Academic literature on the topic 'Oxidative stress factors'

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Journal articles on the topic "Oxidative stress factors"

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Borodin, E. A. "OXIDATIVE STRESS AND BRONCHIAL HYPERSENSITIVITY TO LOW TEMPERATURE AND OSMOTIC FACTORS." Amur Medical Journal, no. 3 (2017): 17–19. http://dx.doi.org/10.22448/amj.2017.3.17-19.

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Dorszewska, Jolanta, Marta Kowalska, Michał Prendecki, Thomas Piekut, Joanna Kozłowska, and Wojciech Kozubski. "Oxidative stress factors in Parkinson’s disease." Neural Regeneration Research 16, no. 7 (2021): 1383. http://dx.doi.org/10.4103/1673-5374.300980.

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Brini, Faiçal, and Walid Saibi. "Oxidative stress and antioxidant defense in Brassicaceae plants under abiotic stresses." SDRP Journal of Plant Science 5, no. 1 (2021): 232–44. http://dx.doi.org/10.25177/jps.5.1.ra.10694.

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Brassicaceae plants, as an important source of primary and secondary metabolites, are becoming a research model in plant science. Plants have developed different ways to ward off environmental stress factors. This is lead to the activation of various defense mechanisms resulting in a qualitative and/or quantitative change in plant metabolite production. Reactive oxygen species (ROS) is being continuously produced in cell during normal cellular processes. Under stress conditions, there are excessive production of ROS causing progressive oxidative damage and ultimately cell death. Despite their destructive activity, ROS are considered as important secondary messengers of signaling pathway that control metabolic fluxes and a variety of cellular processes. Plant response to environmental stress depends on the delicate equilibrium between ROS production, and their scavenging. This balance of ROS level is required for performing its dual role of acting as a defensive molecule in signaling pathway or a destructive molecule. Efficient scavenging of ROS produced during various environmental stresses requires the action of several non-enzymatic as well as enzymatic antioxidants present in the tissues. In this review, we describe the ROS production and its turnover and the role of ROS as messenger molecules as well as inducers of oxidative damage in Brassicaceae plants. Further, the antioxidant defense mechanisms comprising of enzymatic and non-enzymatic antioxidants have been discussed. Keywords: Abiotic stress, Antioxidant defence, Brassicaceae, Oxidative stress, ROS
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Hao, Yue, Mingjie Xing, and Xianhong Gu. "Research Progress on Oxidative Stress and Its Nutritional Regulation Strategies in Pigs." Animals 11, no. 5 (May 13, 2021): 1384. http://dx.doi.org/10.3390/ani11051384.

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Oxidative stress refers to the dramatic increase in the production of free radicals in human and animal bodies or the decrease in the ability to scavenging free radicals, thus breaking the antioxidation–oxidation balance. Various factors can induce oxidative stress in pig production. Oxidative stress has an important effect on pig performance and healthy growth, and has become one of the important factors restricting pig production. Based on the overview of the generation of oxidative stress, its effects on pigs, and signal transduction pathways, this paper discussed the nutritional measures to alleviate oxidative stress in pigs, in order to provide ideas for the nutritional research of anti-oxidative stress in pigs.
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Lozano-Picazo, Carmen María, and Francisco Fernández-Belda. "Especies reactivas de oxígeno y su implicación en Biomedicina." Anales de Veterinaria de Murcia 34 (December 16, 2020): 17–26. http://dx.doi.org/10.6018/analesvet.332621.

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Las especies reactivas de oxígeno (ROS) actúan como regulador intracelular cuando se generan de forma controlada en puntos concretos de la célula. Modifican la función de proteínas mediante la oxidación reversible de cisteínas. Hay quinasas y fosfatasas de proteínas, factores de transcripción y canales iónicos que están regulados por ROS. Estrés oxidativo y daño celular aparecen cuando los mecanismos antioxidantes de protección son incapaces de mantener bajo el nivel intracelular de ROS. En estas condiciones, ROS inducen pérdida de viabilidad celular en patologías degenerativas de corazón y cerebro y promueven proliferación celular ilimitada en procesos tumorales. La alteración de la función mitocondrial juega un papel clave en la generación del estrés oxidativo y por tanto es una diana terapéutica preferente para evitar o aminorar los daños oxidativos producidos por ROS. Reactive oxygen species (ROS) act as intracellular regulator when they are generated under control in specific cell spots. They modify proteins function by cysteine reversible oxidation. There are protein kinases and phosphatases, transcription factors and ionic channels that are regulated by ROS. Oxidative stress and cell damage arise when the protection antioxidant mechanisms are unable to keep low the intracellular ROS level. Under these conditions, ROS induce cell viability loss in heart and brain degenerative pathologies and promote unlimited cell proliferation in tumor processes. Alteration of the mitochondrial function is a key player in the oxidative stress generation and therefore it is preferential therapeutic target for prevention or attenuation of the ROS-induced oxidative damage.
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Li, Jinjin, Yuan Zhang, Jingyun Zhang, Rongna Dong, Juanjuan Guo, and Qiumei Zhang. "Oxidative Stress and Its Related Factors in Latent Autoimmune Diabetes in Adults." BioMed Research International 2021 (September 13, 2021): 1–6. http://dx.doi.org/10.1155/2021/5676363.

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Aims. Few research was reported to explore oxidative stress in individuals with latent autoimmune diabetes in adults (LADA). Therefore, our goal is to study oxidative stress and related factors in LADA patients. Methods. In this study, 250 Chinese inpatients were diagnosed with LADA ( n = 110 ) and type 2 diabetes mellitus ( n = 140 ) and 140 healthy volunteers were recruited. Moreover, individuals with LADA were followed for 6 months to evaluate whether short-term glycemic control during hospitalization can improve oxidative stress. Clinical and laboratory measurements of height, weight, blood pressure, glycosylated hemoglobin (HbA1c), blood lipids, 8-isoprostaglandin F2α (8-iso-PGF2α), and superoxide dismutase (SOD) were performed. Stepwise multiple regression analyses were used to assess factors that related to oxidative stress in individuals with LADA. Results. Compared with patients with type 2 diabetes, individuals with LADA have better oxidative stress and worse oxidative stress than healthy volunteers. After multiple regression analyses, systolic blood pressure, HbA1c, duration of diabetes, and diabetic retinopathy were associated with 8-iso-PGF2α and HbA1c. Diabetic retinopathy and diabetic ketosis were associated with SOD in individuals with LADA. Our results also revealed that, after 6 months of follow-up, oxidative stress was improved to some extent in persons with LADA. Conclusions. Our results show that compared with type 2 diabetes, LADA means less oxidative stress, and compared with healthy volunteers, it means more oxidative stress. Systolic blood pressure, HbA1c, duration of diabetes, diabetic retinopathy, and ketosis were associated with oxidative stress in individuals with LADA. Furthermore, short-term glycemic control can improve oxidative stress to some extent in individuals with LADA.
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Ryan, Sarah M., Kaitie Wildman, Briseida Oceguera-Perez, Scott Barbee, Nathan T. Mortimer, and Alysia D. Vrailas-Mortimer. "Evolutionarily conserved transcription factors drive the oxidative stress response in Drosophila." Journal of Experimental Biology 223, no. 14 (June 12, 2020): jeb221622. http://dx.doi.org/10.1242/jeb.221622.

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ABSTRACTAs organisms are constantly exposed to the damaging effects of oxidative stress through both environmental exposure and internal metabolic processes, they have evolved a variety of mechanisms to cope with this stress. One such mechanism is the highly conserved p38 MAPK (p38K) pathway, which is known to be post-translationally activated in response to oxidative stress, resulting in the activation of downstream antioxidant targets. However, little is known about the role of p38K transcriptional regulation in response to oxidative stress. Therefore, we analyzed the p38K gene family across the genus Drosophila to identify conserved regulatory elements. We found that oxidative stress exposure results in increased p38K protein levels in multiple Drosophila species and is associated with increased oxidative stress resistance. We also found that the p38Kb genomic locus includes conserved AP-1 and lola-PT transcription factor consensus binding sites. Accordingly, over-expression of these transcription factors in D. melanogaster is sufficient to induce transcription of p38Kb and enhances resistance to oxidative stress. We further found that the presence of a putative lola-PT binding site in the p38Kb locus of a given species is predictive of the species' survival in response to oxidative stress. Through our comparative genomics approach, we have identified biologically relevant putative transcription factor binding sites that regulate the expression of p38Kb and are associated with resistance to oxidative stress. These findings reveal a novel mode of regulation for p38K genes and suggest that transcription may play as important a role in p38K-mediated stress responses as post-translational modifications.
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H., Yeldu M., and Arinola O. G. "Oxidative stress factors in Nigerians with rheumatoid arthritis." International Journal of Research in Medical Sciences 5, no. 5 (April 26, 2017): 1948. http://dx.doi.org/10.18203/2320-6012.ijrms20171823.

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Background: Rheumatoid arthritis (RA) is a chronic progressive inflammatory autoimmune disorder characterized by symmetric erosive synovitis and sometimes with multi-system involvement. But the exact mechanism of the disease is not fully understood. In the light of above explanation, the present study measured the plasma levels of total peroxide potential (TPP), total antioxidant potential (TAP), malondialdehyde (MDA), oxidative stress index (OSI) and nitric oxide (NO) in relation to the titer of rheumatoid factor among RA patients compared with controls.Methods: This study included 28 rheumatoid arthritis patients and 28 apparently healthy subjects as controls who were matched for age (50-60 years), sex, and socioeconomic status. Rheumatoid factor was estimated using latex method as described by manufacturer. Anthropometric parameters and plasma levels of TPP, TAP, OSI, MDA and NO were determined using standard techniques.Results: The result indicated that with the exception of mean body weight which was significantly (p<0.001) higher among RA patients (90.61±2.02 years) as compared with controls (77.91±2.51 years), mean age, height and body mass index of RA patients (55.68±1.05kg, 1.65±0.01m and 33.40±0.83 kg/m2 respectively) were not significantly different compared with controls (54.07±1.04kg, 1.61±0.02m and 30.44±1.28 kg/m2 respectively). Plasma TPP, NO, OSI and MDA were significantly (p<0.01; p<0.001) higher while, plasma TAP is significantly lower among RA patients compared with controls. Plasma MDA was positively correlated with titer of rheumatoid factor in the RA patients.Conclusions: Our findings therefore may raise the concept that there are some yet unknown key events in the pathogenesis of RA determination of sex of the skull along with other parameters.
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Block, G. "Factors Associated with Oxidative Stress in Human Populations." American Journal of Epidemiology 156, no. 3 (August 1, 2002): 274–85. http://dx.doi.org/10.1093/aje/kwf029.

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Møller, Peter, Håkan Wallin, and Lisbeth E. Knudsen. "Oxidative stress associated with exercise, psychological stress and life-style factors." Chemico-Biological Interactions 102, no. 1 (September 1996): 17–36. http://dx.doi.org/10.1016/0009-2797(96)03729-5.

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Dissertations / Theses on the topic "Oxidative stress factors"

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Wong, Hoi-kin, and 黃凱健. "New factors that affect adrenomedullin expression." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/195971.

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ADM is a 52-amino acid peptide which carries out multiple biological functions in cardiovascular system such as vasodilation and hypotension, and is a prognostic marker for cardiovascular diseases. Recent studies show that its plasma level is elevated in diabetes, however the reason and significance for such an increase has not been understood. Recent research has proposed that inflammation and oxidative stress both contribute to the pathogenesis of diabetes. If ADM is a marker in diabetes, it is possible that ADM is regulated by these two mechanisms, and so this project aims to investigate how these mechanisms could affect ADM expression. Recent studies have demonstrated that advanced glycation endproducts (AGEs) could lead to development of various diabetic complications. AGEs are formed as intermediate product in the non-enzymatic glycation of reducing sugars. Formation of these products is stimulated by hyperglycemia and oxidative stress, which could also induce ADM expression. Hence one of the studies investigated the direct effect of AGEs on ADM expression in an in vitro model. A rat macrophage cell line NR8383 was used to investigate the dose-response and time-point responses of macrophage cells in expressing ADM stimulated by AGEs. 6 hours of AGEs treatment resulted in no significant effect on ADM gene expression. The gene expression increased in all time points in which the change was at maximum after 1 hour of AGE treatment compared with other time points (P<0.05). However the time-dependent effect on ADM gene expression was insignificant compared with controls. How oxidative stress could lead to increased ADM expression deserves further investigation. ADM plays a role in inflammation that it could influence IL-6 and adiponectin expressions. This project also investigated whether IL-6 and adiponectin could affect ADM levels on the opposite. The associations between IL6 and adiponectin single nucleotide polymorphisms (SNPs) with plasma ADM levels were studied using a cohort of 476 subjects from the Cardiovascular Risk Factor Prevalence Study (CRISPS). Specific tagging SNPs were genotyped for the 476 subjects. Significant associations were identified for the IL6 SNP rs17147230 and adiponectin SNP rs182052 with plasma ADM levels in additive model (β=-0.096, P=0.034, and β=0.104, P=0.023 respectively adjusting for age and sex). The associations remained significant after adjusting for various covariates (P<0.05). Genotypic model shows that the minor alleles of rs17147230 and rs182052 resulted in 12.8% decrease and 17.7% increase in plasma ADM levels. These findings show that ADM level could be regulated by IL-6 which is an inflammatory cytokine, and adiponectin which is a protective peptide in inflammation. Reducing inflammation could lower ADM level and adiponectin might be a therapeutic candidate.
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Medicine
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Master of Philosophy
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Goumenaki, Eleni. "Factors governing the sensitivity of lettuce to ozone-induced oxidative stress." Thesis, University of Newcastle Upon Tyne, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432760.

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Poljak, Anne Medical Sciences Faculty of Medicine UNSW. "Oxidative, inflammatory and vascular factors in Alzheimer's disease." Publisher:University of New South Wales. Medical Sciences, 2008. http://handle.unsw.edu.au/1959.4/41273.

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In spite of impressive recent progress, the aetiopathogenesis of Alzheimer’s disease (AD) remains incompletely understood. The distinctive neuropathological features of AD, in particular the plaques and tangles, have been the particular focus of most aetiological theories. It is well accepted that AD is a multifactorial disease, with alterations to a variety of brain structures and cell types, including neurons, glia and the brain vasculature. Studies of risk factors have revealed a diversity of genetic variables that interact with health, diet and lifestyle-related factors in the causation of AD. These factors influence the structure, aggregation and function of a set of proteins that are increasingly the focus of research. The work in this thesis has focused on the pathophysiological aspects of some of these proteins in a number of cellular compartments and brain. Several assays have been established and techniques utilized in the completion of this work, including; differential detergent fractionation of brain tissue, 1D and 2D PAGE, western blotting with chemiluminescence detection, ELISA assays of Abeta 1-40 and 1-42, quantitative ECNI GCMS of o- and m-tyrosine as well as metabolites of the kynurenine pathway, quantitative MALDI-TOF assay of hemorphins and LCMSMS based proteomics, to identify proteins with altered expression levels in AD relative to control brain tissue. A variety of regional differences have been observed in the biochemistry of the AD cortex which are probably the outcome of local response variations to AD pathology. One of the most consistent threads throughout this work has been an apparent resilience of the occipital lobe relative to the other brain regions, as reflected in lower overall levels of oxidative stress and increased levels of proteins associated with metabolic processes, neuronal remodeling and stress reduction.
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Yuan, Jianfeng. "Effects of hyperbaric oxygen on oxidative stress, angiogenesis factors and endothelial cell injury." Thesis, University of Plymouth, 2007. http://hdl.handle.net/10026.1/2451.

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Hyperbaric oxygen (HBO) therapy is the administration of 100% oxygen at more than one atmosphere. It greatly improves tissue oxygenation and facilitates mechanisms of wound healing, which in turn benefits some patients with chronic wounds. A prominent fact in therapeutic HBO is the acceleration of neoangiogenesis during granulation tissue formation. Angiogenesis is a highly orchestrated event, a diverse range of cells and angiogenesis factors are involved in the process. The formation of reactive oxidative species (ROS) during HBO has been controversially considered as signalling regulator for angiogenic factors, as well as harmful originator for oxidative stress-induced cyto- and geno-toxicity in cells. This thesis contributes to this interesting while challenging topic. The project starts with investigation the direct HBO effects on blood vessel in vitro under physiological conditions and pathological conditions. The data clearly show that a single HBO treatment does not induce oxidative stress and cell damage under physiological conditions. Nevertheless, under pathological conditions, HBO induces oxidative stress with more ROS formation and cell damage. Interestingly, no evidence has been shown that HBO alone or synergically promotes nitric oxide and vascular endothelial growth factor production in either condition. The response of blood vessel to HBO treatment is not explained by autocrine release of angiogenesis factors locally in the blood vessel. Next, HBO-induced intracellular calcium (Ca2) changes and DNA damage were investigated using cultured human umbilical vein endothelial cells. A single HBO treatment significantly elevates intracellular Ca2+ level without inducing cell damage. Furthermore, HBO treatment has small but significant effect on DNA migration when evaluated by comet assay (e. g. 6.8 ± 0.8 % comparing to 4.6 ± 0.2 % DNA in tail of air treatment). However, this effect is totally reversible after 24h recovery. Importantly, HBO treatment protects endothelial cells against subsequent oxidative stress attack, and an increased antioxidant capacity was found as reflected in higher ratio of GSH to GSSG. The findings suggest that the beneficial effect of HBO is possibly via HBO-induced adaptation in cellular redox status. However, the details of Ca2+ signalling and roles of antioxidants in HBO treatment are areas for further research. Keywords: Hyperbaric Oxygen, Oxidative Stress, Vascular Endothelial Growth Factor, Nitric Oxide, Endothelial Cells, Calcium, DNA Damage
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Perry, Leslie M. "Regulation of Alternative Sigma Factors During Oxidative and Ph Stresses in the Phototroph Rhodopseudomonas Palustris." Thesis, University of North Texas, 2014. https://digital.library.unt.edu/ark:/67531/metadc700009/.

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Rhodopseudomonas palustris is a metabolically versatile phototrophic α-proteobacterium. The organism experiences a wide range of stresses in its environment and during metabolism. The oxidative an pH stresses of four ECF (extracytoplasmic function) σ-factors are investigated. Three of these, σ0550, σ1813, and σ1819 show responses to light-generated singlet oxygen and respiration-generated superoxide reactive oxygen species (ROS). The EcfG homolog, σ4225, shows a high response to superoxide and acid stress. Two proteins, one containing the EcfG regulatory sequence, and an alternative exported catalase, KatE, are presented to be regulated by σ4225. Transcripts of both genes show similar responses to oxidative stress compared to σ4225, indicating it is the EcfG-like σ-factor homolog and controls the global stress response in R. palustris.
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Mullan, B. A. "Factors influencing endothelial function and arterial pulse wave morphology : the role of oxidative stress." Thesis, Queen's University Belfast, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398095.

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Sarrafee, Sara. "ROLE OF THE PORPHYROMONAS GINGIVALIS ECF SIGMA FACTOR, SIGH, IN OXIDATIVE STRESS RESPONSE." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1804.

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Periodontal disease affects a majority of the US population. Porphyromonas gingivalis is the major etiological agent for development and progression of the disease. P. gingivalis is a hemin-dependent, obligate anaerobe that is found predominantly in periodontal pockets in infected patients. So for, little is known regarding the mechanisms which allow P. gingivalis to survive and sustain itself in the oral cavity. To better understand the adaptive mechanisms of the bacterium to the varying conditions in the oral cavity, regulatory mechanisms must be characterized. Sigma factors (σ) are responsible for initiating transcription by guiding RNA polymerase binding to specific DNA promoter sites. There are several sigma factors present in P. gingivalis, yet their roles have to be identified. Previous unpublished data indicate that a gene coding for an extracytoplasmic function sigma factor (ECF), SigH, is differentially regulated by exposure to molecular oxygen. Different assays were conducted to assess any variation in survival and/or growth between wild-type and SigH deficient strains of P. gingivalis. The ability to grow and survive in the presence of oxidative stress was compared between the mutant deficient in SigH and that of the parental strain. In addition, transcriptional profiles of the two strains were compared. Our assays indicate that growth was slower in the presence of oxygen in the Sigh-deficient mutant with an average difference of 27% compared to the wild-type. Transcriptional profiling showed down-regulation of genes encoding key enzymes associated with oxidative stress protection and oxidative metabolism in the absence of SigH, indicating that the sigma factor is a positive regulator of transcription required for survival of the bacterium in the presence of oxygen. If oxygen sensitivity can be established for this ECF-σ factor, it will aid in better understanding of P. gingivalis’ ability to survive in the oral cavity despite the presence of oxygen.
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Helmersson, Johanna. "Prostaglandins and Isoprostanes in Relation to Risk Factors for Atherosclerosis : Role of Inflammation and Oxidative Stress." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4803.

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Takahashi, Ken-ichi. "Humoral factors for oxidative stress and regulation of body weight in patients with Obstructive Sleep Apnea." Kyoto University, 2008. http://hdl.handle.net/2433/124218.

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Nälsén, Cecilia. "Measurement and Evaluation of Antioxidant Status and Relation to Oxidative Stress in Humans." Doctoral thesis, Uppsala University, Clinical Nutrition Research, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6742.

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Numerous diseases are associated with reduced antioxidant defence and oxidative stress. The antioxidant defence includes dietary and endogenous antioxidants and involves complex interactions between them. The effects of dietary factors on antioxidant status and oxidative stress of healthy humans were investigated in the studies described in this thesis. Assays of plasma antioxidant capacity encompass interactions between various antioxidants. Although uric acid has an unclear function as an antioxidant, it is a major determinant of antioxidant capacity. We measured antioxidant capacity in the presence and absence of uric acid to provide more information on the application of measures of antioxidant capacity. Individuals with high dietary intakes of various antioxidants and antioxidant rich foods, especially when combined, had higher plasma antioxidant capacities than those with lower antioxidant intakes. However, there were no associations between dietary intake of antioxidants or antioxidant rich foods and the plasma concentration of F2-isoprostanes, which is considered a reliable biomarker for oxidative stress. Intakes of various doses of a mixture of bilberry juice and black tea, rich in flavonoids for four weeks, increased antioxidant capacity in some groups, but urine levels of F2-isoprostanes were not affected. There were substantial individual variations in responses to the drinks related to baseline antioxidant capacity. Supplementation with eicosapentaenoic acid and docosahexaenoic acid decreased the plasma levels of F2-isoprostanes, but not prostaglandin F formation or antioxidant capacity.

It was concluded that a high intake of foods rich in antioxidants is related to improved antioxidant status. After intake of foods rich in antioxidants, the antioxidant status may increase, but with considerable individual variation in the responses, which warrants further investigation. Lipid peroxidation in vivo is not easily affected by dietary antioxidants in healthy humans. Although n-3 fatty acids are highly unsaturated, they reduce nonenzymatic free radical-catalyzed lipid peroxidation, but not enzymatic lipid peroxidation.

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Books on the topic "Oxidative stress factors"

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Packer, Lester, and Karel W. A. Wirtz, eds. Signalling Mechanisms — from Transcription Factors to Oxidative Stress. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79675-3.

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Saavedra-Molina, Alfredo. Mitochondrial dysfunctions related to oxidative stress. Hauppauge, N.Y: Nova Science Publishers, 2010.

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Packer, Lester, and Karel W. A. Wirtz. Signalling Mechanisms -- from Transcription Factors to Oxidative Stress. Springer London, Limited, 2013.

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Signalling mechanisms-- from transcription factors to oxidative stress. [Berlin: Springer-Verlag, 1995.

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Packer, Lester, and Karel W. A. Wirtz. Signalling Mechanisms - From Transcription Factors to Oxidative Stress. Springer London, Limited, 2012.

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Josse, Andrea R. Almonds, glycemic excursions, oxidative stress and risk factors for coronary heart disease. 2006.

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Hinds, Terry D. Jr, David E. Stec, and Barbara Wegiel, eds. Oxidative Stress, Antioxidants, Transcription Factors, and Assimilation of Signal Transduction Pathways in Obesity-Related Disorders. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-527-5.

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Shultz, Lawrence B. Cell Apoptosis: Regulation and Environmental Factors. Nova Science Publishers Inc, 2006.

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B, Shultz Lawrence, ed. Cell apoptosis: Regulation and environmental factors. New York: Nova Biomedical Books, 2007.

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Focus On Atherosclerosis Research. Nova Science Publishers, 2004.

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Book chapters on the topic "Oxidative stress factors"

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Yamamoto, Yorihiro. "Biological Antioxidants Under Oxidative Stress." In Food Factors for Cancer Prevention, 424–27. Tokyo: Springer Japan, 1997. http://dx.doi.org/10.1007/978-4-431-67017-9_83.

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Fyhrquist, Frej Y., and Outi J. Saijonmaa. "Modifiable Factors Influencing Telomere Length and Aging." In Inflammation, Aging, and Oxidative Stress, 67–80. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-33486-8_4.

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Emerit, Ingrid. "Clastogenic Factors as Biomarkers of Oxidative Stress." In Free Radicals, Oxidative Stress, and Antioxidants, 375–84. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4757-2907-8_32.

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Harlev, Avi, Stefan S. du Plessis, Deepak Kumar, and Luay AlKattan. "Extrinsic Factors Inducing Oxidative Stress (OS) in Male and Female Reproductive Systems." In Oxidative Stress in Human Reproduction, 89–105. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48427-3_5.

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Bartekova, Monika, Kristina Ferenczyova, Marek Jelemensky, and Naranjan S. Dhalla. "Role of Oxidative Stress and Cardiovascular Risk Factors in Ischemic Heart Disease." In Oxidative Stress in Heart Diseases, 375–94. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8273-4_16.

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Madill, Janet, Bianca Arendt, Chung-Wai Chow, and Johane Allard. "Nutritional Factors, Oxidative Stress and Lung Transplantation." In Inflammatory Response in Cardiovascular Surgery, 403–10. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4429-8_48.

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Fearon, Ian M. "Risk Factors, Oxidative Stress, and Cardiovascular Disease." In Systems Biology of Free Radicals and Antioxidants, 765–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-30018-9_46.

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Schulze-Osthoff, Klaus, Manuel Bauer, Markus Vogt, Sebastian Wesselborg, and Patrick A. Baeuerle. "Reactive Oxygen Intermediates as Primary Signals and Second Messengers in the Activation of Transcription Factors." In Oxidative Stress and Signal Transduction, 239–59. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5981-8_10.

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Sies, Helmut. "Strategies of Antioxidant Defense: Relations to Oxidative Stress." In Signalling Mechanisms — from Transcription Factors to Oxidative Stress, 165–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79675-3_15.

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Al-Gubory, Kaïs Hussain. "Environmental Factors, Oxidative Stress, and Adverse Developmental Outcomes." In Systems Biology of Free Radicals and Antioxidants, 581–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-30018-9_38.

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Conference papers on the topic "Oxidative stress factors"

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Tyumonbaeva, N. B., K. G. Berbolot, А. А. Vishnevsky, and A. A. Kazybekova. "Biomarkers of oxidative stress in the mountains." In VIII Vserossijskaja konferencija s mezhdunarodnym uchastiem «Mediko-fiziologicheskie problemy jekologii cheloveka». Publishing center of Ulyanovsk State University, 2021. http://dx.doi.org/10.34014/mpphe.2021-194-198.

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The data presented in the work indicate probable membrane indicators of functional disorders, closely related to oxidative processes (LPO) under the influence of unfavorable factors of the mountain environment. Key words: membranes, adaptation to the physical factors of mountains, lysophospholipids.
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Generozova, I. P., P. A. Butsanets, and A. G. Shugaev. "OXIDATIVE STRESS AT PEAS SEEDLINGS DURING RESTORATION AFTER ADVERSE FACTORS." In The All-Russian Scientific Conference with International Participation and Schools of Young Scientists "Mechanisms of resistance of plants and microorganisms to unfavorable environmental". SIPPB SB RAS, 2018. http://dx.doi.org/10.31255/978-5-94797-319-8-221-225.

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Alexander, Robert E., Manuela Plate, Rachel C. Chambers, and Chris J. Scotton. "Oxidative Stress Regulates The Production Of Functional Coagulation Factors By Primary Human Lung Epithelium." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1258.

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Al-Dujaili, Emad A. S., and Maha N. Abu Hajleh. "Effects of Curcumin Intake on CVD Risk Factors and Exercise-Induced Oxidative Stress in Healthy Volunteers—An Exploratory Study." In IECN 2022. Basel Switzerland: MDPI, 2022. http://dx.doi.org/10.3390/iecn2022-12363.

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Singh, K. P., G. Lawyer, T. Muthumalage, N. A. Khan, S. R. McDonough, D. Ye, K. P. Maremanda, S. McIntosh, and I. Rahman. "Biomarkers of Inflammation, Oxidative Stress, Pro-Resolving Lipid Mediators, Triglycerides, Growth Factors and Tissue Injury in Electronic Cigarette Users: Implications for Non-Invasive Assessment of Vaping Associated Lung Injuries." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1225.

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Nogueira, Fábio Dias, Ana Klara Rodrigues Alves, Barbara Beatriz Lira da Silva, Ana Kamila Rodrigues Alves, Marlilia Moura Coelho Sousa, Ana Karla Rodrigues Alves, Wanderson da Silva Nery, Breno Carvalho de Almeida, Flávia Dias Nogueira, and Leiz Maria Costa Véras. "The relationship of diabetes mellitus with Alzheimer’s disease: a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.280.

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Introduction: Alzheimer’s disease (AD) is closely related to diabetes mellitus (DM), and AD is also considered to be type 3 diabetes (T3D). Glycogen synthase kinase-3β (GSK-3β) may be the potential link between DM and AD. GSK-3β is one of the main factors that lead to insulin deficiency and insulin resistance, and insulin resistance is a characteristic of the development of DM. In AD, GSK-3β plays an important role in hyperphosphorylation of the tau protein (tau) associated with microtubules, which is one of the pathological features in AD. Objective: To analyze DM as a factor for the development of AD. METHODOLOGY: This is an integrative review of the literature, which is a construction of a comprehensive analysis of the literature with pre-defined steps, carried out through PubMed, 1.501 articles were found, of which 10 were selected, through the simultaneous crossing between the descriptors “Diabetes mellitus”, “Alzheimer “. Articles written in Portuguese and English published between 2016 and 2021 were inserted. Results: DM associated with insulin resistance affects psychomotor efficiency, attention, learning memory, mental flexibility, speed and executive function of the brain, thus being an independent risk factor for cognitive impairment and damage to the central nervous system, hyperglycemia, which can cause increased oxidative stress leading to progressive functional and structural abnormalities in the brain. Conclusion:The risk of dementia in patients with DM is higher than in nondiabetic patients and it is also well known that DM2 / insulin resistance is involved in AD.
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White, Elshaddai, Jada R. Carter, and Cimona V. Hinton. "Abstract 890: Nuclear factor kappa B (NF-κB) promotes oxidative stress adaptation and survivorship." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-890.

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White, Elshaddai, Jada R. Carter, and Cimona V. Hinton. "Abstract 890: Nuclear factor kappa B (NF-κB) promotes oxidative stress adaptation and survivorship." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-890.

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Ahmed, Amira, Huda Farah, Omnia Ahmed, Dina Elsayegh, Abdelrahman Elgamal, and Nasser Moustafa Rizk. "Profile Of Oxidative Stress Genes In Response To Obesity Treatment." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0150.

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Background: Oxidative stress (OS) is an imbalance between free radical production and the antioxidants defense in the body. Previous studies demonstrated the correlation of OS to the increased risk of developing metabolic disorders such as obesity. Sulforaphane (SFN), a bioactive compound, can protect against inflammation and OS, thus an effective anti-obesity supplement. Aim: This study explores the impact of SNF on OS in diet induced obese (DIO) mice via profiling of OS genes and pathways in skeletal muscles related to the anti-obesity effect. Methods: Wild-type CD1 male mice and the knockout of nuclear factor (erythroid-derived 2) like 2 (NrF2) mice were fed a high-fat diet (HFD) for 16 weeks; to induce obesity. Subsequently, each group was subdivided into two subgroups and received either Vehicle (25μl) or SFN (5 mg/kg BW) for four weeks. Body weight was measured daily, and a glucose tolerance test (GTT) was performed after 21 days of treatment. Afterward, mice were decapitated, blood and tissue samples were collected and snap-frozen immediately. Total RNA was extracted from Skeletal muscle and epididymal white adipose tissue (eWAT), leptin expression was measured in (eWAT), and 84 OS genes in skeletal muscle were examined using RT-PCR. Results: Significant reduction in body weight in SFN treated WT mice, while no change in KO mice. Plasma glucose, leptin, and leptin gene expression (eWAT) were significantly reduced in the WT-DIO SFN treated group, while no changes were detected in KO mice. SFN decreases OS damage in skeletal muscles, such as lipid peroxidation and production of reactive oxygen species (ROS). Conclusion: This study demonstrated that SFN had lowered body weight in WT-DIO mice by decreasing OS damage in skeletal muscles through the NrF2 pathway and can be a potential anti-obesity drug.
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Abalenikhina, Y. V., A. A. Seidkuliyeva, E. D. Rokunov, D. S. Nemtinov, A. V. Shchulkin, and E. N. Yakusheva. "PARTICIPATION OF NUCLEAR FACTOR OF ERYTHROID ORIGIN-2 IN REGU-LATION P-GLYCOPROTEIN IN MODELING ENDOGENOUS OXIDATIVE STRESS." In NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2022. http://dx.doi.org/10.47501/978-5-6044060-2-1.251-257.

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The article discusses the mechanisms of regulation of the P-glycoprotein transporter protein (Pgp) in cells of the Caco2 line under conditions of modeling endogenous oxidative stress caused by exposure to DL-butyonine sulfoximine (BSO, a glutathione synthesis inhibitor). Ex-periments have shown that exposure to BSO at concentrations of 10-100 μM leads to a de-crease in the concentration of glutathione, an increase in the amount of Pgp and nuclear factor of erythroid origin 2 (Nrf2). Inhibition of Nrf2 contributed to the normalization of Pgp levels, which proves the participation of the transcription factor in the regulation of the transporter protein under the conditions of modeling endogenous oxidative stress.
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Reports on the topic "Oxidative stress factors"

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Wu, Guangyu. Preventive Role of Specific Dietary Factors and Natural Compounds Against DNA Damage and Oxidative Stress. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada377925.

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Horwitz, Benjamin A., and Barbara Gillian Turgeon. Fungal Iron Acquisition, Oxidative Stress and Virulence in the Cochliobolus-maize Interaction. United States Department of Agriculture, March 2012. http://dx.doi.org/10.32747/2012.7709885.bard.

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Our project focused on genes for high affinity iron acquisition in Cochliobolus heterostrophus, a necrotrophic pathogen of maize, and their intertwined relationship to oxidative stress status and virulence of the fungus on the host. An intriguing question was why mutants lacking the nonribosomal peptide synthetase (NRPS) gene (NPS6) responsible for synthesis of the extracellular siderophore, coprogen, are sensitive to oxidative stress. Our overall objective was to understand the mechanistic connection between iron stress and oxidative stress as related to virulence of a plant pathogen to its host. The first objective was to examine the interface where small molecule peptide and reactive oxygen species (ROS) mechanisms overlap. The second objective was to determine if the molecular explanation for common function is common signal transduction pathways. These pathways, built around sensor kinases, response regulators, and transcription factors may link sequestering of iron, production of antioxidants, resistance to oxidative stress, and virulence. We tested these hypotheses by genetic manipulation of the pathogen, virulence assays on the host plant, and by following the expression of key fungal genes. An addition to the original program, made in the first year, was to develop, for fungi, a genetically encoded indicator of redox state based on the commercially available Gfp-based probe pHyper, designed for animal cell biology. We implemented several tools including a genetically encoded indicator of redox state, a procedure to grow iron-depleted plants, and constructed a number of new mutants in regulatory genes. Lack of the major Fe acquisition pathways results in an almost completely avirulent phenotype, showing how critical Fe acquisition is for the pathogen to cause disease. Mutants in conserved signaling pathways have normal ability to regulate NPS6 in response to Fe levels, as do mutants in Lae1 and Vel1, two master regulators of gene expression. Vel1 mutants are sensitive to oxidative stress, and the reason may be underexpression of a catalase gene. In nps6 mutants, CAT3 is also underexpressed, perhaps explaining the sensitivity to oxidative stress. We constructed a deletion mutant for the Fe sensor-regulator SreA and found that it is required for down regulation of NPS6 under Fe-replete conditions. Lack of SreA, though, did not make the fungus over-sensitive to ROS, though the mutant had a slow growth rate. This suggests that overproduction of siderophore under Fe-replete conditions is not very damaging. On the other hand, increasing Fe levels protected nps6 mutants from inhibition by ROS, implying that Fe-catalyzed Fenton reactions are not the main factor in its sensitivity to ROS. We have made some progress in understanding why siderophore mutants are sensitive to oxidative stress, and in doing so, defined some novel regulatory relationships. Catalase genes, which are not directly related to siderophore biosynthesis, are underexpressed in nps6 mutants, suggesting that the siderophore product (with or without bound Fe) may act as a signal. Siderophores, therefore, could be a target for intervention in the field, either by supplying an incorrect signal or blocking a signal normally provided during infection. We already know that nps6 mutants cause smaller lesions and have difficulty establishing invasive growth in the host. Lae1 and Vel1 are the first factors shown to regulate both super virulence conferred by T-toxin, and basic pathogenicity, due to unknown factors. The mutants are also altered in oxidative stress responses, key to success in the infection court, asexual and sexual development, essential for fungal dissemination in the field, aerial hyphal growth, and pigment biosynthesis, essential for survival in the field. Mutants in genes encoding NADPH oxidase (Nox) are compromised in development and virulence. Indeed the triple mutant, which should lack all Nox activity, was nearly avirulent. Again, gene expression experiments provided us with initial evidence that superoxide produced by the fungus may be most important as a signal. Blocking oxidant production by the pathogen may be a way to protect the plant host, in interactions with necrotrophs such as C. heterostrophus which seem to thrive in an oxidant environment.
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Handa, Avtar K., Yuval Eshdat, Avichai Perl, Bruce A. Watkins, Doron Holland, and David Levy. Enhancing Quality Attributes of Potato and Tomato by Modifying and Controlling their Oxidative Stress Outcome. United States Department of Agriculture, May 2004. http://dx.doi.org/10.32747/2004.7586532.bard.

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General The final goal and overall objective of the current research has been to modify lipid hydroperoxidation in order to create desirable phenotypes in two important crops, potato and tomato, which normally are exposed to abiotic stress associated with such oxidation. The specific original objectives were: (i) the roles of lipoxygenase (LOX) and phospholipids hydroperoxide glutathione peroxidase (PHGPx) in regulating endogenous levels of lipid peroxidation in plant tissues; (ii) the effect of modified lipid peroxidation on fruit ripening, tuber quality, crop productivity and abiotic stress tolerance; (iii) the effect of simultaneous reduction of LOX and increase of PHGPx activities on fruit ripening and tuber quality; and (iv) the role of lipid peroxidation on expression of specific genes. We proposed to accomplish the research goal by genetic engineering of the metabolic activities of LOX and PHGPx using regulatable and tissue specific promoters, and study of the relationships between these two consecutive enzymes in the metabolism and catabolism of phospholipids hydroperoxides. USA Significant progress was made in accomplishing all objectives of proposed research. Due to inability to regenerate tomato plants after transforming with 35S-PHGPx chimeric gene construct, the role of low catalase induced oxidative stress instead of PHGPx was evaluated on agronomical performance of tomato plant and fruit quality attributes. Effects of polyamine, that protects DNA from oxidative stress, were also evaluated. The transgenic plants under expressing lipoxygenase (LOX-sup) were crossed with catalase antisense (CAT-anti) plants or polyamine over producing plants (SAM-over) and the lines homozygous for the two transgenes were selected. Agronomical performance of these line showed that low catalase induced oxidative stress negatively affected growth and development of tomato plants and resulted in a massive change in fruit gene expression. These effects of low catalase activity induced oxidative stress, including the massive shift in gene expression, were greatly overcome by the low lipoxygenase activity. Collectively results show that oxidative stress plays significant role in plant growth including the fruit growth. These results also for the first time indicated that a crosstalk between oxidative stress and lipoxygenase regulated processes determine the outcome during plant growth and development. Israel Regarding PHGPx, most of the study has concentrated on the first and the last specific objectives, since it became evident that plant transformation with this gene is not obvious. Following inability to achieve efficient transformation of potato and tomato using a variety of promoters, model plant systems (tobacco and potato cell cultures, tobacco calli and plantlets, and Arabidopsis) were used to establish the factors and to study the obstacles which prohibited the regeneration of plants carrying the genetic machinery for overproduction of PHGPx. Our results clearly demonstrate that while genetic transformation and over-expression of PHGPx occurs in pre-developmental tissue stage (cell culture, calli clusters) or in completed plant (Arabidopsis), it is likely that over-expression of this enzyme before tissue differentiation is leading to a halt of the regeneration process. To support this assumption, experiments, in which genetic engineering of a point-mutated PHGPx gene enable transformation and over-expression in plants of PhSPY modified in its catalytic site and thus inactive enzymatically, were successfully carried out. These combined results strongly suggest, that if in fact, like in animals and as we established in vitro, the plant PHGPx exhibits PH peroxidase activity, these peroxides are vital for the organisms developmental process.
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Mateș, Letiția, Marius Emil Rusu, Ionel Fizeșan, Daniela-Saveta Popa, and Daniel Leucuța. Walnut intake interventions targeting biomarkers of metabolic syndrome and inflammation in middle-aged and older adults: a systematic review and meta-analysis of randomized controlled trials research protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0058.

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Review question / Objective: The aim of this study was to conduct a systematic review and meta-analysis of randomized controlled trials (RCTs) in order to properly examine the evidence on the effects of walnut consumption on chosen indicators of inflammation and metabolic syndrome in mature adults. Condition being studied: Metabolic syndrome (MetS), chronic, low-grade inflammation, and oxidative stress are all important risk factors for morbidity and death, with a higher frequency in the elderly population. Information sources: We conducted a comprehensive search in five databases: Pubmed, EMBASE, Scopus, Cochrane, ClinicalTrials, from inception.
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Horwitz, Benjamin, and Barbara Gillian Turgeon. Secondary Metabolites, Stress, and Signaling: Roles and Regulation of Peptides Produced by Non-ribosomal Peptide Synthetases. United States Department of Agriculture, 2005. http://dx.doi.org/10.32747/2005.7696522.bard.

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Fungal pathogens of plants produce a diverse array of small molecules. Often referred to as secondary metabolites because they were thought to be dispensable for basic functions, they may indeed have central roles as signals for the fungal cell, and in interactions with the host. We have identified more than a dozen genes encoding nonribosomal peptide synthetases (NPS) in Cochliobolusheterostrophus, the agent of southern corn leaf blight. The aim of this project was to identify roles of these genes in stress responses and signaling. The first objective was to test a complete collection of C. heterostrophus nonribosomal peptide synthetase (NRPS)-encoding gene deletion mutant and wildtype (WT) strains for sensitivity to various agents of oxidative (ROS) and nitrosative (RNOS) stress, in vitro. The second objective and next step in this part of the project was to study the relevance of sensitivity to ROS and RNOS in the host pathogen interaction, by measuring the production of ROS and RNOS in planta, when plants are inoculated with wild type and mutant strains. A third objective was to study expression of any genes shown to be involved in sensitivity to ROS or RNOS, in vitro and in planta. Another objective was to determine if any of the genes involved in oxidative or nitrosative stress responses are regulated by components of signal transduction pathways (STP) that we have identified and to determine where mechanisms overlap. Study of the collection of nps mutants identified phenotypes relevant for virulence, development and oxidative stress resistance for two of the genes, NPS2 and NPS6. Mutants in genes related to RNOS stress have no virulence phenotypes, while some of those related to ROS stress have reduced virulence as well as developmental phenotypes, so we focused primarily on ROS stress pathways. Furthermore, the identification of NPS2 and NPS6 as encoding for NRPS responsible for siderophore biosynthesis lent a new focus to the project, regulation by Fe. We have not yet developed good methods to image ROS in planta and work in this direction is continuing. We found that NPS6 expression is repressed by Fe, responding over the physiological Fe concentration range. Studying our collection of mutants, we found that conserved MAPK and G protein signal transduction pathways are dispensable for Fe regulation of NPS6, and initiated work to identify other pathways. The transcription factor SreA is one candidate, and is responsible for part, but not all, of the control of NPS6 expression. The results of this project show that the pathogen contends with oxidative stress through several signaling pathways. Loss of the siderophore produced by Nps6 makes the fungus sensitive to oxidative stress, and decreases virulence, suggesting a central role of the ability to sequester and take up extracellular iron in the host-pathogen interaction. Siderophores, and manipulation of Fe levels, could be targets for new strategies to deal with fungal pathogens of maize and other plants.
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Paran, Ilan, and Allen Van Deynze. Regulation of pepper fruit color, chloroplasts development and their importance in fruit quality. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598173.bard.

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Pepper exhibits large natural variation in chlorophyll content in the immature fruit. To dissect the genetic and molecular basis of this variation, we conducted QTL mapping for chlorophyll content in a cross between light and dark green-fruited parents, PI 152225 and 1154. Two major QTLs, pc1 and pc10, that control chlorophyll content by modulation of chloroplast compartment size in a fruit-specific manner were detected in chromosomes 1 and 10, respectively. The pepper homolog of GOLDEN2- LIKE transcription factor (CaGLK2) was found as underlying pc10, similar to its effect on tomato fruit chloroplast development. A candidate gene for pc1was found as controlling chlorophyll content in pepper by the modulation of chloroplast size and number. Fine mapping of pc1 aided by bulked DNA and RNA-seq analyses enabled the identification of a zinc finger transcription factor LOL1 (LSD-One-Like 1) as a candidate gene underlying pc1. LOL1 is a positive regulator of oxidative stress- induced cell death in Arabidopsis. However, over expression of the rice ortholog resulted in an increase of chlorophyll content. Interestingly, CaAPRR2 that is linked to the QTL and was found to affect immature pepper fruit color in a previous study, did not have a significant effect on chlorophyll content in the present study. Verification of the candidate's function was done by generating CRISPR/Cas9 knockout mutants of the orthologues tomato gene, while its knockout experiment in pepper by genome editing is under progress. Phenotypic similarity as a consequence of disrupting the transcription factor in both pepper and tomato indicated its functional conservation in controlling chlorophyll content in the Solanaceae. A limited sequence diversity study indicated that null mutations in CaLOL1 and its putative interactorCaMIP1 are present in C. chinensebut not in C. annuum. Combinations of mutations in CaLOL1, CaMIP1, CaGLK2 and CaAPRR2 are required for the creation of the extreme variation in chlorophyll content in Capsicum.
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Firon, Nurit, Prem Chourey, Etan Pressman, Allen Hartwell, and Kenneth J. Boote. Molecular Identification and Characterization of Heat-Stress-Responsive Microgametogenesis Genes in Tomato and Sorghum - A Feasibility Study. United States Department of Agriculture, October 2007. http://dx.doi.org/10.32747/2007.7591741.bard.

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Exposure to higher than optimal temperatures - heat-stress (HS) - is becoming increasingly common to all crop plants worldwide. Heat stress coinciding with microgametogenesis, especially during the post-meiotic phase that is marked by starch biosynthesis, is often associated with starch-deficient pollen and male sterility and ultimately, greatly reduced crop yields. The molecular basis for the high sensitivity of developing pollen grains, on one hand, and factors involved in pollen heat-tolerance, on the other, is poorly understood. The long-term goal of this project is to provide a better understanding of the genes that control pollen quality under heat-stress conditions. The specific objectives of this project were: (1) Determination of the threshold heat stress temperature(s) that affects tomato and sorghum pollen quality whether: a) Chronic mild heat stress conditions (CMHS), or b) Acute heat stress (AHS). (2) Isolation of heat-responsive, microgametogenesis-specific sequences. During our one-year feasibility project, we have accomplished the proposed objectives as follows: Objectrive 1: We have determined the threshold HS conditions in tomato and sorghum. This was essential for achieving the 2nd objective, since our accumulated experience (both Israeli and US labs) indicate that when temperature is raised too high above "threshold HS levels" it may cause massive death of the developing pollen grains. Above-threshold conditions have additional major disadvantages including the "noise" caused by induced expression of genes involved in cell death and masking of the differences between heatsensitive and heat-tolerant pollen grains. Two different types of HS conditions were determined: a) Season-long CMHS conditions: 32/26°C day/night temperatures confirmed in tomato and 36/26°C day maximum/night minimum temperatures in sorghum. b) Short-term AHS: In tomato, 2 hour exposure to 42-45°C (at 7 to 3 days before anthesis) followed by transfer to 28/22±2oC day/night temperatures until flower opening and pollen maturation, caused 50% reduced germinating pollen in the heat-sensitive 3017 cv.. In sorghum, 36/26°C day/night temperatures 10 to 5 days prior to panicle emergence, occurring at 35 days after sowing (DAS) in cv. DeKalb28E, produced starch-deficient and sterile pollen. Objective 2: We have established protocols for the high throughput transcriptomic approach, cDNA-AFLP, for identifying and isolating genes exhibiting differential expression in developing microspores exposed to either ambient or HS conditions and created a databank of HS-responsivemicrogametogenesis-expressed genes. A subset of differentially displayed Transcript-Derived Fragments (TDFs) that were cloned and sequenced (35 & 23 TDFs in tomato and sorghum, respectively) show close sequence similarities with metabolic genes, genes involved in regulation of carbohydrate metabolism, genes implicated in thermotolerance (heat shock proteins), genes involved in long chain fatty acids elongation, genes involved in proteolysis, in oxidation-reduction, vesicle-mediated transport, cell division and transcription factors. T-DNA-tagged Arabidopsis mutants for part of these genes were obtained to be used for their functional analysis. These studies are planned for a continuation project. Following functional analyses of these genes under HS – a valuable resource of genes, engaged in the HS-response of developing pollen grains, that could be modulated for the improvement of pollen quality under HS in both dicots and monocots and/or used to look for natural variability of such genes for selecting heat-tolerant germplasm - is expected.
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Miller, Gad, and Jeffrey F. Harper. Pollen fertility and the role of ROS and Ca signaling in heat stress tolerance. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7598150.bard.

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The long-term goal of this research is to understand how pollen cope with stress, and identify genes that can be manipulated in crop plants to improve reproductive success during heat stress. The specific aims were to: 1) Compare heat stress dependent changes in gene expression between wild type pollen, and mutants in which pollen are heat sensitive (cngc16) or heat tolerant (apx2-1). 2) Compare cngc16 and apx2 mutants for differences in heat-stress triggered changes in ROS, cNMP, and Ca²⁺ transients. 3) Expand a mutant screen for pollen with increased or decreased thermo-tolerance. These aims were designed to provide novel and fundamental advances to our understanding of stress tolerance in pollen reproductive development, and enable research aimed at improving crop plants to be more productive under conditions of heat stress. Background: Each year crop yields are severely impacted by a variety of stress conditions, including heat, cold, drought, hypoxia, and salt. Reproductive development in flowering plants is highly sensitive to hot or cold temperatures, with even a single hot day or cold night sometimes being fatal to reproductive success. In many plants, pollen tube development and fertilization is often the weakest link. Current speculation about global climate change is that most agricultural regions will experience more extreme environmental fluctuations. With the human food supply largely dependent on seeds, it is critical that we consider ways to improve stress tolerance during fertilization. The heat stress response (HSR) has been intensively studied in vegetative tissues, but is poorly understood during reproductive development. A general paradigm is that HS is accompanied by increased production of reactive oxygen species (ROS) and induction of ROS-scavenging enzymes to protect cells from excess oxidative damage. The activation of the HSR has been linked to cytosolic Ca²⁺ signals, and transcriptional and translational responses, including the increased expression of heat shock proteins (HSPs) and antioxidative pathways. The focus of the proposed research was on two mutations, which have been discovered in a collaboration between the Harper and Miller labs, that either increase or decrease reproductive stress tolerance in a model plant, Arabidopsis thaliana (i.e., cngc16--cyclic nucleotide gated channel 16, apx2-1--ascorbate peroxidase 2,). Major conclusions, solutions, achievements. Using RNA-seq technology, the expression profiles of cngc16 and apx2 pollen grains were independently compared to wild type under favourable conditions and following HS. In comparison to a wild type HSR, there were 2,776 differences in the transcriptome response in cngc16 pollen, consistent with a model in which this heat-sensitive mutant fails to enact or maintain a normal wild-type HSR. In a comparison with apx2 pollen, there were 900 differences in the HSR. Some portion of these 900 differences might contribute to an improved HSR in apx2 pollen. Twenty-seven and 42 transcription factor changes, in cngc16 and apx2-1, respectively, were identified that could provide unique contributions to a pollen HSR. While we found that the functional HS-dependent reprogramming of the pollen transcriptome requires specific activity of CNGC16, we identified in apx2 specific activation of flavonol-biosynthesis pathway and auxin signalling that support a role in pollen thermotolerance. Results from this study have identified metabolic pathways and candidate genes of potential use in improving HS tolerance in pollen. Additionally, we developed new FACS-based methodology that can quantify the stress response for individual pollen in a high-throughput fashion. This technology is being adapted for biological screening of crop plant’s pollen to identify novel thermotolerance traits. Implications, both scientific and agricultural. This study has provided a reference data on the pollen HSR from a model plant, and supports a model that the HSR in pollen has many differences compared to vegetative cells. This provides an important foundation for understanding and improving the pollen HSR, and therefor contributes to the long-term goal of improving productivity in crop plants subjected to temperature stress conditions. A specific hypothesis that has emerged from this study is that pollen thermotolerance can be improved by increasing flavonol accumulation before or during a stress response. Efforts to test this hypothesis have been initiated, and if successful have the potential for application with major seed crops such as maize and rice.
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