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本文引用的文献

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A mitochondria-targeted nitroxide/hemigramicidin S conjugate protects mouse embryonic cells against gamma irradiation.一种线粒体靶向的氮氧化物/短杆菌肽S缀合物可保护小鼠胚胎细胞免受γ射线照射。
Int J Radiat Oncol Biol Phys. 2008 Mar 1;70(3):816-25. doi: 10.1016/j.ijrobp.2007.10.047.
2
The hierarchy of structural transitions induced in cytochrome c by anionic phospholipids determines its peroxidase activation and selective peroxidation during apoptosis in cells.阴离子磷脂在细胞色素c中诱导的结构转变层次决定了其在细胞凋亡过程中的过氧化物酶激活和选择性过氧化作用。
Biochemistry. 2007 Dec 11;46(49):14232-44. doi: 10.1021/bi701237b. Epub 2007 Nov 16.
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Mitochondria, oxidative stress and cell death.线粒体、氧化应激与细胞死亡。
Apoptosis. 2007 May;12(5):913-22. doi: 10.1007/s10495-007-0756-2.
4
Cardiolipin: setting the beat of apoptosis.心磷脂：掌控细胞凋亡的节奏。
Apoptosis. 2007 May;12(5):877-85. doi: 10.1007/s10495-007-0718-8.
5
Structural requirements for optimized delivery, inhibition of oxidative stress, and antiapoptotic activity of targeted nitroxides.靶向氮氧化物的优化递送、氧化应激抑制及抗凋亡活性的结构要求
J Pharmacol Exp Ther. 2007 Mar;320(3):1050-60. doi: 10.1124/jpet.106.114769. Epub 2006 Dec 19.
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Interaction of peroxidized cardiolipin with rat-heart mitochondrial membranes: induction of permeability transition and cytochrome c release.过氧化心磷脂与大鼠心脏线粒体膜的相互作用：诱导通透性转变和细胞色素c释放。
FEBS Lett. 2006 Nov 27;580(27):6311-6. doi: 10.1016/j.febslet.2006.10.036. Epub 2006 Oct 27.
7
Cardiolipin deficiency releases cytochrome c from the inner mitochondrial membrane and accelerates stimuli-elicited apoptosis.心磷脂缺乏会使细胞色素c从线粒体内膜释放出来，并加速刺激引发的细胞凋亡。
Cell Death Differ. 2007 Mar;14(3):597-606. doi: 10.1038/sj.cdd.4402020. Epub 2006 Aug 4.
8
Peroxidase activity and structural transitions of cytochrome c bound to cardiolipin-containing membranes.与含心磷脂膜结合的细胞色素c的过氧化物酶活性及结构转变
Biochemistry. 2006 Apr 18;45(15):4998-5009. doi: 10.1021/bi0525573.
9
Cytochrome c acts as a cardiolipin oxygenase required for release of proapoptotic factors.细胞色素c作为一种心磷脂加氧酶，是促凋亡因子释放所必需的。
Nat Chem Biol. 2005 Sep;1(4):223-32. doi: 10.1038/nchembio727. Epub 2005 Aug 14.
10
Complex I deficiency primes Bax-dependent neuronal apoptosis through mitochondrial oxidative damage.复合体I缺陷通过线粒体氧化损伤引发依赖于Bax的神经元凋亡。
Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):19126-31. doi: 10.1073/pnas.0508215102. Epub 2005 Dec 19.

凋亡过程中bax、活性氧生成与心磷脂氧化之间的相互作用。

Interplay between bax, reactive oxygen species production, and cardiolipin oxidation during apoptosis.

作者信息

Jiang Jianfei, Huang Zhentai, Zhao Qing, Feng Weihong, Belikova Natalia A, Kagan Valerian E

机构信息

Center for Free Radical and Antioxidant Health, Department of Environmental and Occupational Health, University of Pittsburgh, Bridgeside Point, 100 Technology Drive, Suite 350, Pittsburgh, PA 15219, USA.

出版信息

Biochem Biophys Res Commun. 2008 Mar 28;368(1):145-50. doi: 10.1016/j.bbrc.2008.01.055. Epub 2008 Jan 22.

DOI:10.1016/j.bbrc.2008.01.055
PMID:18211809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2373413/
Abstract

Bax/Bak activation and cardiolipin peroxidation are essential for cytochrome c release during apoptosis, yet, the link between them remains elusive. We report that sequence of events after exposure of mouse embryonic fibroblast (MEF) cells to actinomycin D followed the order: Bax translocation-->superoxide production-->cardiolipin peroxidation. Genetic ablation of Bax/Bak inhibited actinomycin D induced superoxide production and cardiolipin peroxidation. Rotenone caused robust superoxide generation but did not trigger cardiolipin peroxidation in Bax/Bak double knockout MEF cells. This suggests that, in addition to participating in ROS generation, Bax/Bak play another specific role in cardiolipin oxidation. In isolated mitochondria, recombinant Bax enhanced succinate induced cardiolipin oxidation and cytochrome c release. Mitochondrial peroxidase activity, likely involved in cardiolipin peroxidation, was enhanced upon incubation with recombinant Bax. Thus, cardiolipin peroxidation may be causatively and time-dependently related to Bax/Bak effects on ROS generation and peroxidase activation of cytochrome c.

摘要

在细胞凋亡过程中，Bax/Bak激活和心磷脂过氧化对于细胞色素c的释放至关重要，然而，它们之间的联系仍然难以捉摸。我们报道，小鼠胚胎成纤维细胞（MEF）暴露于放线菌素D后的事件顺序如下：Bax易位→超氧化物产生→心磷脂过氧化。Bax/Bak的基因敲除抑制了放线菌素D诱导的超氧化物产生和心磷脂过氧化。鱼藤酮在Bax/Bak双敲除的MEF细胞中可引起强烈的超氧化物生成，但不会触发心磷脂过氧化。这表明，除了参与活性氧生成外，Bax/Bak在心磷脂氧化中还发挥另一种特定作用。在分离的线粒体中，重组Bax增强了琥珀酸诱导的心磷脂氧化和细胞色素c释放。与重组Bax孵育后，可能参与心磷脂过氧化的线粒体过氧化物酶活性增强。因此，心磷脂过氧化可能与Bax/Bak对活性氧生成和细胞色素c过氧化物酶激活的影响存在因果关系且具有时间依赖性。