Release of cytochromes from hypoxic and reoxygenated guinea pig heart.

Cardioscience Pub Date : 1993-09-01
F Naro, A Fazzini, C Grappone, G Citro, G Dini, A Giotti, F Malatesta, F Franconi, M Brunori
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引用次数: 0

Abstract

Isolated, perfused hearts from guinea pigs were subjected to hypoxia for 30 minutes followed by reoxygenation for 30 minutes. Cellular damage was assessed by measuring the release of the cytoplasmic enzyme lactate dehydrogenase and the mitochondrial markers cytochrome c and cytochrome oxidase. The release of the enzymes was correlated with electron microscopy. Hypoxia induced an increase in the release of lactate dehydrogenase and cytochrome c. During reoxygenation, the release of lactate dehydrogenase was exacerbated while that of cytochrome c decreased, suggesting a partial recovery of the mitochondria. Cytochrome oxidase was not detectable in the extracellular space during hypoxia or reoxygenation. It is suggested that cytochrome c is a specific marker for damage to mitochondria caused by hypoxia and its loss may affect respiratory chain function.

缺氧和复氧豚鼠心脏细胞色素的释放。
从豚鼠分离的灌注心脏进行缺氧30分钟,然后再充氧30分钟。通过测定细胞质乳酸脱氢酶和线粒体标记物细胞色素c和细胞色素氧化酶的释放来评估细胞损伤。酶的释放与电子显微镜相关。缺氧诱导乳酸脱氢酶和细胞色素c的释放增加,再氧化时乳酸脱氢酶的释放加剧,细胞色素c的释放减少,表明线粒体部分恢复。细胞色素氧化酶在缺氧或再氧化时未在细胞外间隙检测到。提示细胞色素c是缺氧引起线粒体损伤的特异性标志物,其缺失可能影响呼吸链功能。
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