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Department of Veterans Affairs Medical Center, Birmingham 35233; and University of Alabama at Birmingham, Birmingham, Alabama 35294
Exacerbation of hypoxic
injury after restoration of oxygenation (reoxygenation) is an important
mechanism of cellular injury in transplantation and in myocardial,
hepatic, intestinal, cerebral, renal, and other ischemic
syndromes. Cellular hypoxia and reoxygenation are two essential
elements of ischemia-reperfusion injury. Activated neutrophils
contribute to vascular reperfusion injury, yet posthypoxic cellular
injury occurs in the absence of inflammatory cells through mechanisms
involving reactive oxygen (ROS) or nitrogen species (RNS). Xanthine
oxidase (XO) produces ROS in some reoxygenated cells, but other
intracellular sources of ROS are abundant, and XO is not required for
reoxygenation injury. Hypoxic or reoxygenated mitochondria may produce
excess superoxide (O
anoxia; ischemia; reperfusion
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