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[体外钙依赖性缺氧损伤时肝线粒体膜的阳离子通透性]

[Cation permeability of liver mitochondrial membranes during Ca+-dependent anoxic damage in vitro].

作者信息

Bragin E O, Sorokovoĭ V I, Chernikov V P, Kogan E M, Vladimirov Iu A

出版信息

Vopr Med Khim. 1977 May-Jun(3):297-302.

PMID:888394
Abstract

Ca2+ ions are responsible for impairment of oxidative phosphorylation in rat liver mitochondria under anoxia in vitro. The decrease in this function is due to inhibition of electron transport over respiratory chain and to uncoupling. The increase in membrane permeability for H+, K+ and Na+ was observed on incubation of mitochondria under anoxic condition together with Ca2+. Uncoupling of phosphorylation depends on the increased permeability of the membranes for H+. The increased permeability of membranes for Na+ and K+ under energy liberation and in presence of penetrating anions led to active swelling of organelles and to secondary (osmotic) impairment. Ca2+-activated mitochondrial phospholipase A2 appears to participate in the organelle impairment under anoxia.

摘要

钙离子在体外缺氧条件下会导致大鼠肝脏线粒体氧化磷酸化功能受损。该功能的下降是由于呼吸链上电子传递受到抑制以及解偶联作用。在缺氧条件下将线粒体与钙离子一起孵育时,观察到线粒体对氢离子、钾离子和钠离子的膜通透性增加。磷酸化解偶联取决于膜对氢离子通透性的增加。在能量释放且存在渗透性阴离子的情况下,膜对钠离子和钾离子通透性的增加导致细胞器的主动肿胀和继发性(渗透性)损伤。钙离子激活的线粒体磷脂酶A2似乎参与了缺氧条件下的细胞器损伤。

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