Oxygen-derived free radicals in postischemic tissue injury.
Oxygen-derived free radicals in postischemic tissue injury.
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DOI：
10.1056/nejm198501173120305
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发表时间：
1985-01
期刊：
影响因子：
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通讯作者：
J. McCord
中科院分区：
文献类型：
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作者：
J. McCord
现在很清楚，氧自由基在几种实验诱导的再灌注损伤模型中起重要作用。虽然临床缺血和再灌注损伤肯定有多种成分，但自由基的产生可能在损伤进展的某些阶段起主要作用。在再灌注复氧组织中，超氧化物的主要来源似乎是黄嘌呤氧化酶，在缺血期间通过钙触发的黄嘌呤脱氢酶的蛋白水解攻击释放。在各种实验室模型中，再灌注组织受到超氧自由基或羟基自由基清除剂或别嘌呤醇或其他黄嘌呤氧化酶抑制剂的保护。因此，由自由基引起的功能障碍可能是心、肠、肝、肾和脑的缺血性疾病的主要组成部分。
It is now clear that oxygen-derived free radicals play an important part in several models of experimentally induced reperfusion injury. Although there are certainly multiple components to clinical ischemic and reperfusion injury, it appears likely that free-radical production may make a major contribution at certain stages in the progression of the injury. The primary source of superoxide in reperfused reoxygenated tissues appears to be the enzyme xanthine oxidase, released during ischemia by a calcium-triggered proteolytic attack on xanthine dehydrogenase. Reperfused tissues are protected in a variety of laboratory models by scavengers of superoxide radicals or hydroxyl radicals or by allopurinol or other inhibitors of xanthine oxidase. Dysfunction induced by free radicals may thus be a major component of ischemic diseases of the heart, bowel, liver, kidney, and brain.