Ceramide induces cytochrome c release from isolated mitochondria.
Ceramide induces cytochrome c release from isolated mitochondria.
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神经酰胺诱导分离的线粒体释放细胞色素 c。
DOI：
10.1042/bss0660027
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
P. Ghafourifar
中科院分区：
文献类型：
--
作者：
Christoph Richter;P. Ghafourifar
本章讨论线粒体在细胞凋亡中的作用。重点放在最近观察到的神经酰胺对线粒体功能的影响。我们在这里报告，N-乙酰鞘氨醇（C2-神经酰胺），N-己酰鞘氨醇（C6-神经酰胺），并在较小程度上，C2-二氢神经酰胺，诱导细胞色素C（细胞色素C）从离体大鼠肝线粒体释放。神经酰胺诱导的cyt c释放被低浓度的Bcl-2阻止。当cyt c被氧化时会发生释放，而当它被还原时则不会。在cyt c释放后，线粒体氧消耗、线粒体跨膜电位（Δ psi m）和Ca 2+滞留减少。Bcl-2阻止了这些线粒体功能的改变，而加入cyt c则逆转了这些功能的改变。在ATP供能的线粒体神经酰胺不改变Δ psi m，无论是当细胞色素c被氧化，也不当它被还原。这排除了神经酰胺对神经膜完整性的非特异性干扰。它的结论是，神经酰胺介导的一些致突变特性通过其与线粒体细胞色素c的相互作用，然后由其释放。
This chapter addresses the role of mitochondria in apoptosis. Emphasis is put on the recently observed influence of ceramides on mitochondrial functions. We report here that N-acetylsphingosine (C2-ceramide), N-hexanoylsphingosine (C6-ceramide) and, to a much lesser extent, C2-dihydroceramide, induce cytochrome c (cyt c) release from isolated rat liver mitochondria. Ceramide-induced cyt c release is prevented by a low concentration of Bcl-2. The release takes place when cyt c is oxidized, but not when it is reduced. Upon cyt c release mitochondrial oxygen consumption, mitochondrial transmembrane potential (delta psi m) and Ca2+ retention are diminished. Bcl-2 prevents, and addition of cyt c reverses, the alteration of these mitochondrial functions. In ATP-energized mitochondria ceramides do not alter delta psi m, neither when cyt c is oxidized nor when it is reduced. This rules out a non-specific disturbance by ceramides of mitochondrial-membrane integrity. It is concluded that some of the apoptogenic properties of ceramides are mediated via their interaction with mitochondrial cyt c followed by its release.