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[缺血时心脏线粒体中镁离子的释放:是防御机制还是损伤?]

[Mg2+ release from heart mitochondria in ischemia: is it the defense mechanism or damage?].

作者信息

Lemeshko V V, Malanda P

出版信息

Ukr Biokhim Zh (1978). 1989 Jan-Feb;61(1):64-71.

PMID:2525829
Abstract

It is established that at the early stage of total heart ischemia in rats (5-10 min) the oligomycin-sensitive ATPase activity of mitochondria measured in heart homogenates in the medium and containing no Mg2+ decreases considerably, whereas the activity of respiratory chain, the value of respiratory control and Mg2+-ATPase activity are practically unchanged. The hypothetic trigger mechanism is suggested for Mg2+ ejection from mitochondria under conditions of respiration cessation. It is supposed to be a defence reaction of cells aimed to prevent ATP hydrolysis by mitochondria under ischemia.

摘要

已经确定,在大鼠全心缺血的早期阶段(5 - 10分钟),在不含Mg2 +的培养基中测定的心脏匀浆中线粒体的寡霉素敏感ATP酶活性显著降低,而呼吸链活性、呼吸控制值和Mg2 + -ATP酶活性实际上没有变化。提出了在呼吸停止条件下线粒体中Mg2 +排出的假设触发机制。推测这是细胞的一种防御反应,旨在防止缺血状态下线粒体对ATP的水解。

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