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[急性肝缺血过程中腺嘌呤核苷酸线粒体转运破坏的机制]

[Mechanisms of disruption of mitochondrial transport of adenine nucleotides in the course of acute hepatic ischemia].

作者信息

Vavilin V A, Filippova S N, Panov A V, Levandovskiĭ I V

出版信息

Biull Eksp Biol Med. 1980 Apr;89(4):424-6.

PMID:7388158
Abstract

Suppression of mitochondrial transport of adenine nucleotides (AN) in the ischemized liver is caused by inhibition of adenine nucleotide translocase by long chain acyl-KoA and by reduced exchange fund of intramitochondrial AN. It preceeds the disunion of oxidizing phosphorylation which develops during the period of marked structural disturbances of the mitochondrial membrane. The preincubation of mitochondria from the ischemized liver with carnitine and alpha-ketoglutarate stimulates breathing in the metabolic state. The ischemic toxin blocking SH-groups of the membrane proteins also inhibits the transport of AN. However, its effect on the mitochondrial membrane is dominated by the disintegrating component.

摘要

缺血肝脏中腺嘌呤核苷酸(AN)线粒体转运的抑制是由长链酰基辅酶A对腺嘌呤核苷酸转位酶的抑制以及线粒体内AN交换库的减少所引起的。它先于氧化磷酸化的解偶联,氧化磷酸化解偶联发生在线粒体膜明显结构紊乱的时期。用肉碱和α-酮戊二酸对缺血肝脏的线粒体进行预孵育可刺激代谢状态下的呼吸。阻断膜蛋白SH基团的缺血毒素也抑制AN的转运。然而,其对线粒体膜的作用主要由解体成分主导。

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