Regulation of apoptosis by respiration:: cytochrome c release by respiratory substrates

被引:36
作者
Nishimura, G
Proske, RJ
Doyama, H
Higuchi, M
机构
[1] Univ Texas, MD Anderson Canc Ctr, Dept Mol Therapeut, Houston, TX 77030 USA
[2] Univ Texas, Hlth Sci Ctr, Res Ctr Cardiovasc Dis, Inst Mol Med Prevent Human Dis, Houston, TX 77030 USA
[3] Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA
[4] VA Med Ctr Neurol Svc, Houston, TX 77030 USA
关键词
cytochrome c; apoptosis; mitochondrial respiration;
D O I
10.1016/S0014-5793(01)02859-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cytochrome c release from mitochondria is essential for apoptosis. Using human myelogenous leukemia ML-la, its respiration-deficient and reconstituted cells, we demonstrated that respiratory function is essential for tumor necrosis factor-induced cytochrome c release. In a cell free system using mitochondrial fraction from ML-Ia, initiation of respiration by substrates for complexes I, II, and III but not IV released cytochrome c, suggesting that reduction of coenzyme Q or complex III is essential for cytochrome c release. In the same system, disruption of mitochondrial outer membrane was neither enough nor the cause for cytochrome c release by succinate. These observations define an early pathway in which a change in respiration releases cytochrome c. (C) 2001 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.
引用
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页码:399 / 404
页数:6
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