1a), glutathione peroxidase 6 (Gpx6), dual oxidase 1 (Duox1), heme oxygenase 1 (Hmox1) and stearoyl-CoA denaturase 1 (Scd1). These genes, together with the peroxiredoxin 4 (Prdx4), play an important role in pancreatic cell physiology and/or DG. The gene expression was also studied in the preincubation of RINm5F cells with vitamin E and C. These antioxidants were generally able to increase the Hmox1 and Prdx4 expression, genes with antioxidant functions, and decrease the Scd1 expression, a gene with pro-oxidant function. At the cytoplasmic level, it was found that the amounts of Hmox1 and Prdx4 proteins were also modulated by PG and / or vitamin E and C. The results suggest that these antioxidants play an important role in the RINm5F protection cells against the oxidative damage induced by PG. Thus, the results obtained in this project, together, should contribute to a better understanding of the pathogenesis of DG, opening new perspectives not only to elucidate the molecular mechanism involved in the action of PG on pancreatic cells and its relationship with DG, but for the development of strategies for the prevention and treatment of this disease based on antioxidant therapy

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34

Marmolino, Daniele. "Alterations of mitochondrial biogenesis and alterations of mitochondrial antioxidant defense in Friedreich's ataxia." Doctoral thesis, Universite Libre de Bruxelles, 2011. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209972.

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Friedreich’s ataxia (FRDA) is an autosomal recessive inherited disorder affecting approximately 1 every 40,000 individuals in Western Europe, is characterized by progressive gait and limb ataxia, dysarthria, areflexia, loss of vibratory and position sense, and a progressive weakness of central origin. Additional features particularly include an hypertrophic cardiomyopathy that can cause premature death. A large GAA repeat expansion in the first intron of the FXN gene is the most common mutation underlying FRDA. Patients show severely reduced levels of the FXN-encoded mitochondrial protein frataxin.

Frataxin function is not yet completely elucidated. In frataxin deficiency conditions abnormalities of iron metabolism occur: decreased activities of iron-sulfur cluster (ISC) containing proteins, accumulation of iron in mitochondria and depletion in the cytosol, enhanced cellular iron uptake, and, in some models, reduced heme synthesis.

Evidence of oxidative stress has also been found in most though not all models of frataxin deficiency. Accordingly, yfh1-deficient yeast and cells from FRDA patients are highly sensitive to oxidants. Respiratory chain dysfunction further aggravate oxidative stress by increasing leakage of electrons and the formation of superoxide. Frataxin deficient cells not only generate more free radicals, but, they also show a reduced ability to mobilize antioxidant defenses, in particular to induce superoxide dismutase 2 (SOD2).

Peroxisome proliferator-activated receptor (PPAR) isoform-gamma play a key role in numerous cellular functions and is a key regulator of mitochondrial biogenesis and of the ROS metabolism. Recruitment of the PPAR coactivator-1a (PGC-1a) mediates many effects of the PPAR-γ activation.

In a first work we assessed the potential beneficial effects of a potent PPAR-gamma agonist on frataxin expression in primary fibroblasts from healthy controls and FRDA patients, and Neuroblastoma cells. We used the APAF molecule (1-0-hexadecyl-2-azelaoyl-sn-glycero-3-phosphocoline; C33H66NO9P). Our results show that this compound is able to increase frataxin amount both at transcriptional and post-transcriptional level. At a dose of 20µM frataxin mRNA significantly increases in both controls (p=0.03) and FRDA patients (p=0.002) fibroblasts (1). The finding was confirmed in Neuroblastoma cells (p=0.042). According to previous publications APAF, as others PPAR-gamma agonists is able to up-regulate PGC-1a transcription.

In a second part of the study we investigate the role of the PPAR-gamma/PGC-1a pathway in the pathogenesis of FRDA. We performed a microarray analysis of heart and skeletal muscle in a mouse model of frataxin deficiency and we found molecular evidence of increased lipogenesis in skeletal muscle and alteration of fiber-type composition in heart, consistent with insulin resistance and cardiomyopathy, respectively. Since the PPAR-gamma pathway is known to regulate both processes, we hypothesized that dysregulation of this pathway could play a key role in frataxin deficiency. We confirmed this by showing a coordinate dysregulation of Pgc1a and the transcription factor Srebp1 in cellular and animal models of frataxin deficiency, and in cells from FRDA patients, who have marked insulin resistance. Particularly, PGC-1a was found significantly reduced (2) in primary fibroblasts and lymphocytes from FRDA patients (p<0.05). Furthermore, PGC-1a mRNA levels strongly correlate with frataxin relative mRNA levels (r2=0.9, p<0.001). According to this observation, in C2C12 myoblasts, PGC-1a and a reporter gene under the control of the PGC-1a promoter are rapidly down-regulated (p<0.05) when frataxin expression is inhibited by an shRNA in vitro. To further investigate this relation, we then generate PGC-1a deficient fibroblasts cells using a specific siRNA; at 72 hours of transfection frataxin was found down-regulate (p<0.05) in control cells.

Taken together those data indicate that some mechanism directly links an early effect of frataxin deficiency with reduced PGC-1a transcription in this cell type, and presumably in other cells that also down-regulate PGC-1α when frataxin levels are low.

Finally, since PGC-1a has also emerged as a key factor in the induction of many antioxidant programs in response to oxidative stress, both in vivo and in vitro, in particular in neurons, we tested whether the PGC-1a down-regulation occurring in FRDA cells could be in part responsible for the blunted antioxidant response observed in frataxin deficiency.

Using primary fibroblasts from FRDA patients we found reduced SOD2 levels (p<0.05), according to PGC1&
Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished

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Silva, Maria Isabel Afonso da. "Alterações hematológicas e bioquímicas em uma população de Phrynops geoffroanus (Schweigger, 1812) em reposta a estressores ambientes /." São José do Rio Preto : [s.n.], 2011. http://hdl.handle.net/11449/92533.

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Orientador: Claudia Regina Bonini Domingos
Banca: Lilian Castiglioni
Banca: Fabiano Gazzi Taddei
Resumo: Os quelônios estão entre os grupos de vertebrados com maior risco de extinção, sendo as principais ameaças para as populações, a degradação e poluição ambiental. A espécie Phrynops geoffroanus, popularmente conhecida como "Cágado-de-Barbelas", tem se proliferado em ambiente poluído, sujeita a condições adversas que podem influenciar nos seus hábitos de vida e condições fisiológicas. Estudos que monitorem os efeitos da contaminação ambiental são fundamentais para o conhecimento da biologia da espécie e delineamento de estratégias de conservação efetivas. Deste modo, as análises dos parâmetros hematológicos e bioquímicos mostram-se importantes na avaliação da saúde de animais silvestres e riscos para o animal e ecossistema. O objetivo do trabalho foi verificar a influência do ambiente na fisiologia de uma população de Phrynops geoffroanus por meio da avaliação da capacidade antioxidante e respostas aos estressores ambientais, em comparação com espécimes de local sob condições controladas. Foram avaliadas, por meio do hemograma completo, dosagem de espécies reativas ao ácido tiobarbitúrico (TBARS), ensaio da capacidade antioxidante em equivalência ao Trolox (TEAC) e atividades das enzimas antioxidantes catalase e glicose-6-fosfato desidrogenase (G6PDH), amostras sanguíneas de sessenta espécimes, sendo trinta provenientes do córrego Felicidade, ambiente poluído, no perímetro urbano de São José do Rio Preto-SP; e trinta do criatório "Reginaldo Uvo Leone", Tabapuã-SP, local sob condições controladas, cujas amostras constituem o grupo controle dos experimentos. Houve grande variação nos parâmetros hematológicos de Phrynops geoffroanus de ambiente urbano. Os valores de glóbulos vermelhos e hemoglobina foram significantemente menores que os observados em animais do criatório (p = 0,0004; p = 0,0371, respectivamente)... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: The turtles are among the most endangered vertebrates groups, and the main threats to populations are the environmental pollution and degradation. The species Phrynops geoffroanus, popularly known as "Geoffroy's side-necked turtle", has proliferated in polluted environments, subject to adverse conditions that could influence their living habits and physiological conditions. Studies that monitor the effects of environmental pollution are the key to understand the species biology and design effective conservation strategies. Thus, the analysis of hematological and biochemical parameters showed to be important in assessing the health of wild animals and for the animal and ecosystem risks. This work aimed to assess the environmental influence on the physiology of a Phrynops geoffroanus population through the evaluation of antioxidant status and responses to environmental stressors, compared to specimens from a place under controlled conditions. They were evaluated by hemogram, measuring thiobarbituric acid reactive species assay (TBARS), Trolox-equivalent antioxidant capacity evaluation (TEAC) and the activities of antioxidant enzymes, catalase and glucose-6-phosphate dehydrogenase (G6PDH), blood samples of sixty specimens, thirty from the Felicidade stream, polluted environment, within the São José do Rio Preto city, and thirty from the "Reginaldo Uvo Leone" breeding farm, Tabapuã-SP, place under controlled conditions, whose samples constitute the control group of the experiments. There was a wide variation in hematological parameters of Phrynops geoffroanus from the urban environment. The red blood cells and hemoglobin values were significantly less than those observed in animals from breeding farm (p = 0.0004; p = 0.0371, respectively). There was significant increase of thrombocytes (p < 0.0001) and leukocytes (p < 0.0001) to the animals from the Felicidade stream... (Complete abstract click electronic access below)
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Anschau, Valesca. "Estresse oxidativo e parâmetros hematológicos como biomarcadores da infecção experimental com Trypanosoma evansi em ratos." Universidade do Estado de Santa Catarina, 2011. http://tede.udesc.br/handle/handle/843.

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Trypanosoma evansi is a hemoflagellate parasite that had known to cause infection in a variety of mammals, such as camels, cattles, horses, buffaloes, pigs, dogs and other animal species in tropical and subtropical áreas. In Brazil, T. evansi is considered endemic only at Pantanal, but has been also found in the central region of Rio Grande do Sul and Santa Catarina also. High levels of parasitemia with rapid development of anemia characterize the disease, however the mechanisms of development are still unknown. In this study we aimed to investigate the effect of oxidative stress in erythrocytes and evaluate hematological parameters in rats experimentally infected with T. evansi. Due to, sixty male Wistar rats, were inoculated intraperitoneally with blood containing 103 trypanosomes and fifteen were negative control. The parasitemia was evaluated each 12 hours and the animals were allocated in five groups according to average parasitemia in 10 random homogeneous microscopic fields: (A) uninfected group (control); (B) rats with 1-10 trypanosomes/field; (C) 11-30 trypanosomes/field; (D) 31-60 trypanosomes/field; and (E) more than 61 trypanosomes/field. The animals that achieved the number of trypanosomes equivalent to the groups were sacrificed and blood samples collected to measurement the activities of glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), glucose-6-phosphate dehydrogenase (G6PD), catalase (CAT), and glutathione (total and oxidized), protein thiols (PSH) and non-protein (NPSH). As well as, serum iron, plasma glucose, osmotic fragility, methemoglobin levels, markers of oxidative stress as total and lipid peroxides levels and protein carbonyl concentration (PC) were quantified. Hematological parameters were also analyzed such as erythrocyte count, hematocrit, hemoglobin concentration, packed cell volume, mean corpuscular volume, mean corpuscular hemoglobin concentration, total plasma proteins, platelets, reticulocytes and differential leukocytes count. The infected groups with greater development of the disease developed anemia, with low reticulocytes and platelets levels. Besides that, the increasing of erythrocyte osmotic fragility and methemoglobin levels was observed in groups D and E. In group E was observed a significant reduction of plasma glucose levels when compared with the control group (64%). The serum iron decreased to 58% in group B, but increased to 78% in group E. The acute infection caused an increase in GPx activity in group C, D and E, and enhances CAT activity in group D and E respectively. However, decreased the GR activity in group E approximately 52%. There were no significant differences in the activities of GST and G6PD in the groups comparing to the control. Infection with T. evansi caused a consumption of GSH-t (48%) and a reduction of the levels of PSH and NPSH, around 55%. As well, infected animals showed an increase of the levels of total and lipid peroxides, more than 90% PC concentration compared with the control. Finally, T. evansi promoted oxidative damage in infected rats through increasing antioxidant activities of GPx, CAT, depletion of GSH-t, PSH and NPSH, and inhibition of GR activity. Moreover, the infection also increased the levels of PC, total and lipid peroxides in higher stages of infection caused by T. evansi. Therefore, we can to state that oxidative damage in erythrocytes contributes decisively to the development of anemia in infection by T. evansi in rats
O Trypanosoma evansi é um hemoparasita flagelado conhecido por causar infecção em uma diversidade de mamíferos como camelos, bovinos, equinos, bubalinos, suínos, caninos e outras espécies animais em áreas tropicais e subtropicais. No Brasil, T. evansi é considerado endêmico apenas no Pantanal, mas também já foi encontrada na região central do Rio Grande do Sul e em Santa Catarina. Altos níveis de parasitemia com rápido desenvolvimento de anemia caracterizam a doença, contudo seus mecanismos de desenvolvimento ainda são desconhecidos. Este estudo teve como objetivo investigar o efeito do estresse oxidativo em eritrócitos e avaliar parâmetros hematológicos de ratos infectados experimentalmente com T. evansi. Para isso, sessenta ratos Wistar machos foram inoculados via intraperitonial com sangue contendo 103 tripanossomas e quinze foram usados como controle negativo. A parasitemia foi avaliada a cada 12 horas e os animais foram alocados em cinco grupos de acordo com a média de tripanossomas em 10 campos homogêneos focados aleatoriamente sendo: (A) grupo não infectado (controle); (B) ratos com 1-10 tripanossomas/campo; (C) 11-30 tripanossomas/campo; (D) 31 a 60 tripanossomas/campo; and (E) com mais de 61 tripanossomas/campo. Os animais que apresentaram o número de tripanossomas equivalente ao grupo, foram sacrificados e amostras de sangue coletadas para mensuração das atividades da glutationa peroxidase (GPx), glutationa redutase (GR), glutationa-S-transferase (GST), glicose-6-fosfato desidrogenase (G6PD), catalase (CAT), e glutationa (total e oxidada), tióis protéicos (PSH) e não protéicos (NPSH). Assim como ferro sérico, glicose plasmática, fragilidade osmótica, níveis de metahemoglobina, marcadores de estresse oxidativo como peróxidos totais e lipídicos e níveis de proteína carbonilada (PC) foram quantificados. Também foram analisados parâmetros hematológicos tais como contagem total eritrócitos, hematócrito, concentração de hemoglobina, volume globular, volume globular médio, concentração hemoglobina corpuscular média, proteínas plasmáticas totais, plaquetas, reticulócitos, e contagem diferencial de leucócitos. Os grupos infectados com maior desenvolvimento da doença apresentaram anemia, com diminuição nos reticulócitos e plaquetas. Além disso, o aumento na fragilidade osmótica eritrocitária e nos níveis de metahemoglobina nos grupos D e E foi observada. No grupo E foi observada uma redução significativa nos níveis de glicose plasmática quando comparado ao grupo controle (64%). O ferro sérico diminuiu 78% no grupo B, mas aumentou 78% no grupo E. A infecção aguda causou um aumento da atividade da GPx nos grupos C, D e E e um aumento da atividade da CAT nos grupos D e E respectivamente. Entretanto, ocorreu uma diminuição da atividade da GR no grupo E de aproximadamente 52%. Não foram encontradas diferenças significativas nas atividades da GST e G6PD nos grupos comparados com o controle. Infecção com T. evansi causou um consumo da GSH-t (48%) e uma redução nos níveis de PSH e NPSH, de aproximadamente 55%. Assim como, animais infectados mostraram um aumento nos níveis de peróxidos totais e lipídicos, na concentração de PC de mais de 90% comparado com o controle. Em resumo, T. evansi promoveu insulto oxidativo em ratos infectados através do aumento das atividades da GPx, CAT, depleção da GSH-t, PSH e NPSH, inibição da atividade da GR. Além disso, a infecção também aumentou os níveis de PC, peróxidos totais e lipídicos nos estágios de maior infecção causada pelo T. evansi. Diante disso, é possível afirmar que danos oxidativos em eritrócitos contribuem decisivamente para o desenvolvimento de anemia na infecção por T. evansi em ratos

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Baker, Amanda Fern 1969. "Modulation of the antioxidant defense during dexamethasone-induced apoptosis in WEHI7.2 mouse lymphoid cells." Diss., The University of Arizona, 1997. http://hdl.handle.net/10150/282473.

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The modulation of the antioxidant defense during dexamethasone-induced apoptosis in WEHI7.2 cells mouse lymphoid cells was studied. When treated with dexamethasone, antioxidant defense transcripts including catalase, MnSOD, CuZnSOD, DT-diaphorase, GPX, and thioredoxin exhibited a progressive decrease over 24 hours (h) in apoptosis-sensitive wild-type WEHI7.2 and apoptosis-resistant bcl-2 transfected (W.Hb12) cells. Catalase activity was maintained and total SOD and DT-diaphorase activity showed smaller decreases following dexamethasone treatment of bcl-2 transfected cells. Treatment of wild-type and bcl-2 transfected WEHI7.2 cells with a catalase inhibitor, amino-triazole, was not sufficient to induce apoptosis. Antioxidants, including bovine liver catalase, bovine erythrocyte CuZnSOD, sodium selenite and Trolox, a water soluble vitamin E analogue, as well as hypoxia, inhibited dexamethasone-induced apoptosis. Transfection of the WEHI7.2 cells with catalase and thioredoxin resulted in a significant level of protection against dexamethasone-induced apoptosis. Thioredoxin-transfected cells were also protected from apoptosis induced by staurosporine, N-acetyl-sphingosine, etoposide and thapsigargin. When inoculated into severe combined immunodeficient (scid) mice the trx transfected cells formed tumors that showed increased growth compared to wild-type as well as bcl-2 transfected WEHI7.2 cells. The trx and bcl-2 transfected cell tumors both showed less spontaneous apoptosis than tumors formed by the wild-type cells. Unlike tumors formed by the wild-type and bcl-2 transfected WEHI7.2 cells, trx transfected cell tumors did not show growth inhibition upon treatment with dexamethasone. These results suggest that modulation of the antioxidant defense may play a role in dexamethasone-induced apoptosis and that Bcl-2 may prevent apoptosis by maintaining the level of critical antioxidant defense mechanisms including catalase. In addition, the thioredoxin study suggests that increased thioredoxin expression may result in a increased tumor growth through inhibition of spontaneous apoptosis and a decrease in the sensitivity of the tumor to drug-induced apoptosis.

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Battisti, Vanessa. "ESTUDO DO PERFIL OXIDATIVO E AVALIAÇÃO DE PARÂMETROS ENZIMÁTICOS EM PACIENTES COM CÂNCER DE PRÓSTATA." Universidade Federal de Santa Maria, 2012. http://repositorio.ufsm.br/handle/1/4450.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico
Prostate cancer is recognized as one of the most important medical problems in the male population. Inherent or acquired alterations in cellular metabolism that occur over the years may be involved in the process of developing this cancer. Thus, oxidative stress may play an important role in cellular processes associated with the initiation and development of prostate cancer. On the other hand, the cancer may be associated with changes in platelet aggregation and metabolism of nucleotides. In addition, enzymes that degrade esters of choline are well known as participating in non-cholinergic functions and intervene in important cell processes such as proliferation, differentiation and apoptosis. Considering such statements, this study aimed to evaluate the oxidative profile, through the determination of parameters such as the TBARS and protein carbonyl content and antioxidant defenses, by determine the catalase (CAT) and superoxide dismutase (SOD) activity and non-protein thiols, vitamin C and vitamin E levels. Also, determine ectonucleotidases enzyme activities represented by the enzymes NTPDase, E-NPP, 5'nucleotidase and adenosine deaminase (ADA) and verified the acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) activities. In addition, we evaluated the influence of Gleason score, the presence or absence of metastasis and type of treatment used by patients in the parameters analyzed. The results show that the content of TBARS and protein carbonylation levels increased in patients when compared with the control group. In addition, changes in the antioxidant defenses were observed. The CAT activity was decreased and SOD activity increased in patients compared to controls. We found also an increase in the levels of non-protein thiols in plasma and erythrocytes and a decrease in serum levels of vitamin C and vitamin E in patients. These results suggest an increased formation of reactive species and an imbalance in the enzymatic and non-enzymatic antioxidant system defense in patients with prostate cancer. Moreover, it was observed that advanced prostate cancer is associated with a state of high oxidative stress. The results showed that nucleotides hydrolysis (ATP, ADP and AMP) were increased in patients compared to controls, which maybe observed by the increase in the enzymes activity (NTPDase, E-NPP and 5'Nucleotidase). On the other hand, our results showed a decrease in ADA activity in serum of these patients. These results reflect the increase in the nucleotide hydrolysis and the consequent increase in the adenosine concentrations that may be envolved in the tumorigenesis process. Our results also showed that inhibition of platelet aggregation was decreased only in patients with prostate cancer before starting treatment. The AChE and BuChE activities were decreased in patients in relation to the control group. The decrease in the cholinesterases activities and the consequently increase in acetylcholine levels suggest the participation of this molecule in the process of cancer development. Finally, changes in the NTPDase, 5' nucleotidase, E-NPP, ADA, AChE and BuChE activities when patients were divided in groups considering the Gleason score, presence or absence of bone metastasis and the treatment, indicate that these parameters must be considered.
O câncer de próstata é reconhecido como um dos mais importantes problemas médicos enfrentados pela população masculina. Alterações inerentes ou adquiridas no metabolismo celular que ocorrem ao longo dos anos podem ter envolvimento no processo de desenvolvimento deste tipo de câncer. Dessa forma, o estresse oxidativo pode desempenhar um papel importante nos processos celulares associados com a iniciação e o desenvolvimento do câncer de próstata. Por outro lado, o câncer pode estar associado com alterações na agregação plaquetária e no metabolismo dos nucleotídeos. Além disso, as enzimas que degradam ésteres de colina desempenham funções não colinérgicas e parecem estar envolvidas com a proliferação e diferenciação celular. Levando em consideração tais afirmativas, este trabalho teve como objetivos avaliar o perfil oxidativo, através da determinação do conteúdo de substâncias reativas ao ácido tiobarbitúrico (TBARS) e de proteína carbonil, e as defesas antioxidantes, através da determinação das atividades das enzimas catalase (CAT) e superóxido dismutase (SOD) e dos níveis de tióis nãoprotéicos, vitamina C e vitamina E. Além disso, realizar a determinação das atividades das enzimas ectonucleotidases representadas pelas enzimas NTPDase, E-NPP, 5 nucleotidase e adenosina deaminase (ADA). Por fim, verificar as atividades das enzimas acetilcolinesterase (AChE), butirilcolinesterase (BuChE) e os parâmetros bioquímicos em pacientes e controles. Esse trabalho teve ainda como objetivo, avaliar a influência da escala de Gleason, da presença ou ausência de metástase e do tipo de tratamento a que foram submetidos os pacientes, nas dosagens realizadas. Os resultados demonstram que o conteúdo de TBARS e os níveis de carbonilação de proteínas aumentaram nos pacientes quando comparados com o grupo controle e mudanças no sistema de defesa antioxidante foram observadas. A atividade da CAT estava diminuída e a atividade da SOD aumentada nos pacientes quando comparados aos controles. Verificamos ainda um aumento nos níveis de tióis não-protéicos no plasma e eritrócitos e uma diminuição nos níveis séricos de vitamina C e de vitamina E em pacientes com câncer próstata. Os resultados mostraram que a hidrólise dos nucleotídeos ATP, ADP e AMP estava aumentada nos pacientes quando comparado ao grupo controle, o que pode ser comprovado pelo aumento nas atividades das enzimas NTPDase, E-NPP e 5 Nucleotidase. Por outro lado, nossos resultados revelaram uma diminuição na atividade da ADA no soro desses pacientes. Os resultados mostraram também que a agregação plaquetária foi diminuída apenas nos pacientes com câncer de próstata antes do início do tratamento. As atividades da AChE e BuChE foram diminuídas 8 nos pacientes em relação ao grupo controle. Com os dados podemos concluir que há um aumento na formação de espécies reativas e um desequilíbrio no sistema de defesa antioxidante enzimático e não-enzimático nos pacientes. Além disso, o câncer de próstata avançado pode estar associado com um estado de estresse oxidativo elevado. Os resultados refletem também o aumento na hidrólise de nucleotídeos e o consequente aumento nas concentrações de adenosina nos pacientes, que pode estar participando do processo de tumorogênese. A diminuição nas atividades das colinesterases (AChE e BuChE) e o consequente aumento nos níveis de acetilcolina sugerem a participação da mesma no processo de desenvolvimento do câncer. Finalmente, as alterações nas atividades das enzimas NTPDase, 5 Nucleotidase, E-NPP, ADA, BuChE e AChE quando os pacientes foram divididos em grupos considerando a escala de Gleason, a presença ou ausência de metástase óssea e o fato de estar ou não em tratamento, indicam que esses parâmetros devem ser considerados.

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Peña, Ahumada Andrea Alejandra. "Antioxidant defence and the role of the peroxiredoxins during silique development and seedling establishment in oilseed plants." [S.l.] : [s.n.], 2006. http://deposit.ddb.de/cgi-bin/dokserv?idn=980373115.

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Jiang, Mingyi. "Role and mechanism of abscisic acid in the induction of antioxidant defense in maize leaves." HKBU Institutional Repository, 2002. http://repository.hkbu.edu.hk/etd_ra/415.

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Saccol, Etiane Medianeira Hundertmarck. "ADIÇÃO DO ÓLEO ESSENCIAL DE Lippia alba (MILL) N. E. BROWN NA DIETA DO JUNDIÁ: ANÁLISE DO CRESCIMENTO E DA RESPOSTA ANTIOXIDANTE." Universidade Federal de Santa Maria, 2013. http://repositorio.ufsm.br/handle/1/9015.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
Fish become more susceptible to stress and, consequently, to the onset of disease with the intensification of rearing. In an attempt to minimize this problem, farmers use agrochemicals that, besides harming the environment, can also affect producers and consumers health. The essential oil (EO) of Lippia alba may be a natural alternative since it has several effects that can reduce the physiological changes resulting from stress inherent in aquaculture. The influence of five diets containing L. alba EO (0, 0.25, 0.5, 1.0 and 2.0 mL of EO per kg of diet) on growth and antioxidant response in juvenile silver catfish was evaluated. After a feeding period of 60 days, the silver catfish were weighed and measured individually, and euthanized for sampling of brain, gill, liver, kidney and muscle. The oxidative stress biomarkers, thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST) and non-protein thiols groups (NPSH), were determined. Growth parameters were not affected by the diet containing L. alba EO. As for biomarkers of oxidative stress, lipoperoxidation (LPO) evaluated through TBARS and LOOH was reduced by the EO in the gills, liver, kidney and muscle of silver catfish; no effect was observed in the brain. The diet with the EO improved the activity of antioxidant enzymes: SOD, CAT, GPx, GST and NPSH levels in the brain; SOD, GR and GST in the gills; CAT, GR and NPSH levels in the liver; CAT, GR and NPSH levels in the kidney; and SOD, GPx and NPSH levels in the muscle. These results indicate that L. alba EO does not interfere with growth, decreases LPO levels and increases antioxidant enzymes activities in most tissues evaluated, and thus may be added to silver catfish diet to increase the antioxidant response.
Com a intensificação do cultivo, os peixes se tornam mais susceptíveis ao estresse e, por consequência, ao aparecimento de doenças. Para tentar minimizar este problema, os produtores utilizam agroquímicos que, além de prejudicarem o meio ambiente, podem também prejudicar a saúde dos produtores e consumidores. O óleo essencial (EO, do inglês essential oil) da Lippia alba pode ser uma alternativa natural, pois apresenta diversos efeitos que podem reduzir as alterações fisiológicas decorrentes do estresse inerente à aquicultura. Neste estudo foi avaliada a influência de cinco dietas contendo o EO de L. alba (0, 0.25, 0.5, 1.0 e 2.0 mL de EO por kg de dieta) sobre o crescimento e a resposta antioxidante em juvenis de jundiás. Após um período de 60 dias de alimentação, os jundiás foram pesados e medidos individualmente e eutanasiados para amostragem do encéfalo, brânquias, fígado, rim e músculo. Os biomarcadores de estresse oxidativo, substâncias que reagem ao ácido tiobarbitúrico (TBARS), hidroperóxidos lipídicos (LOOH), superóxido dismutase (SOD), catalase (CAT), glutationa peroxidase (GPx), glutationa redutase (GR), glutationa-S-transferase (GST) e o conteúdo dos grupos tióis não proteicos (NPSH) foram determinados. A dieta contendo o EO de L. alba não influenciou o crescimento. Quanto aos biomarcadores de estresse oxidativo, o EO diminuiu a lipoperoxidação (LPO) avaliada através do TBARS e dos LOOH nas brânquias, fígado, rim e músculo do jundiá, não mostrando nenhum efeito sobre a LPO no encéfalo. A dieta com o EO aumentou a atividade das enzimas antioxidantes, SOD, CAT, GPx, GST e o conteúdo de NPSH no encéfalo; SOD, GR e GST nas brânquias; CAT, GR e o conteúdo de NPSH no fígado; CAT, GR e o conteúdo de NPSH no rim e SOD, GPx e o conteúdo de NPSH no músculo, em comparação ao grupo controle. Estes resultados indicam que o EO de L. alba não interfere no crescimento, diminui a LPO e aumenta a atividade das enzimas antioxidantes na maioria dos tecidos avaliados, podendo ser adicionado à dieta de jundiás para aumentar a resposta antioxidante.

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Di, Maggio Paula. "Dietary lipids and inflammation : chylomicron remnants suppress pro-inflammatory pathways and activate antioxidant defence mechanisms in human macrophages." Thesis, Royal Veterinary College (University of London), 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.618287.

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Bagatini, Margarete Dulce. "Avaliação da atividade de enzimas que degradam nucleotídeos de adenina e ésteres de colina e estudo do perfil oxidativo em pacientes com cardiopatia isquêmica." Universidade Federal de Santa Maria, 2010. http://repositorio.ufsm.br/handle/1/4422.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico
Ischemic heart disease (IHD) is a major cardiovascular disease. The term ischemia refers to a lack of oxygen due to inadequate perfusion, which results from an imbalance between oxygen supply and demand. The most common cause of myocardial ischemia is atherosclerotic obstructive coronary artery disease caused by rupture or ulceration of atheromatous plaque and subsequent thrombus formation. Platelets are one of the most important blood components that participate in and regulate thrombus formation by releasing active substances such as adenine nucleotides ATP and ADP. Once their action is exerted, the nucleotides are degraded by a group of enzymes called ectonucleotidases. These enzymes are responsible for the hydrolysis of ATP and ADP to AMP, and consequent formation of adenosine, a cardioprotective and anti-inflammatory molecule. Another important anti-inflammatory molecule is acetylcholine (ACh). However, ACh is rapidly hydrolyzed by the enzymes acetylcholinesterase (AChE) and tyrylcholinesterase (BuChE). Following ischemia, an elevated production of reactive oxygen species (ROS) occurs. The imbalance between ROS production and degradation may lead to an increase in oxidative stress. This study aimed to determine the activity of enzymes involved in thromboregulation, such as NTPDase, 5'-nucleotidase, E-NPP and ADA, the activity of enzymes that degrade choline esters: AChE and BuChE, as well as the parameters of oxidative stress in IHD patients and controls. Evaluation of the oxidant system was carried out by lipid peroxidation and carbonyl protein determination, and the enzymatic and nonenzymatic antioxidant defense measurements were performed in total blood, plasma, and serum of IHD patients. Results showed an increase in the NTPDase and 5'-nucleotidase activities as revealed by nucleotides hydrolysis ATP, ADP and AMP. An increase in E-NPP activity was also observed in IHD patients. However, a decrease in ADA activity was observed. Based on the results presented here we suggest that the pathological condition in IHD produced alterations in ectonucleotidase activities as a compensatory organic response, with the objective of maintaining the levels of adenosine, which is a cardioprotective molecule. An increase in the activity of enzymes that degrade choline esters (AChE and BuChE) in IHD patients was observed. Increasing total blood and serum activities of AChE and BuChE enzymes indirectly reflect reduced levels of ACh. The enhancement of local and systemic inflammatory events is observed due to the absence of the negative feedback control exerted by ACh. Regarding oxidant levels, an increase in TBARS and carbonyl protein levels was observed in acute myocardial infarction (AMI) patients when compared to the control group. The same occurred for the activities of the enzymatic antioxidants, superoxide dismutase (SOD), and catalase (CAT). However, a decrease in nonenzymatic antioxidants, such as vitamin C and vitamin E, was observed in AMI patients when compared to control. These results suggest an increase in oxidative stress in AMI, which was probably a result of the ischemic/reperfusion moment, as well as a decrease of antioxidant defenses. Furthermore, the increased antioxidant defense may act as a compensatory mechanism in consequence of the overproduction of ROS after AMI. In conclusion, IHD results in oxidative and inflamatory damages as well as an increase in the organism defenses as a compensatory response.
A cardiopatia isquêmica (CI) é uma das principais doenças cardiovasculares. O termo isquemia refere-se à falta de oxigênio, secundária à perfusão inadequada do miocárdio, que gera desequilíbrio entre a oferta e a demanda deste gás. A causa mais comum de isquemia miocárdica é a doença aterosclerótica obstrutiva das artérias coronárias, causada por ruptura ou ulceração da placa ateromatosa e consequente formação de trombo. As plaquetas são um dos mais importantes componentes do sangue que participam na regulação dos processos tromboembólicos por liberação de substâncias ativas como os nucleotídeos de adenina, ATP e ADP. Uma vez exercida sua ação esses nucleotídeos são degradados por um grupo de enzimas denominadas de ectonucleotidases. Essas são responsáveis pela hidrólise do ATP e ADP até AMP e consequente formação da adenosina, uma molécula cardioprotetora e anti-inflamatória. Outra importante molécula anti-inflamatória é a acetilcolina (ACh). Entretanto, a ACh é rapidamente hidrolisada pelas enzimas acetilcolinesterase (AChE) e butirilcolinesterase (BuChE). Acompanhando a isquemia temos uma produção elevada de espécies reativas de oxigênio (EROs). Um desequilíbrio entre a produção e a degradação de EROs pode levar a um aumento do estresse oxidativo. Neste trabalho determinaram-se a atividade das enzimas envolvidas na tromboregulação: NTPDase, 5 -nucleotidase, E-NPP e ADA, e a atividade de enzimas que degradam ésteres de colina: AChE e BuChE, além dos parâmetros de estresse oxidativo em pacientes cardiopatas e controles. Foi realizada a avaliação do sistema oxidante através da determinação da peroxidação lipídica e da carbonilação protéica e a medida das defesas antioxidantes enzimáticas e não enzimáticas do organismo, em sangue total, plasma e soro destes pacientes. Os resultados demonstraram um aumento na atividade da NTPDase e da 5 -nucleotidase, revelada através da hidrólise dos nucleotídeos ATP, ADP e AMP. Para a enzima E-NPP também foi observado um aumento na sua atividade em pacientes cardiopatas. Entretanto, para a ADA observou-se uma diminuição na atividade. Esses resultados sugerem uma resposta orgânica compensatória do organismo frente ao estado patológico formado, com o objetivo de manter os níveis de adenosina, uma molécula cardioprotetora. Para as enzimas que degradam ésteres de colina foi observado um aumento tanto na atividade da AChE quanto da BuChE em pacientes cardiopatas. Um aumento na atividade sérica e no sangue total da atividade da BuChE e da AChE pode refletir indiretamente níveis reduzidos de ACh que, por sua vez, irá reforçar eventos inflamatórios locais e sistêmicos, devido à ausência do controle de retroalimentação negativa exercido pela ACh. Em relação aos níveis de oxidantes determinados, observou-se um aumento nos níveis de TBARS e proteína carbonil em soro de pacientes com infarto agudo do miocárdio (IAM) quando comparados com o grupo controle. Esse aumento também foi observado para as defesas antioxidantes enzimáticas superóxido dismutase (SOD) e catalase (CAT). Entretanto, observou-se um decréscimo das defesas antioxidantes não enzimáticas como a vitamina C e a vitamina E no soro de pacientes com IAM. Estes dados sugerem um aumento do estresse oxidativo como resultado do momento de isquemia/reperfusão e da diminuição das defesas antioxidantes não enzimáticas. Além disso, o aumento das defesas antioxidantes enzimáticas poderiam agir como um mecanismo compensatório como consequência da superprodução de EROs após o IAM. Concluí-se então, que a CI resulta tanto em danos oxidativos e inflamatórios como mobilização das defesas do organismo para uma resposta compensatória.

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D’Avila, Roseane Farias. "Efeito da redução de aporte hídrico e aplicação de radiação UV-C sobre compostos relacionados à qualidade e ao metabolismo de glicosinolatos em brócolis (Brassica oleracea L. var. italica)." Universidade Federal de Pelotas, 2017. http://guaiaca.ufpel.edu.br:8080/handle/prefix/4138.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Características diversas das habituais durante o cultivo de vegetais e na pós-colheita podem ser reconhecidas como fatores de estresse pelo metabolismo e, dependendo da intensidade, levar ao acúmulo de compostos de defesa, relacionados ao aumento da vida de prateleira e a atividades antioxidantes e anticancerígenas in vivo. Deste modo, o efeito do cultivo de brócolis sob condições de estresse hídrico e da aplicação de radiação UV-C durante a pós-colheita sobre compostos relacionados a atributos sensoriais e funcionais foram analisados durante colheitas realizadas no verão e inverno. O cultivo sob estresse hídrico ocasionou a diminuição do teor de ácido L-ascórbico em todas as amostras, e os teores de glicosinolatos nos brócolis colhidos no verão, o que também ocorreu para clorofila a e carotenoides. No inverno, o estresse hídrico levou ao aumento de glicosinolatos somente após o armazenamento. Observaram-se diferenças significativas pela aplicação de UV-C após sete dias de armazenamento. No verão, a utilização da dose de 7 kJ.m-2 de UV-C resultou no aumento do conteúdo de clorofilas a e b e de carotenoides nos brócolis cultivados sob aporte hídrico regular. A mesma dose, quando aplicada a plantas cultivadas sob estresse hídrico, promoveu aumento significativo apenas de carotenoides e ácido L-ascórbico. O teor de glicosinolatos em brócolis cultivados no verão foi intensificado pelo cultivo sob condições de estresse hídrico combinado com aplicação de 10 kJ.m-2 de UV-C. No inverno, o aumento do teor de glicosinolatos foi observado aplicando a dose de 7 kJ.m-2, e foi acompanhado pela redução da atividade de mirosinases. Em ambos os cultivos conduzidos no inverno, houve um aumento de isotiocianatos quando brócolis cultivados sob estresse hídrico foram tratados com 10 kJ.m-2 de UV-C. Em vista dos resultados, conclui-se que as respostas metabólicas à redução do aporte hídrico e à aplicação de radiação UV-C são diferentes devido à época de cultivo da hortaliça, com exceção do teor do ácido L-ascórbico, que é reduzido pelo cultivo com estresse independentemente da estação.
Characteristics different from the usual ones during the growing and in the post-harvest of vegetables can be recognized as stress factors by the metabolism and, depending on the level, lead to the accumulation of defense compounds, related to the increase of the shelf life and to the antioxidant and anticancer activities in vivo. Thus, the effect of broccoli cultivation under water stress and of the application of UV-C radiation during post-harvest on compounds related to sensorial and functional attributes were analyzed during summer and winter harvests. The cultivation under water stress caused a decrease in the L-ascorbic acid content in all the samples, and the glycosinolate content in the broccoli harvested in the summer, which also occurred for chlorophyll a and carotenoids. In winter, water stthe pigments presented opposite patterns between the years analyzed, which also occurred with the isothiocyanates, compounds derived from glucosinolates. The stress led to the increase of glucosinolates only after storage. Significant differences were observed by application of UV-C after seven days of storage. In the summer, the use of the 7 kJ.m-2 UV-C dose resulted in increased content of chlorophyll a and b and carotenoids in broccoli grown under regular water intake. The same dose, when applied to the plants grown under water stress, promoted a significant increase only of carotenoids and L-ascorbic acid. The glucosinolates content in broccoli grown in summer was intensified by the cultivation under water stress conditions combined with the application of 10 kJ.m-2 of UV-C. In the winter, the glucosinolates content increase was observed by applying the 7 kJ.m-2 dose, and it was accompanied by a reduction in myrosinase activity. In both cultures conducted in winter, there was an increase in isothiocyanates when broccoli cultivated under water stress were treated with 10 kJ.m-2 of UV-C. In view of the results, it is concluded that the metabolic responses to the reduction of the water supply and to the application of UV-C radiation are different due to the season of cultivation of the vegetable, except for the L-ascorbic acid content, which is reduced by the cultivation with water stress regardless of the season.

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Roberts, Blaine R. "Structural studies of the antioxidant defense enzymes : copper, zinc superoxide dismutase and alkyl hydroperoxide reductase flavoprotein /." Connect to this title online, 2007. http://hdl.handle.net/1957/5054.

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Xu, Chenping. "The effects of solar ultraviolet-B on the proteome and antioxidant defense systems in soybean leaves." College Park, Md. : University of Maryland, 2007. http://hdl.handle.net/1903/6762.

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Thesis (Ph. D.) -- University of Maryland, College Park, 2007.
Thesis research directed by: Natural Resource Sciences. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.

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Peixoto, Luanna Fernandes. "Avaliação do efeito protetor do extrato bruto hidroalcoólico das folhas de Eugenia dysenterica DC. sobre a neurotoxicidade induzida pelo alumínio." Universidade Federal de Goiás, 2015. http://repositorio.bc.ufg.br/tede/handle/tede/6134.

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incidence of neurodegenerative disease (ND) is increasing with the world population aging. Among them, Alzheimer's disease (AD) is the most common of dementia in the elderly population. The AD has been linked to oxidative stress resulting in neurodegenerative disorders, such as the impairment of the antioxidant and cholinergic systems. AChE inhibitors drugs are a treatment option used for AD. However, until now, the drug treatment only temporary attenuates the AD symptoms and new drug targets, as the medicinal plants, are necessary for a better treatment of this disease. Eugenia dysenterica DC (Myrtaceae), popularly known as cagaita, is a native plant from the Cerrado region of Brazil. It is used in the folk medicine to treat diarrhea, jaundice and diabetes. Data from literature reported the presence of phenolic compounds, such as flavonoids and tannins, in the leaves of E. dysenterica. Thus, the aim of this study was to evaluate the neuroprotective effect of crude hydroalcoholic extract of E. dysenterica leaves (HEED), using a model of neurotoxicity induced by aluminium in mice and that causes similar cellular alterations of that observed in the Alzheimer’s disease. The results showed the HEED increased the mice performance in the passive avoidance test, showing the reversion of the cognitive damage promoted by aluminium. In addition, the HEED reduced the neuronal lipid peroxidation and restored the activity of superoxide dismutase (SOD), catalase (CAT) and acetylcholinesterase (AChE) enzymes in mice brain. The histological analysis showed the HEED decreased the incidence of neuronal death by necrosis. Taken together, the results here obtained suggest that the antioxidant properties of HEED are the responsible for its neuroprotective effect.
A incidência de doenças neurodegenerativas (DN) vem aumentando com o envelhecimento populacional. Dentre as DN a doença de Alzheimer (DA) é a forma mais comum de demência na população idosa. Um dos fatores envolvidos no desenvolvimento da DA é o estresse oxidativo neuronal que pode resultar em diversas desordens neurodegenerativas, como o comprometimento dos sistemas antioxidante e colinérgico. Um dos tratamentos utilizados para esta doença são os fármacos inibidores de acetilcolinesterase (AChE) porém, as terapias disponíveis apenas atenuam temporariamente os sintomas. Nesse sentido, novas terapias são necessárias para o tratamento da DA e o estudo de plantas pode ser uma fonte para obtenção de novas opções terapêuticas. Eugenia dysenterica DC (Myrtaceae), popularmente conhecida como cagaita, é uma planta encontrada em região de Cerrado, utilizada na medicina popular para tratar doenças diarreicas, icterícia e diabetes. Dados da literatura relatam a presença de compostos fenólicos, como flavonoides e taninos, nas folhas de E. dysenterica., substâncias descritas como potenciais antioxidantes e anticolinesterásicos. Dessa forma, o objetivo deste trabalho foi avaliar o efeito neuroprotetor do extrato bruto hidroalcoólico das folhas de Eugenia dysenterica (EHED) em camundongos, em um modelo de neurotoxicidade induzida por alumínio. O EHED aumentou o tempo de latência na memória de curta e longa duração no teste esquiva passiva, demonstrando a reversão do prejuízo cognitivo promovido pelo alumínio. Os testes chaminé e campo aberto demonstraram que não houve comprometimento na atividade locomotora dos animais. As análises histológicas demonstraram que o tratamento com EHED diminuiu a incidência da morte neuronal por necrose causada pelo AlCl3. Nos ensaios bioquímicos, observou-se que o EHED foi capaz de reduzir a lipoperoxidação e restaurar a atividade das enzimas antioxidantes superóxido dismutase (SOD) e catalase (CAT). Além disso, o EHED foi capaz de restaurar a atividade da AChE, revertendo os danos causados pelo AlCl3. Em conclusão, os resultados obtidos são sugestivos de que o EHED apresenta atividade neuroprotetora por apresentar propriedades antioxidantes, inibindo os efeitos deletérios centrais promovidos pelo alumínio e que se assemelham às alterações celulares descritas para a Doença de Alzheimer.

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Murphy, Kelsey E. "BBB-bypassing polysaccharide mini-GAGR activates the neuronal Nrf2- mediated antioxidant defense system for the treatment of Alzheimer’s disease." University of Toledo Health Science Campus / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=mco1576192220098119.

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Melendez, Juan Andres. "The effects of cellular quiescence on the antioxidant defense enzymes of bovine embryonic lung fibroblasts: a survey." Thesis, Virginia Polytechnic Institute and State University, 1989. http://hdl.handle.net/10919/52088.

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The aging phenomena is a process to which all organisms eventually succumb. The universality of this phenomena suggests that there may be one overwhelming factor involved. The exact biochemical basis of aging is still unclear. Free radicals such as the superoxide radical (O₂⁻) and the hydroxyl radical (OH⁻), formed in biological oxidation reactions may be responsible for cellular aging. Because of the high reactivity of the O₂⁻ and the OH⁻ they can produce extensive damage to lipids, proteins, and nucleic acids. In this study we have developed an in vitro quiescent model using density dependent bovine embryonic lung fibroblast (BELF). The effect of this process on the antioxidant defense enzymes such as, the superoxide dismutases, catalase, glutathione reductase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase, was studied. We have also extensively monitored the levels of free radical in the cell by both direct and indirect methods. The results indicate that no significant (p<0.05) changes in the activity of any of the major antioxidant enzymes in our quiescent model. Significant increases were observed in the intracellular levels of lipofuscin (age pigment) with time, but no changes in the generation of free radicals were observed using electron spin resonance spectrometry, cytochrome c reduction or spectrofluorometric techniques (caution should be placed in statistical interpretation of the data because of the small sample size in some experiments). The transcriptional and translational controls of the one of the major antioxidant defense enzymes (manganese superoxide dismutase) in bovine embryonic lung fibroblasts, human pulmonary artery endothelial cells (HPAE) and bovine PAE cell lines were also studied. Our preliminary data suggest that inhibitors of protein and RNA synthesis both cause a significant decrease in the induction of the manganese SOD in bovine pulmonary endothelial cells.
Master of Science

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Bazito, Olivia Domingues. "Estresse oxidativo e bioluminescência nos fungos Gerronema viridilucens e Mycena lucentipes." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/46/46136/tde-03092012-144815/.

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Espécies reativas de oxigênio (EROs) são produzidas normalmente durante o metabolismo de organismos aeróbios. Fungos degradadores de lignina geram estas espécies também no processo de degradação da lignina. As espécies de fungos bioluminescentes Gerronema viridilucens e Mycena lucentipes foram utilizadas para se estabelecer possível dependência entre intensidade de bioluminescência, viabilidade celular e atividades das enzimas de defesa antioxidante e ligninolíticas nos micélios e corpos de frutificação. Verificou-se o efeito de espécies causadoras de estresse químico (metais e fenóis) na emissão de luz, viabilidade celular, defesas antioxidantes e enzimas de respiração celular no fungo bioluminescente G. viridilucens, com o objetivo de conectar a inibição da bioluminescência com danos oxidativos ao organismo. Constatou-se que diferentes espécies de fungos bioluminescentes podem apresentar características diferentes quanto à emissão de luz e proteção antioxidante. Diferenças na intensidade e variação temporal da emissão de luz de diferentes espécies foram observadas nos corpos de frutificação e também no micélio. Isto foi revelado pela irregularidade do perfil de luz reprodutível para a espécie M. lucentipes, ao contrário do observado para G. viridilucens. A viabilidade celular de ambas as espécies varia com o tempo, sendo que no caso de G. viridilucens seu perfil é similar ao da bioluminescência. Os ensaios enzimáticos indicam maior atividade no micélio dos fungos do que nos corpos de frutificação, provavelmente pela função específica reprodutora do corpo de frutificação, enquanto a atividade metabólica do fungo está concentrada no micélio. As enzimas ligninolíticas também apresentam atividade baixa nas culturas estudadas, provavelmente por serem enzimas de degradação extracelulares. O fato de ambas viabilidade celular e bioluminescência do micélio serem reduzidas na presença dos metais (cobre e cádmio) e fenóis (fenol e 2,4,6-triclorofenol) testados atesta a interrelação entre atividade luminogênica e injúria oxidativa aos fungos. Os metais parecem afetar mais negativamente as defesas antioxidantes dos fungos do que os fenóis, os quais possivelmente são eliminados pela atividade da glutationa S-transferase (GST), sem também afetar as demais defesas antioxidantes. No conjunto, estes resultados possibilitam estabelecer uma relação metabólica entre abatimento da bioluminescência e as defesas antioxidantes do organismo. No caso dos metais, os sistemas de defesa antioxidante envolvendo a glutationa são bastante importantes, tanto para eliminar peróxidos produzidos na presença de cobre, como na quelação de cádmio pela glutationa. Sob condições normais, a bioluminescência, defesas antioxidantes e respiração celular do organismo estariam funcionando e o NAD(P)H seria mobilizado por todos estes sistemas. Quando o fungo é submetido ao estresse químico, o fluxo de NAD(P)H seria desviado da bioluminescência para sustentar prioritariamente as defesas antioxidantes e a respiração celular, essenciais para a proteção, manutenção e reprodução do organismo
Reactive Oxygen Species (ROS) are normally produced during the metabolism of aerobic organisms. Ligninolitic fungi also produce these oxidizing species also during the lignin degradation process. The bioluminescent species Gerronema viridilucens and Mycena lucentipes were studied aiming to establish a correlation between the temporal profiles of bioluminescence, cellular viability and antioxidant defense enzymes and ligninolitic enzymes in mycelium and fruiting bodies. Chemical toxicants such as metals and phenols were here found to affect light emission, cellular viability, antioxidant defenses and cellular respiration enzymes when administered to G. viridilucens, thereby attesting a metabolic connection between bioluminescence inhibition and fungal oxidative damage. Different species of fungi exhibit different characteristics linked to light emission and antioxidant defenses. Differences in light emission displayed by different species do not resume to fruiting bodies, but the light profile and intensity can also vary in the mycelia. This may explain the irreproducibility of the light profile from M. lucentipes, differently to that observed with G. viridilucens. The cellular viability of both species varies with time, G. viridilucens profile being similar to the time course of bioluminescence. The enzymatic data pointed to higher activities in mycelium than in fruiting bodies, probably due to a main reproductive function of the latter, whereas the metabolic activities are prevalent in the mycelium. Ligninolytic enzymes exhibit low activities in the extracts of fungus samples, probably because they are extracellular degradation enzymes. The inhibition effect of phenols and metals (copper and cadmium) on mycelium viability reinforces the notion that cellular oxidative damage hampers bioluminescence emission. Redox active (copper) and heavy metals (cadmium) were found to display higher impact on antioxidant defenses than phenols (phenol and 2,4,6-trichlorophenol), which are expected to be promptly metabolized and excluded by principally glutathione S-transferase (GST). Notably, a metabolic correlation between bioluminescence inhibition and antioxidant defenses was unveiled by the present work. Regarding the metals, glutathione was found to be a crucial antioxidant, both to eliminate peroxides when in the presence of copper, and to act as a cadmium chelating agent. Under normal conditions, the bioluminescence system, the antioxidant defenses and the cellular respiration sets cooperate through the common demand of reducing power of NAD(P)H. Under chemical stress, the NAD(P)H flux would be deviated from bioluminescence, to principally sustain the antioxidant defenses and cellular respiration, essential for the protection, maintenance and reproduction of the organism.

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