Antioxidants in myocardial ischemia–reperfusion injury: therapeutic potential and basic mechanisms

Protective effect of proanthocyanidins on anoxia-reoxygenation injury of myocardial cells mediated by the PI3K/Akt/GSK-3β pathway and mitochondrial ATP-sensitive potassium channel

“…ROS have a highly potent chemical activity, and their active electrons easily militate against the components of cells, enhancing cell membrane lipid peroxidation, restraining the function of cellular proteins and damaging nucleic acids and chromosomes, resulting in overall damage to cellular structure and functioning with harmful consequences (14,15). In the present study, it has been identified that the myocardial cell survival rate decreased following anoxia-reoxygenation injury, ROS production was enhanced and the apoptotic rate of myocardial cells increased.…”

Mitochondria in hematopoiesis and hematological diseases

“…Antioxidants also showed promise for prevention of ischemia/reperfusion injury that involves apoptosis (Marczin et al, 2003) but their ability to affect apoptosis rate in erythroid diseases still remains to be determined. The erythroid apoptosis that characterizes myelodysplastic syndromes could be inhibited by growth factors such as Epo (Tehranchi et al, 2005).…”

Oxidative Stress and Lipid Peroxidation – A Lipid Metabolism Dysfunction

“…Specific aldehydes (e.g., 4-hydroxynonenal acetaldehyde, acrolein) were reported to be transiently increased in the settings of heart failure and ischemia-reperfusion injury [13] and to interfere with transcriptional regulation of endogenous anti-oxidant networks in mitochondria [1]. Recently, accumulation of reactive aldehydes was studied from the point of view of the subsequent protein carbonylation and its implication in cardiovascular pathophysiology [4].…”