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自由基与心肌缺血:综述与展望

Free radicals and myocardial ischemia: overview and outlook.

作者信息

McCord J M

机构信息

Department of Biochemistry, College of Medicine, University of South Alabama, Mobile 36688.

出版信息

Free Radic Biol Med. 1988;4(1):9-14. doi: 10.1016/0891-5849(88)90005-6.

Abstract

Much evidence suggests that free radicals and active oxygen species derived from molecular oxygen (superoxide, hydrogen peroxide, and hydroxyl radical) contribute to the tissue injury which accompanies myocardial ischemia and reperfusion. Three possible sources have been identified for the production of active oxygen species: the enzyme xanthine oxidase; the activated polymorphonuclear leukocyte; the disrupted mitochondrial electron transport system. These sources may be mutually interactive. Once triggered, they may lead to the loss of antioxidant enzymes and to the release of iron, both of which are exacerbatory events.

摘要

大量证据表明,由分子氧衍生而来的自由基和活性氧(超氧化物、过氧化氢和羟基自由基)会导致心肌缺血和再灌注时伴随的组织损伤。活性氧的产生已确定有三个可能来源:黄嘌呤氧化酶;活化的多形核白细胞;受损的线粒体电子传递系统。这些来源可能相互作用。一旦被触发,它们可能导致抗氧化酶的丧失和铁的释放,而这两者都是加剧损伤的事件。

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