Succinate accumulates during ischemia forcing mitochondrial complex I to operate in reversal, while producing oxidant species during reperfusion

by José Carlos Toledo

Ischemia-reperfusion (IR) is a process where blood supply (thus oxygen supply) to an organ is interrupted and then restored. While reperfusion is essential for survival, it is accompanied by a burst of mitochondrial generation of redox species and intermediates such as superoxide and hydrogen peroxide. Such species associate with derived ischemic tissue injury, underling disorders such as heart attack and stroke [1]. Nonetheless, IR mitochondrial ROS production has been considered a nonspecific consequence of a dysfunctional interaction of mitochondrial redox

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