Titlebook: Biochemistry of Oxidative Stress; Physiopathology and Ricardo Jorge Gelpi,Alberto Boveris,Juan José Pode Book 2016 Springer International

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Mitochondrial Complex I Inactivation After Ischemia-Reperfusion in the Stunned Heartof iron-sulfur centers (Fe-S) to ubiquinone (UQ) in a reaction associated with proton translocation across the inner membrane, contributing to the proton-motive force. Complex I produces superoxide anion (O..) through the autoxidation reaction of the flavin-semiquinone (FMNH•) with molecular oxygen.

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Reactive Oxygen Species Are Involved in Myocardial Remote Ischemic Preconditioningmyocardial ischemia/reperfusion injury. Remote ischemic preconditioning (rIPC) was first introduced in 1993 by Przyklenk et al who reported that brief regional occlusion-reperfusion episodes in one vascular bed of the heart render protection to remote myocardial tissue. Subsequently, different studi

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Mitochondrial Transfer by Intercellular Nanotubeslogical processes. In this context, we also discuss the importance of mitochondria transfer from stem cells to recipient cells with nonfunctional mitochondria, which results in a significant improvement in aerobic respiration. The transfer of healthy mitochondria through TNTs may rescue damaged cell

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Role of Oxidative Stress in Subcellular Defects in Ischemic Heart Disease malfunction and changes in enzyme activities. Lipid peroxidation leads to depressed membrane fluidity and increased permeability, as well as changes in gene expression leading to impaired recovery of cardiac dysfunction due to I/R injury. Since the redox status of cardiomyocytes depends mainly on t