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线粒体电子传递链产生的活性氧通过心磷脂过氧化作用诱导细胞色素c从牛心亚线粒体颗粒中解离。其在细胞凋亡中的可能作用。

Reactive oxygen species generated from the mitochondrial electron transport chain induce cytochrome c dissociation from beef-heart submitochondrial particles via cardiolipin peroxidation. Possible role in the apoptosis.

作者信息

Petrosillo G, Ruggiero F M, Pistolese M, Paradies G

机构信息

Department of Biochemistry and Molecular Biology and C.N.R Unit for the Study of Mitochondria and Bioenergetics, University of Bari, Via E, Orabona 4, 70126, Bari, Italy.

出版信息

FEBS Lett. 2001 Dec 14;509(3):435-8. doi: 10.1016/s0014-5793(01)03206-9.

Abstract

Cytochrome c release from mitochondria is a critical event in the apoptosis induction. Dissociation of cytochrome c from the mitochondrial inner membrane (IMM) is a necessary first step for cytochrome c release. In the present study, the effect of reactive oxygen species (ROS) on the dissociation of cytochrome c from beef-heart submitochondrial particles (SMP) and on the cardiolipin content was investigated. Exposure of SMP to mitochondrial-mediated ROS generation resulted in a large dissociation of cytochrome c from SMP and in a parallel loss of cardiolipin. Both these effects were directly and significantly correlated and also abolished by superoxide dismutase+catalase. These results demonstrate that ROS generation induces the dissociation of cytochrome c from IMM via cardiolipin peroxidation. The data may prove useful in clarifying the molecular mechanism underlying the release of cytochrome c from the mitochondria to the cytosol.

摘要

细胞色素c从线粒体释放是诱导细胞凋亡的关键事件。细胞色素c从线粒体内膜(IMM)解离是其释放的必要第一步。在本研究中,研究了活性氧(ROS)对细胞色素c从牛心亚线粒体颗粒(SMP)解离以及对心磷脂含量的影响。将SMP暴露于线粒体介导的ROS生成中,导致细胞色素c从SMP大量解离,同时心磷脂平行丧失。这两种效应直接且显著相关,并且超氧化物歧化酶+过氧化氢酶可消除这种效应。这些结果表明,ROS生成通过心磷脂过氧化诱导细胞色素c从IMM解离。这些数据可能有助于阐明细胞色素c从线粒体释放到细胞质中的分子机制。

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