Bibliografías temáticas / Oxidative stress

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Literatura académica sobre el tema "Oxidative stress"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 23 de noviembre de 2024

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Artículos de revistas sobre el tema "Oxidative stress"

1

Sun, Qi-An, Nageswara Madamanchi y Marschall Runge. "Oxidative stress, NADPH oxidases, and arteries". Hämostaseologie 36, n.º 02 (2016): 77–88. http://dx.doi.org/10.5482/hamo-14-11-0076.

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ZusammenfassungDie Atherosklerose und ihre wichtigsten Komplikationen – Myokardinfarkt und Schlaganfall – sind die Hauptursachen für Tod und Behinderung in den USA und weltweit. Eine dramatische Zunahme bei Adipositas und Diabetes mellitus wird wahrscheinlich auch in Zukunft zu einer hohen Prävalenz kardiovaskulärer Erkrankungen (CVD) und deren Auswirkungen auf das Gesundheitswesen führen. Große Fortschritte gibt es bei der Entwicklung neuer Therapien zur Senkung der Inzidenz von Atherosklerose und CVD, besonders bei der Behandlung der Hypercholesterinämie und Hypertonie. Der gemeinsame mechanistische Nenner bei vielen Risikofaktoren für CVD ist oxidativer Stress. Erst seit kurzem verfügen wir über Methoden, um die Schnittstelle zwischen oxidativem Stress und CVD im Tiermodell zu untersuchen. Die wichtigste Quelle für reaktive Sauerstoffspezies (und damit für oxidativen Stress) in vaskulären Zellen sind die Formen der Nicotin - amidadenindinukleotidphosphat-Oxidase (NADPH-Oxidase). Die jüngsten Studien belegen eindeutig, dass 1. NADPH-Oxidasen im Tiermodell von grundlegender Bedeutung für Atherosklerose und Hypertonie sind und 2. der vaskuläre oxidative Stress, angesichts der gewebespezifischen Expression wichtiger Bestandteile der NADPH-Oxidase, ein Ziel bei der Prävention der CVD sein könnte.
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2

Naziya, Dr Saba. "MITOCHONDRIAL CARBON STRESS AND OXIDATIVE STRESS: IMPLICATIONS FOR HUMAN HEALTH". Era's Journal of Medical Research 11, n.º 1 (junio de 2024): 85–92. http://dx.doi.org/10.24041/ejmr2024.14.

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Avital component of cellular redox equilibrium, mitochondria also play a crucial role in the synthesis of energy within cells. Disturbances in the metabolism of carbon inside the mitochondria may cause malfunction and oxidative stress, which in turn may contribute to the etiology of a number of human diseases. This is supported by newly emerging research. The interaction of oxidative stress and mitochondrial carbon stress is examined in this review, with particular attention on how these effects affect human health. We go over the processes that underlie oxidative stress caused by mitochondrial carbon stress and its consequences for various physiological processes such as aging, cancer, metabolic disorders, and neurodegenerative illnesses. We also highlight prospective therapeutic approaches that focus on redox balance and mitochondrial function in order to lessen the harmful effects of oxidative stress and mitochondrial carbon stress on human health.
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Dorovskikh, V. A., N. V. Simonova, E. Yu Yurtaeva, R. A. Anokhina y M. A. Shtarberg. "PHYTOCORRECTION OF OXIDATIVE STRESS IN EXPERIMENT". Amur Medical Journal, n.º 15-16 (2016): 35–37. http://dx.doi.org/10.22448/amj.2016.15-16.35-37.

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Nsonwu, Magnus, SJ Ozims y JK Nnodim. "Perspective of Cataract and Oxidative Stress". Series of Clinical and Biomedical Research 1, n.º 1 (23 de marzo de 2024): 1–10. http://dx.doi.org/10.54178/2997-2701.v1i1a1994.

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One of the main causes of blindness is the multifactorial condition known as cataract. It is believed that oxidative stress plays a significant role in starting the cataractogenesis process. Today, it is a well-established fact that oxidative stress plays a role in both diabetes-induced cataract (diabetic) and age-related cataract (senile). The most likely cause of oxidative damage to the lens is a compromised antioxidant defense system brought on by age and diabetes-related increases in reactive oxygen species (ROS) production. The main factor contributing to cataract formation is systemic oxidative stress, which is produced externally to the lens. An imbalance between pro- and antioxidant-oxidants leads to oxidative stress. It is essential to eliminate hazardous free radicals because they are a byproduct of normal metabolism. Globally, cataracts are the primary cause of blindness. Oxidative stress is the direct cause of the lens’s opacity. Although age is the main cause of cataracts, diabetes is also a common cause, as higher superoxide levels in the mitochondria arise from hyperglycemia. This review will look into ultraviolet (UV) light, diabetes, and diet (fat, alcohol, and vitamins) as risk factors for cataracts.
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Malenica, Maja y Neven Meseldžić. "Oxidative stress and obesity". Arhiv za farmaciju 72, n.º 2 (2022): 166–83. http://dx.doi.org/10.5937/arhfarm72-36123.

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Obesity is a disease of excessive accumulation of adipose tissue due to an increased energy intake which is disproportionate to the energy expenditure in the body. The visceral adipose tissue in the obese accumulated in that way increases the risk of developing a number of metabolic and cardiovascular diseases. Disorders such as diabetes, dyslipidemia, inflammation, endothelial dysfunction and mitochondria can contribute to the development of oxidative stress, which is especially pronounced in the abdominal type of obesity. Obesity can induce systemic oxidative stress through a variety of biochemical mechanisms. Although ROS is generated in a large number of cells, mitochondria play a significant role in their intracellular production through the process of oxidative phosphorylation of the respiratory chain, and in fatty acid oxidation reactions. Oxidative stress is a unique link between the various molecular disorders present in the development of insulin resistance that plays a key role in the pathogenesis and progression of chronic metabolic, proinflammatory diseases. The progression of insulin resistance is also affected by inflammation. Both of these can be the cause and the consequence of obesity. The synthesis of the inflammatory mediators is induced by oxidative stress, thus bringing the inflammation and the oxidative stress into a very significant relation. This review aims to highlight recent findings on the role of oxidative stress in the pathogenesis of obesity, with special reference to the mechanisms that explain its occurrence.
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BÜYÜKOĞLU, Tülay y Nurcanan ASLAN. "Oxidative Stress and Effects of Oxidative Stress on the Dairy Cattle During Transition Period". Turkiye Klinikleri Journal of Veterinary Sciences 9, n.º 2 (2018): 33–41. http://dx.doi.org/10.5336/vetsci.2018-60899.

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Kibel, Aleksandar, Ana Marija Lukinac, Vedran Dambic, Iva Juric y Kristina Selthofer Relatic. "Oxidative Stress in Ischemic Heart Disease". Oxidative Medicine and Cellular Longevity 2020 (28 de diciembre de 2020): 1–30. http://dx.doi.org/10.1155/2020/6627144.

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One of the novel interesting topics in the study of cardiovascular disease is the role of the oxidation system, since inflammation and oxidative stress are known to lead to cardiovascular diseases, their progression and complications. During decades of research, many complex interactions between agents of oxidative stress, oxidation, and antioxidant systems have been elucidated, and numerous important pathophysiological links to na number of disorders and diseases have been established. This review article will present the most relevant knowledge linking oxidative stress to vascular dysfunction and disease. The review will focus on the role of oxidative stress in endotheleial dysfunction, atherosclerosis, and other pathogenetic processes and mechanisms that contribute to the development of ischemic heart disease.
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8

LATHA, A. "OXIDATIVE STRESS". NARAYANA NURSING JOURNAL 3, n.º 2 (2014): 13. http://dx.doi.org/10.5455/nnj.2014-06-4.

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Poncin, Sylvie, Sandrine Van Eeckoudt, Kevin Humblet, Ides M. Colin y Anne-Catherine Gérard. "Oxidative Stress". American Journal of Pathology 176, n.º 3 (marzo de 2010): 1355–63. http://dx.doi.org/10.2353/ajpath.2010.090682.

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Dabrowski, Andrzej y Antoni Gabryelewicz. "Oxidative stress". International Journal of Pancreatology 12, n.º 3 (diciembre de 1992): 193–99. http://dx.doi.org/10.1007/bf02924357.

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Tesis sobre el tema "Oxidative stress"

1

Gregory, Mary Sarah-Jane y n/a. "Thioredoxin and Oxidative Stress". Griffith University. School of Health Science, 2004. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040301.082639.

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The experiments described in this thesis involve the expression and characterisation of recombinant truncated thioredoxin (tTrx) and the potential involvement that thioredoxin (Trx) has in the cellular responses to oxidative stress. Truncated Trx (80 amino acids) was expressed from a plasmid containing the ORF for tTrx that had been introduced into E.coli BL-21(DE3) cells. The protein was initially extracted using a combination of high concentrations of urea, high pH levels, and multiple sonification steps to remove the tTrx from inclusion bodies formed during expression. This procedure produced a stable solution of tTrx. Purification of tTrx from this protein solution required anion exchange chromatography followed by gel permeation in a HPLC system to obtain fully purified, recombinant tTrx which allowed further characterisation studies to be undertaken. An initial investigation into tTrx was performed to determine some basic physical, biochemical and functional aspects of this hitherto relatively undefined protein. Analysis by sedimentation equilibrium indicated that freshly prepared tTrx forms a single species with a molecular weight of 18.8kDa. This value indicates that recombinant tTrx naturally forms a dimer in solution that was shown to be non-covalent in nature and stable in solution. The capacity of tTrx to reduce protein disulphide bonds was determined using the insulin reduction assay. Results show that tTrx lacks this particular redox ability. The rate of oxidisation at 4 degrees C was analysed using free thiol determination, sedimentation equilibrium and SDS-PAGE patterning. Results indicated a steady rise in the degree of oxidation of tTrx over an eight day period. After six days the oxidated protein consistently displayed the presence of intramolecular disulphide bonds. Covalently-linked disulphide dimers and higher molecular weight oligomers were detectable after eight days oxidation. An investigation of the reducing capacity of the basic Trx system determined that fully oxidised tTrx was unable to act alone as a substrate for thioredoxin reductase (TR). However, when reduced Trx was added to the system, it appeared capable of acting as an electron donor to the oxidised tTrx in order to reduce disulphide groups. Recombinant tTrx was successfully radiolabelled with Trans 35S-methionine/cysteine for use in cell association studies. No evidence was found to indicate the presence of a receptor for tTrx on either MCF-7 or U-937 cells. Findings suggest that a low level of non-specific binding of tTrx to these cell lines rather than a classical ligand-binding mechanism occurs thus suggesting the absence of a cell surface receptor for tTrx. The role that Trx may play in the cellular responses to oxidative stress was also investigated. The chemical oxidants hydrogen peroxide (H2O2) and diamide were used to establish an in vitro model of oxidative stress for the choriocarcinoma cytotrophoblast cell line JEG-3. Cellular function was assessed in terms of membrane integrity, metabolic activity and the ability to synthesis new DNA following exposure to these oxidants. Results indicated that both agents were capable of causing cells to undergo oxidative stress without inducing immediate apoptosis or necrosis. Initially, JEG-3 cells exposed to 38μM or 75μM H2O2 or 100μM diamide were shown to display altered cell metabolism and DNA synthesis without loss to cell viability or membrane integrity. Cells were also shown to be capable of some short-term recovery but later lapsed into a more stressed state. Expression levels of Trx were studied to determine whether this type of chemical stress caused a change in intercellular protein levels. Both cELISA and western blotting results indicated that only cells exposed to 100μM diamide displayed any significant increase in Trx protein levels after 6 or 8hrs exposure to the oxidant. Further studies over a longer time-frame were also performed. These found that when JEG-3 cells were exposed to 18μM H2O2 or 200μM diamide over 12-48hrs, a positive correlation between increasing endogenous Trx protein levels and a decline in cell proliferation was observed. Cytotrophoblast cells, which are responsible for implantation and placentation, are susceptible to oxidative stress in vivo and their anti-oxidant capacity is fundamental to the establishment of pregnancy. The findings obtained during these studies suggest that Trx plays a role in this process.
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2

Gregory, Mary Sarah-Jane. "Thioredoxin and Oxidative Stress". Thesis, Griffith University, 2004. http://hdl.handle.net/10072/367183.

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The experiments described in this thesis involve the expression and characterisation of recombinant truncated thioredoxin (tTrx) and the potential involvement that thioredoxin (Trx) has in the cellular responses to oxidative stress. Truncated Trx (80 amino acids) was expressed from a plasmid containing the ORF for tTrx that had been introduced into E.coli BL-21(DE3) cells. The protein was initially extracted using a combination of high concentrations of urea, high pH levels, and multiple sonification steps to remove the tTrx from inclusion bodies formed during expression. This procedure produced a stable solution of tTrx. Purification of tTrx from this protein solution required anion exchange chromatography followed by gel permeation in a HPLC system to obtain fully purified, recombinant tTrx which allowed further characterisation studies to be undertaken. An initial investigation into tTrx was performed to determine some basic physical, biochemical and functional aspects of this hitherto relatively undefined protein. Analysis by sedimentation equilibrium indicated that freshly prepared tTrx forms a single species with a molecular weight of 18.8kDa. This value indicates that recombinant tTrx naturally forms a dimer in solution that was shown to be non-covalent in nature and stable in solution. The capacity of tTrx to reduce protein disulphide bonds was determined using the insulin reduction assay. Results show that tTrx lacks this particular redox ability. The rate of oxidisation at 4 degrees C was analysed using free thiol determination, sedimentation equilibrium and SDS-PAGE patterning. Results indicated a steady rise in the degree of oxidation of tTrx over an eight day period. After six days the oxidated protein consistently displayed the presence of intramolecular disulphide bonds. Covalently-linked disulphide dimers and higher molecular weight oligomers were detectable after eight days oxidation. An investigation of the reducing capacity of the basic Trx system determined that fully oxidised tTrx was unable to act alone as a substrate for thioredoxin reductase (TR). However, when reduced Trx was added to the system, it appeared capable of acting as an electron donor to the oxidised tTrx in order to reduce disulphide groups. Recombinant tTrx was successfully radiolabelled with Trans 35S-methionine/cysteine for use in cell association studies. No evidence was found to indicate the presence of a receptor for tTrx on either MCF-7 or U-937 cells. Findings suggest that a low level of non-specific binding of tTrx to these cell lines rather than a classical ligand-binding mechanism occurs thus suggesting the absence of a cell surface receptor for tTrx. The role that Trx may play in the cellular responses to oxidative stress was also investigated. The chemical oxidants hydrogen peroxide (H2O2) and diamide were used to establish an in vitro model of oxidative stress for the choriocarcinoma cytotrophoblast cell line JEG-3. Cellular function was assessed in terms of membrane integrity, metabolic activity and the ability to synthesis new DNA following exposure to these oxidants. Results indicated that both agents were capable of causing cells to undergo oxidative stress without inducing immediate apoptosis or necrosis. Initially, JEG-3 cells exposed to 38μM or 75μM H2O2 or 100μM diamide were shown to display altered cell metabolism and DNA synthesis without loss to cell viability or membrane integrity. Cells were also shown to be capable of some short-term recovery but later lapsed into a more stressed state. Expression levels of Trx were studied to determine whether this type of chemical stress caused a change in intercellular protein levels. Both cELISA and western blotting results indicated that only cells exposed to 100μM diamide displayed any significant increase in Trx protein levels after 6 or 8hrs exposure to the oxidant. Further studies over a longer time-frame were also performed. These found that when JEG-3 cells were exposed to 18μM H2O2 or 200μM diamide over 12-48hrs, a positive correlation between increasing endogenous Trx protein levels and a decline in cell proliferation was observed. Cytotrophoblast cells, which are responsible for implantation and placentation, are susceptible to oxidative stress in vivo and their anti-oxidant capacity is fundamental to the establishment of pregnancy. The findings obtained during these studies suggest that Trx plays a role in this process.
Thesis (Masters)
Master of Philosophy (MPhil)
School of Health Sciences
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3

Nälsén, Cecilia. "Measurement and evaluation of antioxidant status and relation to oxidative stress in humans /". Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6742.

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4

Byon, Chang Hyun. "Oxidative stress-stimulated vascular calcification". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2010r/byon.pdf.

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5

Vanderlelie, Jessica y n/a. "Placental Oxidative Stress in Preeclampsia". Griffith University. School of Medical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20060918.161726.

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Affecting 6-8% of all pregnancies, preeclampsia is the leading cause of maternal morbidity in the western world and is charactensed by hypertension, proteinuria, edema and platelet aggregation. Despite its prevalence and severity, no comprehensive theory or single factor has been suggested to explain the pathophysiology of this multi system disorder of pregnancy, with the only therapies being bed rest, pharmacological symptom management and if necessary early delivery. Oxidative stress plays an important role in the pathophysiology of preeclampsia, resulting from defective trophoblast invasion, reductions in placental perfusion and placental hypoxia/reoxygenation. The inability of endogenous antioxidant systems up regulated in normal pregnancy, to control increased levels of oxidative stress, is suggested as a possible factor in the feed forward generation of reactive oxygen species and placental oxidative stress. That in turn may stimulate increased syncytiotrophoblast apoptosis, endothelial cell activation and the maternal hyper immune response characteristic of preeclampsia. Analysis of the research literature revealed that previous evaluations of placental oxidation and antioxidant enzyme activity in preeclampsia were by no means comprehensive, and exhibited significant inter-study variations. It was the aim of this thesis to clarify the placental oxidative state and the endogenous antioxidant activity of glutathione peroxidase, thioredoxin reductase, thioredoxin and superoxide dismutase in human placentae in an attempt to determine if variations in antioxidant function were due to changes in gene expression or protein oxidation. The findings reported in this thesis indicate the presence of increased levels of oxidative stress in the preeclamptic placenta, associated with significant reductions in antioxidant enzyme capacity. Quantitative real-time PCR analysis of placental samples revealed that deceases in antioxidant capacity in the placenta are more likely to be related to the significant oxidative burden within the tissue rather than reductions in gene expression. A number of animal models exist to investigate components of preeclampsia pathophysiology, however the ability of these models to mimic the oxidative and antioxidant features of preeclampsia remains unclear. The exposure of pregnant rats to N(G)-nitro-L-arginine methyl ester is a widely used model of endothelial cell dysfunction during preeclampsia. It was the aim of this thesis to determine the biochemical characteristics of this model in an attempt to assess its effectiveness in mimicking oxidative changes in the preeclamptic placenta. Although this model is capable of producing a syndiome in rats similar to the disorder in terms of physiology, this is not manifest in terms of placental biochemistry. The importance of selenium in the synthesis of selenobased antioxidants such as glutathione peroxidase and thioredoxin reductase is well documented. Increasing demand for selenium by the developing fetus may be linked to reductions in selenium status during pregnancy. Considering preeclampsia is associated with significant reductions in selenium status it may be hypothesised that reductions in antioxidant function may be linked to selenium inadequacy. The modulation of dietary selenium in pregnant rats was used to determine the importance of selenium during pregnancy and its effect on antioxidant function and placental oxidative stress. The results of this analysis revealed that selenium deficiency causes a pregnancy specific condition similar to preeclampsia. This condition was found to be associated with increased placental oxidative stress and significant reductions in the systemic activity of selenobased antioxidants that could be modified through selenium supplementation. In summary, data obtained in this thesis indicate that placental oxidative stress and reduced antioxidant enzyme activity play a significant role in the pathogenesis of preeclampsia. These studies support the hypothesis that antioxidant sufficiency is crucial in the maintenance of oxidative balance and that antioxidant dysfunction may result in damage to the placenta and the progression of the disease. These novel data further our understanding of the pathophysiology of preeclampsia and provide new insight into the pathogenesis of clinical complications exhibited in this condition, suggesting antioxidant therapy as a possible means for improving the health outcomes of both mother and baby.
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6

Afzal, Maryam. "Breast cancer and oxidative stress". Thesis, Cardiff University, 2009. http://orca.cf.ac.uk/55856/.

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Endocrine and anti-EGFR strategies are used to treat breast cancer. Unfortunately, resistance can be acquired. Deciphering resistance mechanisms remains essential to design treatments for this adverse state. Oxidative stress is the cellular imbalance of pro-oxidants (promoting cell death) and antioxidants (facilitating cell survival and chemotherapy/radiotherapy resistance). However, it remains unexplored whether endocrine or anti-EGFR resistance also associates with altered redox balance. In this project, redox balance was examined using in vitro human resistant breast cancer models TAMR, FASR, X-MCF and NEW DUBS, comparing with responsive w/tMCF7 cells using microarray analysis, PCR, and TAC, ROS, or MTT assays. Pro-oxidant levels increased significantly in all resistant models but this did not impact adversely on growth. Significantly increased antioxidant levels were also observed in all resistant models, perhaps limiting pro-oxidant increases to maintain cell survival. Antioxidants were also significantly induced by antihormones in w/tMCF7 cells that may limit apoptosis with early treatment. Expression of 15 antioxidant genes increased in resistant cells spanning multiple resistant states. While gefitinib challenge revealed many antioxidant genes were EGFR/kinase signalling-regulated in TAMR cells, gefitinib and further signal transduction inhibitors (STIs) indicated total antioxidant capacity was not. Thus, additional genes/signalling probably drive increased antioxidants in resistant cells future deciphering and depletion of antioxidants could feasibly block cell survival in multiple resistant states. Several STIs further increased pro-oxidants in TAMR cells, indicating oxidative stress was also not EGFR/kinase-promoted since STIs also further increased antioxidant capacity, this may again limit pro-oxidant increases and hence apoptotic effect. Importantly, the thesis revealed resistant cells may be particularly sensitive to agents inducing excessive oxidative stress. Redox balance and feasibility of agents influencing redox remains complex. However, new findings and concepts emerging from this thesis are worthy of future exploration for potential treatments for resistance to endocrine/anti-EGFR agents.
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7

Wood, Christopher. "Oxidative stress and seed survival". Thesis, Abertay University, 1998. https://rke.abertay.ac.uk/en/studentTheses/79d28b74-9210-4ebd-a3b8-66a610bd8c87.

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Free radical and aldehydic breakdown product content were determined, by EPR and UV / visible spectroscopy, primarily in intermediate (desiccation tolerant) seeds of Carica papaya L. (Papaya) and recalcitrant (desiccation intolerant) seeds of Aesculus hippocastanum L. (Horse chestnut), but also in other species covering a range of desiccation tolerances, with a view to determining the role of oxidative stress as a diagnostic marker for desiccation tolerance. Axes of non-senescent highly viable recalcitrant seeds of horse chestnut were metabolically active, contained products of lipid peroxidation, displayed low levels of enzymatic protection against activated oxygen and peroxides, and a two-peak free radical EPR signal. During fully hydrated storage at 16 °C for up to 18 months, seeds exhibited, sequentially, an increase in germination rate, a transient increase in intensities of both the low field and high field EPR peaks, a significant increase in membrane leakage and decrease in seed viability, germination rate, and SOD and peroxidase activities. Drying 'unstored' seeds below and embryonic axis moisture content of 40 to 50 % initiated viability loss. At < 25 % moisture content all axes were inviable and displayed a 2- to 4-fold increase in solute leakage, lipid peroxidation products and the low field EPR signal. Seed desiccation sensitivity increased with hydrated storage. The accumulation of lipid peroxidation products and free radicals on drying generally occurred to a greater extent, or at a higher moisture content, than observed with unstored seeds. The results indicate a mediating role for oxidative stress in recalcitrant seed viability loss which is differentially expressed during hydrated, 'natural' ageing and desiccation. Similar trends were seen in other recalcitrant species with the increase in lipid peroxidation products occurring around the point of viability loss. However the study of a more orthodox species (papaya) revealed no such trends.
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8

Bennett, Stuart James. "Oxidative stress biomarkers in dementia". Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/1449/.

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Alzheimer’s disease (AD) is a devastating neurodegenerative disorder which is thought to affect 26.6 million individuals worldwide. There is growing concern over a worldwide dementia epidemic that is predicted to develop over the coming decades. The evidence thus far suggests that increased levels of oxidative stress and vascular risk factors are two major contributors, amongst others, to AD development. The thesis aimed to investigate markers of oxidative stress in AD plasma. Moreover, the oxidative status of specific proteins was investigated using both hypothesis driven and proteomic approaches. Results presented in this thesis suggest that global plasma protein oxidation levels are not different when AD and control subjects are compared, but that individual plasma proteins are specific targets for oxidative modification in AD. The thesis explores different methodologies to assess oxidative changes in AD. In addition it demonstrates that emerging novel and powerful mass spectrometry techniques can be employed successfully to identify several proteins modified by oxidation, providing an initial starting point for further investigation.
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9

Vanderlelie, Jessica. "Placental Oxidative Stress in Preeclampsia". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365679.

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Affecting 6-8% of all pregnancies, preeclampsia is the leading cause of maternal morbidity in the western world and is charactensed by hypertension, proteinuria, edema and platelet aggregation. Despite its prevalence and severity, no comprehensive theory or single factor has been suggested to explain the pathophysiology of this multi system disorder of pregnancy, with the only therapies being bed rest, pharmacological symptom management and if necessary early delivery. Oxidative stress plays an important role in the pathophysiology of preeclampsia, resulting from defective trophoblast invasion, reductions in placental perfusion and placental hypoxia/reoxygenation. The inability of endogenous antioxidant systems up regulated in normal pregnancy, to control increased levels of oxidative stress, is suggested as a possible factor in the feed forward generation of reactive oxygen species and placental oxidative stress. That in turn may stimulate increased syncytiotrophoblast apoptosis, endothelial cell activation and the maternal hyper immune response characteristic of preeclampsia. Analysis of the research literature revealed that previous evaluations of placental oxidation and antioxidant enzyme activity in preeclampsia were by no means comprehensive, and exhibited significant inter-study variations. It was the aim of this thesis to clarify the placental oxidative state and the endogenous antioxidant activity of glutathione peroxidase, thioredoxin reductase, thioredoxin and superoxide dismutase in human placentae in an attempt to determine if variations in antioxidant function were due to changes in gene expression or protein oxidation. The findings reported in this thesis indicate the presence of increased levels of oxidative stress in the preeclamptic placenta, associated with significant reductions in antioxidant enzyme capacity. Quantitative real-time PCR analysis of placental samples revealed that deceases in antioxidant capacity in the placenta are more likely to be related to the significant oxidative burden within the tissue rather than reductions in gene expression. A number of animal models exist to investigate components of preeclampsia pathophysiology, however the ability of these models to mimic the oxidative and antioxidant features of preeclampsia remains unclear. The exposure of pregnant rats to N(G)-nitro-L-arginine methyl ester is a widely used model of endothelial cell dysfunction during preeclampsia. It was the aim of this thesis to determine the biochemical characteristics of this model in an attempt to assess its effectiveness in mimicking oxidative changes in the preeclamptic placenta. Although this model is capable of producing a syndiome in rats similar to the disorder in terms of physiology, this is not manifest in terms of placental biochemistry. The importance of selenium in the synthesis of selenobased antioxidants such as glutathione peroxidase and thioredoxin reductase is well documented. Increasing demand for selenium by the developing fetus may be linked to reductions in selenium status during pregnancy. Considering preeclampsia is associated with significant reductions in selenium status it may be hypothesised that reductions in antioxidant function may be linked to selenium inadequacy. The modulation of dietaty selenium in pregnant rats was used to determine the importance of selenium during pregnancy and its effect on antioxidant function and placental oxidative stress. The results of this analysis revealed that selenium deficiency causes a pregnancy specific condition similar to preeclampsia. This condition was found to be associated with increased placental oxidative stress and significant reductions in the systemic activity of selenobased antioxidants that could be modified through selenium supplementation. In summary, data obtained in this thesis indicate that placental oxidative stress and reduced antioxidant enzyme activity play a significant role in the pathogenesis of preeclampsia. These studies support the hypothesis that antioxidant sufficiency is crucial in the maintenance of oxidative balance and that antioxidant dysfunction may result in damage to the placenta and the progression of the disease. These novel data further our understanding of the pathophysiology of preeclampsia and provide new insight into the pathogenesis of clinical complications exhibited in this condition, suggesting antioxidant therapy as a possible means for improving the health outcomes of both mother and baby.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
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10

Bolotta, Alessandra <1982&gt. "Oxidative Stress and Friedreich’s Ataxia". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amsdottorato.unibo.it/6282/1/Bolotta_Alessandra_tesi.pdf.

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Friedreich’s Ataxia (FRDA) is a neurodegenerative disorder caused by a deficiency of the protein frataxin and characterized by oxidative stress. The first aim of my research project was to analyze the effects of tocotrienol in FRDA patients. Patients received for 2 months a low dose of tocotrienol. A number of biochemical parameters related to oxidative stress were studied. We consistently showed that taking for 2 months a low dose of tocotrienol led to the decrease of oxidative stress indexes in FRDA patients. Also, this study provides a suitable model to investigate the efficacy of natural compounds to counteract the oxidative stress in FRDA. Furthermore, we investigated whether the tocotrienol was able to modulate the expression of the frataxin isoforms (FXN-1, FXN -2, FXN-3) in FRDA patients. We demonstrated that tocotrienol leads to a specific and significant increase of FXN-3 expression. As no structural and functional details were available for FNX-2 and FXN-3, 3D-models were built. FXN-1, the canonical isoform, was then docked on the human iron-sulphur complex and functional interactions were computed; when FXN-1 was replaced by FXN-2 or FNX-3, we found that the interactions were maintained, thus suggesting a possible biological role for both isoforms. The second aim of my research project was to investigate the role of a single nucleotide polymorphism (SNP) in the protein Sirtuin 6 in FRDA patients. In fact, it was known that those who harbour a SNP (Asn46/Ser46) in the gene enconding Sirt6 show a better outcome those individuals who are homozygous for the Asn 46 allele. We found that fibroblasts and iPSC-derived neurons from FRDA patients harboring the SNP (Asn46/Ser46) have a reduced amount of Sirt6 protein compared to cells from individuals who are homozygous for the prevalent Asn allele. Our studies provide new information on the role of Sirtuins in FRDA pathogenesis.
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Libros sobre el tema "Oxidative stress"

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Huang, Canhua y Yuanyuan Zhang, eds. Oxidative Stress. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-0522-2.

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1942-, Sies H., ed. Oxidative stress. London: Orlando, 1985.

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Reyes, Adolfo M. Handbook on oxidative stress: New research. Hauppauge, N.Y: Nova Science Publisher's, 2011.

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1945-, Reznick A. Z., ed. Oxidative stress in skeletal muscle. Basel: Birkhäuser Verlag, 1998.

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Armstrong, Donald y Dhruba J. Bharali, eds. Oxidative Stress and Nanotechnology. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-475-3.

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Miwa, Satomi, Kenneth B. Beckman y Florian L. Muller, eds. Oxidative Stress in Aging. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-420-9.

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Cutler, R. G., L. Packer, J. Bertram y A. Mori, eds. Oxidative Stress and Aging. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7337-6.

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Parvez, H. y P. Riederer, eds. Oxidative Stress and Neuroprotection. Vienna: Springer Vienna, 2006. http://dx.doi.org/10.1007/978-3-211-33328-0.

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Gelpi, Ricardo Jorge, Alberto Boveris y Juan José Poderoso, eds. Biochemistry of Oxidative Stress. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45865-6.

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G, Cutler Richard y International Conference on Oxidative Stress and Aging (1st : 1994 : Hawaii), eds. Oxidative stress and aging. Basel: Birkhauser Verlag, 1995.

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Capítulos de libros sobre el tema "Oxidative stress"

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Zeliger, Harold I. "Psychological stress". En Oxidative Stress, 153–58. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-323-91890-9.00015-5.

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"Front Matter". En Oxidative Stress, iii. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-12-642760-8.50001-6.

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"Copyright". En Oxidative Stress, iv. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-12-642760-8.50002-8.

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"Contributors". En Oxidative Stress, xi—xiii. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-12-642760-8.50003-x.

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Sies, Helmut. "Preface". En Oxidative Stress, xv. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-12-642760-8.50004-1.

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SIES, HELMUT. "Oxidative Stress: Introductory Remarks". En Oxidative Stress, 1–8. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-12-642760-8.50005-3.

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SCHULTE-FROHLINDE, DIETRICH y CLEMENS VON SONNTAG. "Radiolysis of DNA and Model Systems in the Presence of Oxygen". En Oxidative Stress, 11–40. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-12-642760-8.50006-5.

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WILLSON, ROBIN L. "Organic Peroxy Free Radicals as Ultimate Agents in Oxygen Toxicity". En Oxidative Stress, 41–72. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-12-642760-8.50007-7.

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SIES, HELMUT. "Hydroperoxides and Thiol Oxidants in the Study of Oxidative Stress in Intact Cells and Organs". En Oxidative Stress, 73–90. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-12-642760-8.50008-9.

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SMITH, MARTYN T., CELIA G. EVANS, HJÖRDIS THOR y STEN ORRENIUS. "Quinone-Induced Oxidative Injury to Cells and Tissues". En Oxidative Stress, 91–113. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-12-642760-8.50009-0.

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Actas de conferencias sobre el tema "Oxidative stress"

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Sridharan, Sriram, Ritwik Layek, Aniruddha Datta y Jijayanagaram Venkatraj. "Modelling oxidative stress response pathways". En 2011 IEEE International Workshop on Genomic Signal Processing and Statistics (GENSIPS). IEEE, 2011. http://dx.doi.org/10.1109/gensips.2011.6169471.

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"24th International Conference on Oxidative Stress Reduction, Redox Homeostasis and Antioxidants". En 24th International Conference on Oxidative Stress Reduction, Redox Homeostasis and Antioxidants. Frontiers Media SA, 2023. http://dx.doi.org/10.3389/978-2-88971-019-5.

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Liu, Junhua, Zhenhua Wang, Bao Ju y Qiusheng Zheng. "Heroin-Induced Hepatotoxicity: Involved Oxidative Stress". En 2008 2nd International Conference on Bioinformatics and Biomedical Engineering (ICBBE '08). IEEE, 2008. http://dx.doi.org/10.1109/icbbe.2008.272.

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Gea, J., S. Mas, E. Balcells, J. Sauleda, F. Gomez, J. Galdiz, E. Monso et al. "Systemic Oxidative Stress and COPD Phenotypes." En American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4329.

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Yang, Kewen. "Oxidative stress and male reproductive health". En International Conference on Modern Medicine and Global Health (ICMMGH 2023), editado por Sheiladevi Sukumaran. SPIE, 2023. http://dx.doi.org/10.1117/12.2692053.

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Shikov, A. E., V. V. Lastochkin, T. V. Chirkova y V. V. Emelyanov. "Oxidative damage to plant lipids and proteins bynatural and artificial oxidative stress". En IX Congress of society physiologists of plants of Russia "Plant physiology is the basis for creating plants of the future". Kazan University Press, 2019. http://dx.doi.org/10.26907/978-5-00130-204-9-2019-481.

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Keyhani, J., E. Keyhani, F. Attar y M. Hadizadeh. "Anti-oxidative stress enzymes in Pleurotus ostreatus". En Proceedings of the II International Conference on Environmental, Industrial and Applied Microbiology (BioMicroWorld2007). WORLD SCIENTIFIC, 2009. http://dx.doi.org/10.1142/9789812837554_0001.

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Jassal, R., D. Talwar, D. Mcmillan y S. Tovey. "Biomarkers of Oxidative Stress in Breast Cancer." En Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-2141.

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Avramouli, Antigoni, Georgia Theocharopoulou y Panayiotis Vlamos. "Detection of oxidative stress in neurodegenerative diseases". En 2015 IEEE International Symposium on Signal Processing and Information Technology (ISSPIT). IEEE, 2015. http://dx.doi.org/10.1109/isspit.2015.7394366.

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Kawai, K., Y.-S. Li, Y. Kawasaki, H. Kasai, S. Watanabe, H. Yamato, T. Honda y M. Ohta. "1218 Salivary oxidative stress biomarker: 8-hydroxyguanosine". En 32nd Triennial Congress of the International Commission on Occupational Health (ICOH), Dublin, Ireland, 29th April to 4th May 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/oemed-2018-icohabstracts.1158.

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Informes sobre el tema "Oxidative stress"

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Vanreusel, Inne, Wendy Hens, Jan Taeymans, Emeline Van Craenenbroeck, An Van Berendoncks, Bernard Paelinck, Vincent Segers y Jacob J. Briedé. Oxidative Stress in Patients with Congenital Heart Disease: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, mayo de 2023. http://dx.doi.org/10.37766/inplasy2023.5.0044.

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Review question / Objective: To conduct a systematic review and meta-analysis of clinical controlled studies comparing parameters measuring oxidative stress in blood of patients with congenital heart disease (CHD). Main objective: to review studies on the presence of oxidative stress in both children and adults with CHD. Secondary objectives: - to review methods to assess oxidative stress levels in peripheral blood of CHD - to review factors with the potential to influence oxidative stress levels - to study whether there are therapeutic options targeting oxidative stress in CHD.
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Paul, Satashree. Oxidative Stress: A Cause of Male Infertility. Science Repository OÜ, octubre de 2020. http://dx.doi.org/10.31487/sr.blog.10.

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zhao, Hua. Oxidative Stress, DNA Repair and Prostate Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, agosto de 2010. http://dx.doi.org/10.21236/ada542698.

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Zhao, Hua. Oxidative Stress, DNA Repair and Prostate Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, agosto de 2009. http://dx.doi.org/10.21236/ada518882.

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Zhao, Hua. Oxidative Stress, DNA Repair, and Prostate Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, agosto de 2011. http://dx.doi.org/10.21236/ada561087.

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Madaeva, I. M., N. A. Kurashova, N. V. Semenova, E. B. Uhinov, S. I. Kolesnikov y L. I. Kolesnikova. HSP70 HEAT SHOCK PROTEIN IN OXIDATIVE STRESS APNEA PATIENTS. Publishing house of the Russian Academy of Medical Sciences, 2020. http://dx.doi.org/10.18411/1695-1978-2020-62730.

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Handa, Avtar K., Yuval Eshdat, Avichai Perl, Bruce A. Watkins, Doron Holland y David Levy. Enhancing Quality Attributes of Potato and Tomato by Modifying and Controlling their Oxidative Stress Outcome. United States Department of Agriculture, mayo de 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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Horwitz, Benjamin A. y Barbara Gillian Turgeon. Fungal Iron Acquisition, Oxidative Stress and Virulence in the Cochliobolus-maize Interaction. United States Department of Agriculture, marzo de 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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Li, Jiaxiao, Suling Liu y Yang Cui. Oxidative and Anti-oxidative stress-linked biomarkers in Ankylosing Spondylitis: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, mayo de 2020. http://dx.doi.org/10.37766/inplasy2020.5.0066.

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Carey, Hannah V. The Adaptive Response to Intestinal Oxidative Stress in Mammalian Hibernation. Fort Belvoir, VA: Defense Technical Information Center, enero de 2006. http://dx.doi.org/10.21236/ada442363.

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