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

来源：

FEBS LETTERS | 2001年 / 505卷 / 03期

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

页码：399 / 404

页数：6

共 30 条

[1] Bcl-2 and the outer mitochondrial membrane in the inactivation of cytochrome c during fas-mediated apoptosis
Adachi, S
Cross, AR
Babior, BM
Gottlieb, RA
[J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (35) : 21878 - 21882
[2] Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death
Boldin, MP
Goncharov, TM
Goltsev, YV
Wallach, D
[J]. CELL, 1996, 85 (06) : 803 - 815
[3] Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization
Bossy-Wetzel, E
Newmeyer, DD
Green, DR
[J]. EMBO JOURNAL, 1998, 17 (01) : 37 - 49
[4] FADD, A NOVEL DEATH DOMAIN-CONTAINING PROTEIN, INTERACTS WITH THE DEATH DOMAIN OF FAS AND INITIATES APOPTOSIS
CHINNAIYAN, AM
OROURKE, K
TEWARI, M
DIXIT, VM
[J]. CELL, 1995, 81 (04) : 505 - 512
[5] SITES OF INHIBITION OF MITOCHONDRIAL ELECTRON-TRANSPORT IN MACROPHAGE-INJURED NEOPLASTIC-CELLS
GRANGER, DL
LEHNINGER, AL
[J]. JOURNAL OF CELL BIOLOGY, 1982, 95 (02) : 527 - 535
[6] Rapid cytochrome c release, activation of caspases 3, 6, 7 and 8 followed by Bap31 cleavage in HeLa cells treated with photodynamic therapy
Granville, DJ
Carthy, CM
Jiang, HJ
Shore, GC
McManus, BM
Hunt, DWC
[J]. FEBS LETTERS, 1998, 437 (1-2): : 5 - 10
[7] The respiratory-chain poison antimycin A promotes the formation of DNA single-strand breaks and reduces toxicity in U937 cells exposed to t-butylhydroperoxide
Guidarelli, A
Brambilla, L
Rota, C
Tomasi, A
Cattabeni, F
Cantoni, O
[J]. BIOCHEMICAL JOURNAL, 1996, 317 : 371 - 375
[8] HARTLEY A, 1994, J NEUROCHEM, V63, P1987
[9] CHARACTERIZATION OF THE APOPTOTIC EFFECTS OF HUMAN TUMOR-NECROSIS-FACTOR - DEVELOPMENT OF HIGHLY RAPID AND SPECIFIC BIOASSAY FOR HUMAN TUMOR-NECROSIS-FACTOR AND LYMPHOTOXIN USING HUMAN TARGET-CELLS
HIGUCHI, M
SINGH, S
AGGARWAL, BB
[J]. JOURNAL OF IMMUNOLOGICAL METHODS, 1995, 178 (02) : 173 - 181
[10] Inhibition of mitochondrial respiratory chain complex I by TNF results in cytochrome c release, membrane permeability transition, and apoptosis
Higuchi, M
Proske, RJ
Yeh, ETH
[J]. ONCOGENE, 1998, 17 (19) : 2515 - 2524

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