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特定线粒体亚群中缺血诱导损伤的发展

Development of ischemia-induced damage in defined mitochondrial subpopulations.

作者信息

Piper H M, Sezer O, Schleyer M, Schwartz P, Hütter J F, Spieckermann P G

出版信息

J Mol Cell Cardiol. 1985 Sep;17(9):885-96. doi: 10.1016/s0022-2828(85)80102-4.

DOI:10.1016/s0022-2828(85)80102-4
PMID:4046049
Abstract

Two mitochondrial subpopulations were isolated from guinea-pig heart by density gradient centrifugation. Under control conditions, both contain functionally intact mitochondria in which ischemic damage develops similarly. However, in one subpopulation adenine nucleotide content, adenine nucleotide translocase activity, oxidative phosphorylation and Ca2+ uptake are a quarter lower than in the other one when related to mitochondrial protein mass. Cytochrome contents and uncoupled electron flux are the same. Changes develop most evidently at the very beginning of ischemia for NAD-linked respiration. When ischemia progresses, cytochromes and the translocator protein are gradually lost or inactivated. Thereupon only partial recovery of mitochondrial function can be obtained after 20 min of reperfusion.

摘要

通过密度梯度离心从豚鼠心脏中分离出两个线粒体亚群。在对照条件下,两者均含有功能完整的线粒体,其中缺血损伤的发展方式相似。然而,在一个亚群中,与线粒体蛋白质质量相关时,腺嘌呤核苷酸含量、腺嘌呤核苷酸转位酶活性、氧化磷酸化和Ca2+摄取比另一个亚群低四分之一。细胞色素含量和解偶联电子通量相同。对于NAD相关呼吸,变化在缺血刚开始时最为明显。当缺血进展时,细胞色素和转位蛋白逐渐丢失或失活。于是,再灌注20分钟后只能部分恢复线粒体功能。

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