摘要：

Excessive generation of superoxide and mitochondrial dysfunction has been described as being important events during ischemia/reperfusion (I/R) injury. Our laboratory has demonstrated that manganese superoxide dismutase (MnSOD), a major mitochondrial antioxidant that eliminates superoxide, is inactivated during renal transplantation and renal I/R, and precedes development of renal failure. We...

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