Regular ArticleGlutathione Protects Against Myocardial Ischemia–reperfusion Injury by Detoxifying Peroxynitrite
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The mechanism of ferroptosis regulating oxidative stress in ischemic stroke and the regulation mechanism of natural pharmacological active components
2022, Biomedicine and PharmacotherapyCitation Excerpt :Antioxidants prevent cellular damage by converting ROS/RNS into harmless molecules. Therefore, O2- can be converted to H2O2 by SOD1 in the cytoplasm and to H2O2 by SOD2 in the mitochondria, and then, peroxidase can reduce H2O2 to water [172]. Lipid peroxidation is considered to be a direct inducer of ferroptosis [173].
Riluzole protects against skeletal muscle ischaemia-reperfusion injury in a porcine model
2020, InjuryCitation Excerpt :ROS accumulates in ischaemic tissues and these products may leak into the systemic circulation following reperfusion, potentially leading to fatal systemic complications in the heart, kidneys and lungs [23,24]. Glutathine has been studied extensively in cardiac IRI and glutathione depletion is associated with cardiac IRI [25–27]. Furthermore, retroinfusion of glutathione demonstrated protective effects against IRI in the pig myocardium [27].
Genetic deletion of CD38 confers post-ischemic myocardial protection through preserved pyridine nucleotides
2018, Journal of Molecular and Cellular CardiologyCitation Excerpt :Accompanying I/R there is reported to be a loss of GSH/GSSG pool secondary to GSSG formation and wash out [31]. With I/R, we found that the levels of GSH in both groups fell significantly (approximately 35%), as previously reported to occur in hearts undergoing I/R [32,33]. Interestingly, this brought the GSH levels in the CD38−/− hearts to levels near the pre-ischemic baseline levels in WT hearts (Fig. 8A).
Cross-talk between lipid and protein carbonylation in a dynamic cardiomyocyte model of mild nitroxidative stress
2017, Redox BiologyCitation Excerpt :It is a highly reactive molecule that can decompose to other reactive species, including •OH and •NO2, which all together lead to complex nitroxidative stress in the myocardium [6,7]. Peroxynitrite production is significantly increased in various CVDs including myocardial IR [8,9], HF [10,11], atherosclerosis [12] and diabetes [13]. Furthermore, numerous experimental results demonstrate a critical role of peroxynitrite in the pathogenesis of CVDs, including HF and IR injury.
Capsaicin-Sensitive Sensory Nerves in Myocardial Ischemia-Reperfusion Injury and Ischemic Stress Adaptation. Role of Nitric Oxide and Calcitonin Gene-Related Peptide
2009, NeuroImmune BiologyCitation Excerpt :Thus nature has a built in a mechanism to return toxic ONOO− into a NO donor. Indeed, hearts with enhanced endogenous GSH levels are less susceptible to ischemia–reperfusion injury [95] and micromolar concentrations of GSH added to the perfusate protects isolated hearts from stunning injury through the reduced formation of ONOO− at reperfusion [96]. Exogenously administered ONOO− was also shown to inhibit leukocyte–endothelial cell interactions and to protect against ischemia–reperfusion injury in rats in vivo[97] Intraventricular infusion of ONOO− reduced myocardial infarct size and preserved coronary endothelium after ischemia and reperfusion in cats [98], which effect was mediated by the intermediate formation of S-nitrosothiols [99].
Inhibition of lipid infusion-induced skeletal muscle insulin resistance by cotreatment with tempol and glutathione in mice
2009, Journal of Pharmacological Sciences
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Please address all correspondence to: Dr Richard Schulz, Departments of Pediatrics and Pharmacology, 462 Heritage Medical Research Centre, University of Alberta, Edmonton, Alberta, T6G 2S2, Canada. E-mail: [email protected]