Journal articles: 'Oxidative stess'

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Horton, Amanda, Kim Boggess, Kevin Moss, James Beck, and Steven Offenbacher. "401: Maternal periodontal infection, oxidative stess, and preeclampsia risk." American Journal of Obstetrics and Gynecology 199, no. 6 (December 2008): S121. http://dx.doi.org/10.1016/j.ajog.2008.09.430.

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Sarvazyan, Narine, Luther M. Swift, Pamela J. Kell, and Jame McHowat. "Oxidant-induced inhibition of phospholipase Ag2 activity and its role in potentiation of oxidative stess." Journal of Molecular and Cellular Cardiology 33, no. 6 (June 2001): A105. http://dx.doi.org/10.1016/s0022-2828(01)90419-5.

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Maharaj, Deepa S., Beverley D. Glass, and Santy Daya. "Melatonin: New Places in Therapy." Bioscience Reports 27, no. 6 (November 20, 2007): 299–320. http://dx.doi.org/10.1007/s10540-007-9052-1.

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The fact that the full extent of the function of the pineal gland has not yet been elucidated, has stimulated melatonin research worldwide. This review introduces melatonin's mechanism of action, direct and indirect antioxidant actions as well as the antioxidant properties of its metabolites, 6-hydroxymelatonin (6-OHM) and N-acetyl-N-formyl-5-methoxykynurenamine (AFMK). At present the mechanism of action is proposed to be receptor-, protein- and nonprotein-mediated. From its popular role in the treatment of jetlag, melatonin is now implicated in the reduction of oxidative stess, both as a free radical scavenger and antioxidant. Melatonin's direct scavenging action in respect of the following will be discussed: superoxide anions, hydrogen peroxide, hydroxyl radicals, singlet oxygen, peroxy radicals and nitric oxide/peroxy nitrite anions. In addition melatonin also possesses indirect antioxidant activity and the role of its metabolites, AFMK and 6-OHM will be presented. It is these free radical scavenging and antioxidant properties of melatonin that has shifted the focus from that of merely strengthening circadian rhythms to that of neuroprotectant: a new place in therapy.

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Sun, Qi-An, Nageswara Madamanchi, and Marschall Runge. "Oxidative stress, NADPH oxidases, and arteries." Hämostaseologie 36, no. 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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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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Rosa, Eloi Francisco, and Vanessa Cristina Coimbra. "Câncer de cólon e estresse oxidativo." O Mundo da Saúde 33, no. 4 (December 4, 2009): 415–18. http://dx.doi.org/10.15343/0104-7809.20094415418.

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Qin, Bei, Kuan Yang, and Ruijun Cao. "Synthesis and Antioxidative Activity of Piperine Derivatives Containing Phenolic Hydroxyl." Journal of Chemistry 2020 (July 21, 2020): 1–9. http://dx.doi.org/10.1155/2020/2786359.

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Piperine was used in this study in its raw form, and different steps, such as amide hydrolysis and amidation, were used to synthesize piperine derivatives containing a phenolic hydroxyl group. DPPH and ABTS free radical scavenging assays were used to assess piperine derivative antioxidant activities. We constructed an AAPH oxidative stress erythrocyte model to study the effect of piperine derivatives on the hemolysis rate of oxidatively damaged erythrocytes as well as the hemoglobin oxidation rate. This AAPH model was also used to determine piperine derivative effects on antioxidant enzyme activity and malondialdehyde (MDA) content. Results showed that spectroscopic methods could synthesize and identify piperine derivatives containing phenolic hydroxyl groups (H-1∼H-3). Moreover, DPPH and ABTS assay results showed that piperine derivative free radical clearance rates were higher compared with the parent compound. Additionally, piperine derivatives (H-1∼H-3) were found to provide protection to AAPH oxidatively damaged erythrocytes in their ability to inhibit AAPH-induced erythrocyte lysis, while hemoglobin oxidation was higher compared with the parent compound. Piperine derivatives may protect intracellular glutathione peroxidase (GSH-Px) antioxidant enzyme system activities, safeguarding against oxidative damage. This study synthesized novel piperine derivatives for use as potential antioxidant agent candidates.

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Dorovskikh, V. A., N. V. Simonova, E. Yu Yurtaeva, R. A. Anokhina, and M. A. Shtarberg. "PHYTOCORRECTION OF OXIDATIVE STRESS IN EXPERIMENT." Amur Medical Journal, no. 15-16 (2016): 35–37. http://dx.doi.org/10.22448/amj.2016.15-16.35-37.

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Chen, Chuck T., Marc-Olivier Trépanier, Kathryn E. Hopperton, Anthony F. Domenichiello, Mojgan Masoodi, and Richard P. Bazinet. "Inhibiting Mitochondrial β-Oxidation Selectively Reduces Levels of Nonenzymatic Oxidative Polyunsaturated Fatty Acid Metabolites in the Brain." Journal of Cerebral Blood Flow & Metabolism 34, no. 3 (December 11, 2013): 376–79. http://dx.doi.org/10.1038/jcbfm.2013.221.

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Schönfeld and Reiser recently hypothesized that fatty acid β-oxidation is a source of oxidative stress in the brain. To test this hypothesis, we inhibited brain mitochondrial β-oxidation with methyl palmoxirate (MEP) and measured oxidative polyunsaturated fatty acid (PUFA) metabolites in the rat brain. Upon MEP treatment, levels of several nonenzymatic auto-oxidative PUFA metabolites were reduced with few effects on enzymatically derived metabolites. Our finding confirms the hypothesis that reduced fatty acid β-oxidation decreases oxidative stress in the brain and β-oxidation inhibitors may be a novel therapeutic approach for brain disorders associated with oxidative stress.

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Shang, F., and A. Taylor. "Oxidative stress and recovery from oxidative stress are associated with altered ubiquitin conjugating and proteolytic activities in bovine lens epithelial cells." Biochemical Journal 307, no. 1 (April 1, 1995): 297–303. http://dx.doi.org/10.1042/bj3070297.

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Roles for ubiquitin (an 8.5 kDa polypeptide) involve its conjugation to proteins as a signal to initiate degradation and as a stress protein. We investigated ubiquitin conjugation and ubiquitin-dependent proteolytic activities in cultured bovine lens epithelial cells (BLECs) upon oxidative challenge. A 44% decrease in intracellular glutathione confirmed oxidative stress upon incubation with 1 mM H2O2. After 30 min incubation, endogenous high-molecular-mass ubiquitin conjugates decreased 73%, and intracellular proteolysis decreased about 50%. In the supernatants of the oxidatively treated BLECs, the ability to form high-molecular-mass ubiquitin conjugates with exogenous 125I-labelled ubiquitin decreased 28%, and ATP-dependent degradation of oxidized alpha-crystallin decreased 36%. When the H2O2-treated BLECs were allowed to recover for 60 min, intracellular proteolysis returned to the level of control cells. There was also a subsequent transient enhancement of intracellular proteolysis and a simultaneous recovery of endogenous high-molecular-mass ubiquitin conjugates. In parallel cell-free experiments, conjugating activity with exogenous 125I-labelled ubiquitin and ATP-dependent degradation of oxidized alpha-crystallin increased 35% and 72% respectively compared with non-oxidatively treated BLECs. ATP-independent proteolysis showed little response to exposure or removal of H2O2. These results indicate that (1) the rate of intracellular proteolysis in BLECs is associated with the level of endogenous high-molecular-mass ubiquitin conjugates and (2) oxidative stress may inactivate the ubiquitin conjugation activity with coordinate depression of proteolytic capability. Enhancement in ubiquitin conjugation and proteolytic activities during recovery from oxidative stress may be important in removal of damaged proteins and restoration of normal function of BLECs. The inactivation of ubiquitin-dependent proteolysis by oxidation may be involved in the accumulation of altered proteins and other adverse sequelae in the oxidatively challenged aging lens.

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11

Saha, Atanu. "Assessment of Oxidative Stress and Association of Oxidative Markers among High School Teachers." Indian Journal of Applied Research 4, no. 2 (October 1, 2011): 7–9. http://dx.doi.org/10.15373/2249555x/feb2014/179.

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12

Singh, Abhishek Kumar, Sandeep Singh, Geetika Garg, and Syed Ibrahim Rizvi. "Rapamycin alleviates oxidative stress-induced damage in rat erythrocytes." Biochemistry and Cell Biology 94, no. 5 (October 2016): 471–79. http://dx.doi.org/10.1139/bcb-2016-0048.

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An imbalanced cellular redox system promotes the production of reactive oxygen species (ROS) that may lead to oxidative stress-mediated cell death. Erythrocytes are the best-studied model of antioxidant defense mechanism. The present study was undertaken to investigate the effect of the immunosuppressant drug rapamycin, an inducer of autophagy, on redox balance of erythrocytes and blood plasma of oxidatively challenged rats. Male Wistar rats were oxidatively challenged with HgCl2 (5 mg/kg body mass (b.m.)). A significant (p < 0.05) induction in ROS production, plasma membrane redox system (PMRS), intracellular Ca2+ influx, lipid peroxidation (LPO), osmotic fragility, plasma protein carbonyl (PCO) content, and plasma advanced oxidation protein products (AOPP) and simultaneously significant reduction in glutathione (GSH) level and ferric reducing ability of plasma (FRAP) were observed in rats exposed to HgCl2. Furthermore, rapamycin (0.5 mg/kg b.m.) provided significant protection against HgCl2-induced alterations in rat erythrocytes and plasma by reducing ROS production, PMRS activity, intracellular Ca2+ influx, LPO, osmotic fragility, PCO content, and AOPP and also restored the level of antioxidant GSH and FRAP. Our observations provide evidence that rapamycin improves redox status and attenuates oxidative stress in oxidatively challenged rats. Our data also demonstrate that rapamycin is a comparatively safe immunosuppressant drug.

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Tiwari, Supriya. "Oxidative Stress and Antioxidant Defense in Cells." Global Journal For Research Analysis 3, no. 8 (June 15, 2012): 11–14. http://dx.doi.org/10.15373/22778160/august2014/4.

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I.A., Maslyukov, Kokoreva T.V., and Pashin S.S. "ПАТОГЕНЕТИЧЕСКИЕ АСПЕКТЫ ОКСИДАТИВНОГО СТРЕССА ПРИ ПАТОСПЕРМИИ." Bulletin "Biomedicine and sociology" 4, no. 2 (June 30, 2019): 25–28. http://dx.doi.org/10.26787/nydha-2618-8783-2019-4-2-25-28.

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Catanzaro, Orlando. "Diabetic oxidative stress and bone loss complications." Endocrinology and Disorders 5, no. 1 (March 5, 2021): 01–04. http://dx.doi.org/10.31579/2640-1045/056.

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Diabetes mellitus is a group of metabolic disorder characterize by and absolute or partial insulin deficiency. Diabetic hyperglycemia is produce by the effect of homeostasis between proteolytic enzymes, their inhibitors and the antioxidants defense that protect and repair vital tissues and molecular components. Bone consist of both component and trabecular bone tissue. Organic matrix and albumin form part of noncollagenous of bone .Initiation of mineralization and collagen fibrils form the phase of mineral matrix. Calcium flux into and out of bone depend of osteoclastic and osteoblastic activity. The remodeling is initiated by resorption and new bone formation at the resorption site. Diabetic complication is a critical factor for bone pathology and could start early inflammatory stage even before hyperglycemia. Diabetic produces bone loss from reduce osteoblast activity. Partly insulin deficiency produce defective bone remodeling indirect by oxidative stress. The current treatment for defective bone in diabetes state include biophosphonate and cinaciguat. Biphosphonate inhibit bone resorption, but may worsen bone quality. A novel type of activation of sGMP is cinaciguat an NO independent activator of oxidative GC, increase c GMP synthesis on diabetic and restore proliferation and survival of osteoblasts. Chronic hyperglycemia interferes with the oseointegration of implants in diabetics. Both diabetic and aging plays a role in abnormal differentiation of osteroblasts. In diabetic patients may improve the oral health to have a positive impact if optimal glycemic control is emphasized. However with cinaciguat present as a novel paradigm enhancing bone formation under hyperglycemia and protect bone implants.

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Mann, Carolina, Solon Thanos, Katrin Brockhaus, Franz H. Grus, Norbert Pfeiffer, and Verena Prokosch. "Reaktion der Endothelzellen auf kurzzeitig physiologisch erhöhte hydrostatische Drücke und oxidativen Stress in vitro." Klinische Monatsblätter für Augenheilkunde 236, no. 09 (April 11, 2018): 1122–28. http://dx.doi.org/10.1055/s-0043-122677.

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Zusammenfassung Hintergrund Im Rahmen der Pathogenese des Glaukoms wird die endotheliale Dysfunktion zunehmend diskutiert. Peripapilläre Blutungen sind diagnostisch wegweisend. Die Korrelation von Glaukomerkrankungen mit vaskulärem Dysregulationssyndrom ist eindeutig. Ziel dieser Studie ist es, die genaue Reaktion der Endothelzellen auf erhöhten hydrostatischen und oxidativen Stress zu untersuchen. Material und Methoden In vitro wurden primär dissoziierte BMECs (brain microvascular endothelial cells) für 3 Tage normalem und leicht erhöhtem hydrostatischem Druck von 60 und 120 mmHg in einer Druckkammer ausgesetzt. Zusätzlich wurden sowohl druckbelastete als auch nicht druckbelastete Zellen oxidativem Stress in Form von geringen Konzentrationen H2O2 ausgesetzt. Ein Live/Dead Assay wurde durchgeführt, um die Zellviabilität zu messen. Morphologisch wurden die Zellen mit immunhistochemischer Aktinfärbung beurteilt. Ergebnisse Interessanterweise zeigten die Endothelzellen sowohl unter 60 mmHg als auch unter 120 mmHg kein vermehrtes Absterben im Vergleich zu den Zellen ohne Belastung. Auch morphologisch zeigten sich keine großen Unterschiede. Gegenüber oxidativem Stress wurden alle Zellen schon bei kleinen Mengen geschädigt. Keinen Unterschied konnte man zwischen oxidativem Stress ohne vorherige Druckbelastung und oxidativem Stress mit vorheriger Druckbelastung von 120 mmHg für 3 Tage feststellen. Schlussfolgerung Wir konnten keinen direkten Effekt in Form von vermehrtem Zelluntergang der Endothelzellen auf erhöhten hydrostatischen Druck feststellen. Allerdings zeigt die Reaktion auf die geringen Konzentrationen von oxidativem Stress, dass die Zellen im Rahmen der Pathogenese des Glaukoms doch in Mitleidenschaft gezogen werden. Der oxidative Stress scheint hier eine besondere Rolle zu spielen.

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Lykkesfeldt, Jens, Gilberto Perez Trueba, Henrik E. Poulsen, and Stephan Christen. "Vitamin C deficiency in weanling guinea pigs: differential expression of oxidative stress and DNA repair in liver and brain." British Journal of Nutrition 98, no. 6 (December 2007): 1116–19. http://dx.doi.org/10.1017/s0007114507787457.

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Neonates are particularly susceptible to malnutrition due to their limited reserves of micronutrients and their rapid growth. In the present study, we examined the effect of vitamin C deficiency on markers of oxidative stress in plasma, liver and brain of weanling guinea pigs. Vitamin C deficiency caused rapid and significant depletion of ascorbate (P < 0·001), tocopherols (P < 0·001) and glutathione (P < 0·001), and a decrease in superoxide dismutase activity (P = 0·005) in the liver, while protein oxidation was significantly increased (P = 0·011). No changes in lipid oxidation or oxidatively damaged DNA were observed in this tissue. In the brain, the pattern was markedly different. Of the measured antioxidants, only ascorbate was significantly depleted (P < 0·001), but in contrast to the liver, ascorbate oxidation (P = 0·034), lipid oxidation (P < 0·001), DNA oxidation (P = 0·13) and DNA incision repair (P = 0·014) were all increased, while protein oxidation decreased (P = 0·003). The results show that the selective preservation of brain ascorbate and induction of DNA repair in vitamin C-deficient weanling guinea pigs is not sufficient to prevent oxidative damage. Vitamin C deficiency may therefore be particularly adverse during the neonatal period.

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Breusing, Nicolle, and Tilman Grune. "Regulation of proteasome-mediated protein degradation during oxidative stress and aging." Biological Chemistry 389, no. 3 (March 1, 2008): 203–9. http://dx.doi.org/10.1515/bc.2008.029.

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Abstract Protein degradation is a physiological process required to maintain cellular functions. There are distinct proteolytic systems for different physiological tasks under changing environmental and pathophysiological conditions. The proteasome is responsible for the removal of oxidatively damaged proteins in the cytosol and nucleus. It has been demonstrated that proteasomal degradation increases due to mild oxidation, whereas at higher oxidant levels proteasomal degradation decreases. Moreover, the proteasome itself is affected by oxidative stress to varying degrees. The ATP-stimulated 26S proteasome is sensitive to oxidative stress, whereas the 20S form seems to be resistant. Non-degradable protein aggregates and cross-linked proteins are able to bind to the proteasome, which makes the degradation of other misfolded and damaged proteins less efficient. Consequently, inhibition of the proteasome has dramatic effects on cellular aging processes and cell viability. It seems likely that during oxidative stress cells are able to keep the nuclear protein pool free of damage, while cytosolic proteins may accumulate. This is because of the high proteasome content in the nucleus, which protects the nucleus from the formation and accumulation of non-degradable proteins. In this review we highlight the regulation of the proteasome during oxidative stress and aging.

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Kiffin, Roberta, Christopher Christian, Erwin Knecht, and Ana Maria Cuervo. "Activation of Chaperone-mediated Autophagy during Oxidative Stress." Molecular Biology of the Cell 15, no. 11 (November 2004): 4829–40. http://dx.doi.org/10.1091/mbc.e04-06-0477.

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Oxidatively damaged proteins accumulate with age in almost all cell types and tissues. The activity of chaperone-mediated autophagy (CMA), a selective pathway for the degradation of cytosolic proteins in lysosomes, decreases with age. We have analyzed the possible participation of CMA in the removal of oxidized proteins in rat liver and cultured mouse fibroblasts. Added to the fact that CMA substrates, when oxidized, are more efficiently internalized into lysosomes, we have found a constitutive activation of CMA during oxidative stress. Oxidation-induced activation of CMA correlates with higher levels of several components of the lysosomal translocation complex, but in particular of the lumenal chaperone, required for substrate uptake, and of the lysosomal membrane protein (lamp) type 2a, previously identified as a receptor for this pathway. In contrast with the well characterized mechanism of CMA activation during nutritional stress, which does not require de novo synthesis of the receptor, oxidation-induced activation of CMA is attained through transcriptional up-regulation of lamp2a. We conclude that CMA is activated during oxidative stress and that the higher activity of this pathway under these conditions, along with the higher susceptibility of the oxidized proteins to be taken up by lysosomes, both contribute to the efficient removal of oxidized proteins.

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Kibel, Aleksandar, Ana Marija Lukinac, Vedran Dambic, Iva Juric, and Kristina Selthofer Relatic. "Oxidative Stress in Ischemic Heart Disease." Oxidative Medicine and Cellular Longevity 2020 (December 28, 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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M V, Sailaja, Sharan B. Singh M, Ch Rajendhra, and N. Mallikarjuna Reddy. "Role of Oxidative Stress on Age and Gender." International Journal of Integrative Medical Sciences 2, no. 2 (February 28, 2015): 61–69. http://dx.doi.org/10.16965/ijims.2015.103.

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Waghmare, P. A. "Some Oxidative Stress Markers in Pregnant Anemic Woman." Journal of Medical Science And clinical Research 05, no. 06 (June 30, 2017): 24121–24. http://dx.doi.org/10.18535/jmscr/v5i6.213.

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Namıduru, Emine Siber, and Mustafa Namıduru. "Oxidative stress in viral HEPATITIS B and C." Asian Pacific Journal of Health Sciences 6, no. 4 (December 2019): 47–48. http://dx.doi.org/10.21276/apjhs.2019.6.4.10.

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Yan, Liang-Jun. "Protein Redox Modification as a Cellular Defense Mechanism against Tissue Ischemic Injury." Oxidative Medicine and Cellular Longevity 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/343154.

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Protein oxidative or redox modifications induced by reactive oxygen species (ROS) or reactive nitrogen species (RNS) not only can impair protein function, but also can regulate and expand protein function under a variety of stressful conditions. Protein oxidative modifications can generally be classified into two categories: irreversible oxidation and reversible oxidation. While irreversible oxidation usually leads to protein aggregation and degradation, reversible oxidation that usually occurs on protein cysteine residues can often serve as an “on and off” switch that regulates protein function and redox signaling pathways upon stress challenges. In the context of ischemic tolerance, including preconditioning and postconditioning, increasing evidence has indicated that reversible cysteine redox modifications such as S-sulfonation, S-nitrosylation, S-glutathionylation, and disulfide bond formation can serve as a cellular defense mechanism against tissue ischemic injury. In this review, I highlight evidence of cysteine redox modifications as protective measures in ischemic injury, demonstrating that protein redox modifications can serve as a therapeutic target for attenuating tissue ischemic injury. Prospectively, more oxidatively modified proteins will need to be identified that can play protective roles in tissue ischemic injury, in particular, when the oxidative modifications of such identified proteins can be enhanced by pharmacological agents or drugs that are available or to be developed.

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Kale, Ravindra, Annette E. Hebert, Laurie K. Frankel, Larry Sallans, Terry M. Bricker, and Pavel Pospíšil. "Amino acid oxidation of the D1 and D2 proteins by oxygen radicals during photoinhibition of Photosystem II." Proceedings of the National Academy of Sciences 114, no. 11 (March 6, 2017): 2988–93. http://dx.doi.org/10.1073/pnas.1618922114.

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The Photosystem II reaction center is vulnerable to photoinhibition. The D1 and D2 proteins, lying at the core of the photosystem, are susceptible to oxidative modification by reactive oxygen species that are formed by the photosystem during illumination. Using spin probes and EPR spectroscopy, we have determined that both O2•− and HO• are involved in the photoinhibitory process. Using tandem mass spectroscopy, we have identified a number of oxidatively modified D1 and D2 residues. Our analysis indicates that these oxidative modifications are associated with formation of HO• at both the Mn4O5Ca cluster and the nonheme iron. Additionally, O2•− appears to be formed by the reduction of O2 at either PheoD1 or QA. Early oxidation of D1:332H, which is coordinated with the Mn1 of the Mn4O5Ca cluster, appears to initiate a cascade of oxidative events that lead to the oxidative modification of numerous residues in the C termini of the D1 and D2 proteins on the donor side of the photosystem. Oxidation of D2:244Y, which is a bicarbonate ligand for the nonheme iron, induces the propagation of oxidative reactions in residues of the D-de loop of the D2 protein on the electron acceptor side of the photosystem. Finally, D1:130E and D2:246M are oxidatively modified by O2•− formed by the reduction of O2 either by PheoD1•− or QA•−. The identification of specific amino acid residues oxidized by reactive oxygen species provides insights into the mechanism of damage to the D1 and D2 proteins under light stress.

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Thomas, Megan M., Maricela Haghiac, Catalin Grozav, Judi Minium, Virtu Calabuig-Navarro, and Perrie O’Tierney-Ginn. "Oxidative Stress Impairs Fatty Acid Oxidation and Mitochondrial Function in the Term Placenta." Reproductive Sciences 26, no. 7 (October 10, 2018): 972–78. http://dx.doi.org/10.1177/1933719118802054.

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Placental fatty acid oxidation (FAO) is impaired and lipid storage is increased in pregnancy states associated with chronic oxidative stress. The effect of acute oxidative stress, as seen in pregnancies complicated with asthma, on placental lipid metabolism is unknown. We hypothesized that induction of acute oxidative stress would decrease FAO and increase esterification. We assessed [3H]-palmitate oxidation and esterification in term placental explants from lean women after exposure to hydrogen peroxide (H2O2) for 4 hours. Fatty acid oxidation decreased 16% and 24% in placental explants exposed to 200 ( P = .02) and 400 µM H2O2 ( P = .01), respectively. Esterification was not altered with H2O2 exposure. Neither messenger RNA nor protein expression of key genes involved in FAO (eg, peroxisome proliferator-activated receptor α, carnitine palmitoyl transferase 1b) were altered. Adenosine triphosphate (ATP) levels decreased with induction of oxidative stress, without increasing cytotoxicity. Acute oxidative stress decreased FAO and ATP production in the term placenta without altering fatty acid esterification. As decreases in placental FAO and ATP production are associated with impaired fetal growth, pregnancies exposed to acute oxidative stress may be at risk for fetal growth restriction.

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Rubbo, H., A. Trostchansky, H. Botti, and C. Batthyány. "Interactions of Nitric Oxide and Peroxynitrite with Low-Density Lipoprotein." Biological Chemistry 383, no. 3-4 (April 12, 2002): 547–52. http://dx.doi.org/10.1515/bc.2002.055.

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Abstract Nitric oxide (NO) is a free radical species that diffuses and concentrates in the hydrophobic core of lowdensity lipoprotein (LDL) to serve as a potent inhibitor of lipid oxidation processes. Peroxynitrite (PN), the product of the diffusionlimited reaction between NO and superoxide (O2), represents a relevant mediator of oxidative modifications in LDL. The focus of this review is the analysis of interactions between NO and PN and its secondary reactions with oxygen radicals on LDL oxidation, which are relevant in the development of the early steps as well as progression of atherosclerosis. We propose that the balance between rates of PN and NO production, which greatly depends on oxidative stress processes within the vascular wall, will critically determine the final extent of oxidative LDL modifications leading or not to scavenger receptormediated LDL uptake and foam cell formation.

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Vodošek Hojs, Nina, Sebastjan Bevc, Robert Ekart, and Radovan Hojs. "Oxidative Stress Markers in Chronic Kidney Disease with Emphasis on Diabetic Nephropathy." Antioxidants 9, no. 10 (September 27, 2020): 925. http://dx.doi.org/10.3390/antiox9100925.

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Diabetes prevalence is increasing worldwide, especially through the increase of type 2 diabetes. Diabetic nephropathy occurs in up to 40% of diabetic patients and is the leading cause of end-stage renal disease. Various factors affect the development and progression of diabetic nephropathy. Hyperglycaemia increases free radical production, resulting in oxidative stress, which plays an important role in the pathogenesis of diabetic nephropathy. Free radicals have a short half-life and are difficult to measure. In contrast, oxidation products, including lipid peroxidation, protein oxidation, and nucleic acid oxidation, have longer lifetimes and are used to evaluate oxidative stress. In recent years, different oxidative stress biomarkers associated with diabetic nephropathy have been found. This review summarises current evidence of oxidative stress biomarkers in patients with diabetic nephropathy. Although some of them are promising, they cannot replace currently used clinical biomarkers (eGFR, proteinuria) in the development and progression of diabetic nephropathy.

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Buss, J. L., J. Neuzil, and P. Ponka. "The role of oxidative stress in the toxicity of pyridoxal isonicotinoyl hydrazone (PIH) analogues." Biochemical Society Transactions 30, no. 4 (August 1, 2002): 755–58. http://dx.doi.org/10.1042/bst0300755.

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Pyridoxal isonicotinoyl hydrazone (PIH) analogues are effective iron chelators in vivo and in vitro, and may be of value for the treatment of secondary iron overload. The sensitivity of Jurkat cells to Fe-chelator complexes was enhanced several-fold by the depletion of the antioxidant glutathione, indicating the role of oxidative stress in their toxicity. K562 cells loaded with eicosapentaenoic acid, a fatty acid particularly susceptible to oxidation, were also more sensitive to the toxic effects of the Fe complexes, and toxicity was proportional to lipid peroxidation. Thus Fechelator complexes cause oxidative stress, which may be a major component of their toxicity. As was the case for their Fe complexes, the toxicity of PIH analogues was enhanced by glutathione depletion of Jurkat cells and eicosapentaenoic acidloading of K562 cells. Thus the toxicity of the chelators themselves is also enhanced by compromised cellular redox status. In addition, the toxicity of the chelators was diminished by culturing Jurkat cells under hypoxic conditions, which may limit the production of the reactive oxygen species that initiate oxidative stress. A significant part of the toxicity of the chelators may be due to intracellular formation of Fe-chelator complexes, which oxidatively destroy the cell.

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Dzyuba, V., J. Cosson, B. Dzyuba, and M. Rodina. "Oxidative stress and motility in tench Tinca tinca spermatozoa." Czech Journal of Animal Science 60, No. 6 (July 15, 2016): 250–62. http://dx.doi.org/10.17221/8238-cjas.

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Junagam, Sreemannarayana, and Balu Jatthavath. "OXIDATIVE STRESS AND ANTIOXIDANT STATUS IN AGRICULTURAL PESTICIDE SPRAYERS." International Journal of Integrative Medical Sciences 5, no. 6 (July 5, 2018): 663–66. http://dx.doi.org/10.16965/ijims.2018.120.

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Konada, Sudhakar, Satyanarayana Rentala, SarvaMangala Dhurjeti, and USN Murthy. "Morinda Citrifolia Implications on Oxidative Stress Induced Cataract Formation." Global Journal For Research Analysis 3, no. 8 (June 15, 2012): 8–10. http://dx.doi.org/10.15373/22778160/august2014/3.

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Solomons, Hilary. "Increased Oxidative Stress In Allergic Rhinitis. Attention; Ruywayda Adams." Journal of Clinical Research and Reports 8, no. 2 (June 11, 2021): 01–02. http://dx.doi.org/10.31579/2690-1919/172.

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There is a sample evidence that allergic disorders such as asthma, rhinitis and atopic dermatitis are mediated by oxidative stress. Excessive exposure to reactive oxygen and nitrogen species is the hallmark of oxidative stress and leads to damage of proteins, lipids and DNA. Oxidative stress occurs not only as a result of inflammation but also from environmental exposure to air pollution and cigarette smoke. The specific localization of antioxidant enzymes in the lung and the rapid reaction of nitric oxide with reactive oxygen species, such as superoxide, suggests that antioxidant enzymes might also function as cell-signalling agents or regulators of cell signalling.

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Solomons, Hilary. "Increased oxidative stress in allergic rhinitis. Attention; Ruywayda Adams." International Journal of Clinical Case Reports and Reviews 8, no. 1 (August 11, 2021): 01–02. http://dx.doi.org/10.31579/2690-4861/142.

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There is ample evidence that allergic disorders such as asthma, rhinitis and atopic dermatitis are mediated by oxidative stress. Excessive exposure to reactive oxygen and nitrogen species is the hallmark of oxidative stress and leads to damage of proteins, lipids and DNA. Oxidative stress occurs not only as a result of inflammation but also from environmental exposure to air pollution and cigarette smoke.

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FU, Shanlin, Min-Xin FU, W. John BAYNES, R. Suzanne THORPE, and T. Roger DEAN. "Presence of dopa and amino acid hydroperoxides in proteins modified with advanced glycation end products (AGEs): amino acid oxidation products as a possible source of oxidative stress induced by AGE proteins." Biochemical Journal 330, no. 1 (February 15, 1998): 233–39. http://dx.doi.org/10.1042/bj3300233.

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Glycation and subsequent Maillard or browning reactions of glycated proteins, leading to the formation of advanced glycation end products (AGEs), are involved in the chemical modification of proteins during normal aging and have been implicated in the pathogenesis of diabetic complications. Oxidative conditions accelerate the browning of proteins by glucose, and AGE proteins also induce oxidative stress responses in cells bearing AGE receptors. These observations have led to the hypothesis that glycation-induced pathology results from a cycle of oxidative stress, increased chemical modification of proteins via the Maillard reaction, and further AGE-dependent oxidative stress. Here we show that the preparation of AGE-collagen by incubation with glucose under oxidative conditions in vitro leads not only to glycation and formation of the glycoxidation product Nε-(carboxymethyl)lysine (CML), but also to the formation of amino acid oxidation products on protein, including m-tyrosine, dityrosine, dopa, and valine and leucine hydroperoxides. The formation of both CML and amino acid oxidation products was prevented by anaerobic, anti-oxidative conditions. Amino acid oxidation products were also formed when glycated collagen, prepared under anti-oxidative conditions, was allowed to incubate under aerobic conditions that led to the formation of CML. These experiments demonstrate that amino acid oxidation products are formed in proteins during glycoxidation reactions and suggest that reactive oxygen species formed by redox cycling of dopa or by the metal-catalysed decomposition of amino acid hydroperoxides, rather than by redox activity or reactive oxygen production by AGEs on protein, might contribute to the induction of oxidative stress by AGE proteins.

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Jana, Sirsendu, Michael Brad Strader, and Abdu I. Alayash. "The Providence Mutation (βK82D) in Human Hemoglobin Substantially Reduces βCysteine 93 Oxidation and Oxidative Stress in Endothelial Cells." International Journal of Molecular Sciences 21, no. 24 (December 11, 2020): 9453. http://dx.doi.org/10.3390/ijms21249453.

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The highly toxic oxidative transformation of hemoglobin (Hb) to the ferryl state (HbFe4+) is known to occur in both in vitro and in vivo settings. We recently constructed oxidatively stable human Hbs, based on the Hb Providence (βK82D) mutation in sickle cell Hb (βE6V/βK82D) and in a recombinant crosslinked Hb (rHb0.1/βK82D). Using High Resolution Accurate Mass (HRAM) mass spectrometry, we first quantified the degree of irreversible oxidation of βCys93 in these proteins, induced by hydrogen peroxide (H2O2), and compared it to their respective controls (HbA and HbS). Both Hbs containing the βK82D mutation showed considerably less cysteic acid formation, a byproduct of cysteine irreversible oxidation. Next, we performed a novel study aimed at exploring the impact of introducing βK82D containing Hbs on vascular endothelial redox homeostasis and energy metabolism. Incubation of the mutants carrying βK82D with endothelial cells resulted in altered bioenergetic function, by improving basal cellular glycolysis and glycolytic capacity. Treatment of cells with Hb variants containing βK82D resulted in lower heme oxygenase-1 and ferritin expressions, compared to native Hbs. We conclude that the presence of βK82D confers oxidative stability to Hb and adds significant resistance to oxidative toxicity. Therefore, we propose that βK82D is a potential gene-editing target in the treatment of sickle cell disease and in the design of safe and effective oxygen therapeutics.

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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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Štikarová, Jana, Roman Kotlín, Tomáš Riedel, Jiří Suttnar, Kristýna Pimková, Leona Chrastinová, and Jan E. Dyr. "The Effect of Reagents Mimicking Oxidative Stress on Fibrinogen Function." Scientific World Journal 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/359621.

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Fibrinogen is one of the plasma proteins most susceptible to oxidative modification. It has been suggested that modification of fibrinogen may cause thrombotic/bleeding complications associated with many pathophysiological states of organism. We exposed fibrinogen molecules to three different modification reagents—malondialdehyde, sodium hypochlorite, and peroxynitrite—that are presented to various degrees in different stages of oxidative stress. We studied the changes in fibrin network formation and platelet interactions with modified fibrinogens under flow conditions. The fastest modification of fibrinogen was caused by hypochlorite. Fibers from fibrinogen modified with either reagent were thinner in comparison with control fibers. We found that platelet dynamic adhesion was significantly lower on fibrinogen modified with malondialdehyde and significantly higher on fibrinogen modified either with hypochlorite or peroxynitrite reflecting different prothrombotic/antithrombotic properties of oxidatively modified fibrinogens. It seems that, in the complex reactions ongoing in living organisms at conditions of oxidation stress, hypochlorite modifies proteins (e.g., fibrinogen) faster and more preferentially than malondialdehyde. It suggests that the prothrombotic effects of prior fibrinogen modifications may outweigh the antithrombotic effect of malondialdehyde-modified fibrinogen in real living systems.

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Sevcikova, M., H. Modra, A. Slaninova, and Z. Svobodova. " Metals as a cause of oxidative stress in fish: a review." Veterinární Medicína 56, No. 11 (December 12, 2011): 537–46. http://dx.doi.org/10.17221/4272-vetmed.

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This review summarizes the current knowledge on the contribution of metals to the development of oxidative stress in fish. Metals are important inducers of oxidative stress in aquatic organisms, promoting formation of reactive oxygen species through two mechanisms. Redox active metals generate reactive oxygen species through redox cycling, while metals without redox potential impair antioxidant defences, especially that of thiol-containing antioxidants and enzymes. Elevated levels of reactive oxygen species lead to oxidative damage including lipid peroxidation, protein and DNA oxidation, and enzyme inactivation. Antioxidant defences include the enzyme system and low molecular weight antioxidants. Metal-binding proteins, such as ferritin, ceruloplasmin and metallothioneins, have special functions in the detoxification of toxic metals and also play a role in the metabolism and homeostasis of essential metals. Recent studies of metallothioneins as biomarkers indicate that quantitative analysis of mRNA expression of metallothionein genes can be appropriate in cases with elevated levels of metals and no evidence of oxidative damage in fish tissue. Components of the antioxidant defence are used as biochemical markers of oxidative stress. These markers may be manifested differently in the field than in results found in laboratory studies. A complex approach should be taken in field studies of metal contamination of the aquatic environment.  

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Badiou, Cristol, Morena, Bosc, Carbonneau, Dupuy, Descomps, and Canaud. "Vitamin E Supplementation Increases LDL Resistance to ex vivo Oxidation in Hemodialysis Patients." International Journal for Vitamin and Nutrition Research 73, no. 4 (July 1, 2003): 290–96. http://dx.doi.org/10.1024/0300-9831.73.4.290.

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Background: Oxidative stress and alterations in lipid metabolism observed in hemodialysis patients potentiate the low-density lipoprotein (LDL) oxidability, recognized as a key event during early atherogenesis. Objective: To explore the effects of an oral vitamin E supplementation on oxidative stress markers and LDL oxidability in hemodialysis patients. Methods: Fourteen hemodialysis patients and six healthy volunteers were given oral vitamin E (500 mg/day) for six months. Oxidative stress was assessed using: plasma and lipoprotein vitamin E levels [high-performance liquid chromatography (HPLC) procedure]; thiobarbituric acid reactive substances (TBARS, Yaggi method); and copper-induced LDL oxidation. All parameters were evaluated before initiation of vitamin E supplementation, and at three and six months thereafter. Results: At baseline, a significantly higher TBARS concentration and a higher LDL oxidability were observed in hemodialysis patients when compared to controls. After six months of vitamin E supplementation, TBARS and LDL oxidability were normalized in hemodialysis patients. Conclusion: Our data confirm that hemodialysis patients are exposed to oxidative stress and increased susceptibility to ex vivo LDL oxidation. Since oral vitamin E supplementation prevents oxidative stress and significantly increases LDL resistance to ex vivo oxidation, supplementation by natural antioxidants such as vitamin E may be beneficial in hemodialysis patients.

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Kobiela, Jarek, Jacek Krajewski, Beata Kalińska-Błach, and Tomasz Stefaniak. "Selectivity of oxidative stress targeting in estrogen-induced experimental nephrocarcinogenesis." Acta Biochimica Polonica 49, no. 1 (March 31, 2002): 51–58. http://dx.doi.org/10.18388/abp.2002_3820.

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Specificity of targeting of the oxidative stress towards lipid and protein fractions in a model of estrogen-induced Syrian hamster nephrocarcinogenesis was evaluated. The amount of proteins modified by oxidative stress was significantly elevated as early as one month after the initial implantation of estradiol to the experimental versus the control group, while the stress did not affect lipids. Subcellular localization of the oxidative stress target was determined by the analysis of protein oxidation in subcellular fractions of kidney cells. The endoplasmic reticulum membranes were the fraction most affected by the oxidative stress.

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Basu, Samar. "Fatty acid oxidation and isoprostanes: Oxidative strain and oxidative stress." Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA) 82, no. 4-6 (April 2010): 219–25. http://dx.doi.org/10.1016/j.plefa.2010.02.031.

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Wang, Xiaole, Chuqiao Shen, Jie Zhu, Guoming Shen, Zegeng Li, and Jingcheng Dong. "Long Noncoding RNAs in the Regulation of Oxidative Stress." Oxidative Medicine and Cellular Longevity 2019 (February 17, 2019): 1–7. http://dx.doi.org/10.1155/2019/1318795.

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Oxidative stress takes responsibility for various diseases, such as chronic obstructive pulmonary disease (COPD), Alzheimer’s disease (AD), and cardiovascular disease; nevertheless, there is still a lack of specific biomarkers for the guidance of diagnosis and treatment of oxidative stress-related diseases. In recent years, growing studies have documented that oxidative stress has crucial correlations with long noncoding RNAs (lncRNAs), which have been identified as important transcriptions involving the process of oxidative stress, inflammation, etc. and been regarded as the potential specific biomarkers. In this paper, we review links between oxidative stress and lncRNAs, highlight lncRNAs that refer to oxidative stress, and conclude that lncRNAs have played a negative or positive role in the oxidation/antioxidant system, which may be helpful for the further investigation of specific biomarkers of oxidative stress-related diseases.

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Sandoval-Salazar, Cuauhtémoc, Cecilia Oviedo-Solís, Edmundo Lozoya-Gloria, Herlinda Aguilar-Zavala, Martha Solís-Ortiz, Victoriano Pérez-Vázquez, Cristina Balcón-Pacheco, and Joel Ramírez-Emiliano. "Strawberry Intake Ameliorates Oxidative Stress and Decreases GABA Levels Induced by High-Fat Diet in Frontal Cortex of Rats." Antioxidants 8, no. 3 (March 20, 2019): 70. http://dx.doi.org/10.3390/antiox8030070.

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It has been proposed that there is a correlation between high-fat diet (HFD), oxidative stress and decreased γ-aminobutyric acid (GABA) levels, but this has not been thoroughly demonstrated. In the present study, we determined the effects of strawberry extract intake on the oxidative stress and GABA levels in the frontal cortex (FC) of obese rats. We observed that an HFD increased lipid and protein oxidation, and decreased GABA levels. Moreover, UV-irradiated strawberry extract (UViSE) decreased lipid peroxidation but not protein oxidation, whereas non-irradiated strawberry extract (NSE) reduced protein oxidation but not lipid peroxidation. Interestingly, NSE increased GABA concentration, whereas UViSE was not as effective. In conclusion, our results suggest that an HFD increases oxidative damage in the FC, whereas strawberry extract intake may ameliorate the disturbances associated with HFD-induced oxidative damage.

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Ussipbek, B. A., L. C. López, N. T. Ablaikhanova, and M. K. Murzakhmetova. "OXIDATIVE STRESS AND MITOCHONDRIAL DYSFUNCTION." Series of biological and medical 2, no. 338 (April 15, 2020): 31–40. http://dx.doi.org/10.32014/10.32014/2020.2519-1629.10.

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The process of cell damage resulting from the action of free radicals – reactive oxygen species (ROS) – is called oxidative stress. Most ROS are constantly formed in the cell – about 5 % of the oxygen consumed by tissues is converted into free radicals, but their level is normally so small that the cell inactivates them with the help of an antioxidant system. Different organs and tissues are exposed to different degrees of ROS and demonstrate different stability during the implementation of oxidative stress. The mechanisms of ROS formation by mitochondria under oxidative stress are still unclear. At the same time, it was found that mitochondrial dysfunction and the accumulation of mitochondrial mutations in tissues make a significant contribution to the aging process, as well as to the pathogenesis of a number of diseases characterized by neurodegeneration. Mutations lead to increased generation of free radicals, reduced ATP levels, and energy failure of cells. Coenzyme Q10 is a component of the mitochondrial respiratory chain. Violation of the biosynthesis of coenzyme Q10 can lead to a number of mitochondrial diseases. When coenzyme Q10 is deficient, sulfide metabolism plays a critical role. Sulfide metabolism in mammalian cells includes trans-sulfuration (biosynthetic) and hydrogen sulfide oxidation (H2S) (catabolic). Violation of H2S oxidation may contribute to oxidative stress in coenzyme Q deficiency or may play a synergistic role with oxidative stress in the pathogenesis of tissue specificity in coenzyme Q deficiency.

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Watson, Walter H., and Dean P. Jones. "Oxidation of nuclear thioredoxin during oxidative stress." FEBS Letters 543, no. 1-3 (April 29, 2003): 144–47. http://dx.doi.org/10.1016/s0014-5793(03)00430-7.

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Gasparovic, Ana Cipak, Neven Zarkovic, and Serge P. Bottari. "Biomarkers of nitro-oxidation and oxidative stress." Current Opinion in Toxicology 7 (February 2018): 73–80. http://dx.doi.org/10.1016/j.cotox.2017.10.002.

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Bjerre, Jenny. "Chronic Heart Failure: An Epidemiological Study Of Impaired Oxidative Stress." Clinical Cardiology and Cardiovascular Interventions 1, no. 1 (June 6, 2018): 01–02. http://dx.doi.org/10.31579/2641-0419/002.

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Tokarchuk, K. О., and О. V. Zaitseva. "Aldehydes participation in oxidative stress in rat thymocytes in vitro." Ukrainian Biochemical Journal 86, no. 3 (June 27, 2014): 61–68. http://dx.doi.org/10.15407/ubj86.03.061.

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Eck, Peter, Yougui Chen, Usha Thiyam-Hollander, and N. A. Michael Eskin. "Phenolics from canola crude extracts protect cells from oxidative stress." SDRP Journal of Food Science & Technology 4, no. 5 (2019): 760–69. http://dx.doi.org/10.25177/jfst.4.5.ra.487.

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Journal articles on the topic 'Oxidative stess'

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