Mitochondrial role in life and death of the cell

被引:212
作者
Lee, HC
Wei, YH [1 ]
机构
[1] Natl Yang Ming Univ, Dept Biochem, Sch Life Sci, Taipei 112, Taiwan
[2] Natl Yang Ming Univ, Ctr Cellular & Mol Biol, Taipei 112, Taiwan
关键词
apoptosis; mitochondria; necrosis; oxidative stress; reactive oxygen species;
D O I
10.1007/BF02255913
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mitochindris are the major ATP producer of the mammalian cell. Moreover, mitochondria are also the main intracellular source and target of reactive oxygen species (ROS) that are continually generated as by-products of aerobic metabolism in human cells. A low level of ROS generated from the respiratory chain was recently proposed to take part in the signaling from mitochondria to the nucleus. Several structural characteristics of mitochondria and the mitochondrial genome enable them to sense and respond to extracellular and intracellular signals or stresses in order to sustain the life of the cell,lt has been established that mitochondrial respiratory function declines with age, and that defects in the respiratory chain increase the production of ROS and free radicals in mitochondria, Within a certain concentration range, ROS may induce stress responses of the cell by altering the expression of a number of genes in order to uphold energy metabolism to rescue the cell. However, beyond this threshold, ROS may elicit apoptosis by induction of mitochondrial membrane permeability transition and release of cytochrome c, Intensive research in the past few years has established that mitochondria play a pivotal role in the early phase of apoptosis in mammalian cells. In this article, the role of mitochondria in the determination of life and death of the cell is reviewed on the basis of recent findings gathered from this and other laboratories. Copyright (C) 2000 National Science Council. ROC and S. Karger AG, Basel.
引用
收藏
页码:2 / 15
页数:14
相关论文
共 108 条
[61]   Oxidative stress and upregulation of mitochondrial biogenesis genes in mitochondrial DNA-depleted HeLa cells [J].
Miranda, S ;
Foncea, R ;
Guerrero, J ;
Leighton, F .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1999, 258 (01) :44-49
[62]  
Miyako K, 1997, J BIOL CHEM, V272, P9605
[63]   X-ray and NMR structure of human Bcl-x(L), an inhibitor of programmed cell death [J].
Muchmore, SW ;
Sattler, M ;
Liang, H ;
Meadows, RP ;
Harlan, JE ;
Yoon, HS ;
Nettesheim, D ;
Chang, BS ;
Thompson, CB ;
Wong, SL ;
Ng, SC ;
Fesik, SW .
NATURE, 1996, 381 (6580) :335-341
[64]   Induction of nuclear respiratory factor-1 expression by an acute bout of exercise in rat muscle [J].
Murakami, T ;
Shimomura, Y ;
Yoshimura, A ;
Sokabe, M ;
Fujitsuka, N .
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS, 1998, 1381 (01) :113-122
[65]   CELL-FREE APOPTOSIS IN XENOPUS EGG EXTRACTS - INHIBITION BY BCL-2 AND REQUIREMENT FOR AN ORGANELLE FRACTION ENRICHED IN MITOCHONDRIA [J].
NEWMEYER, DD ;
FARSCHON, DM ;
REED, JC .
CELL, 1994, 79 (02) :353-364
[66]   BCL-2 HETERODIMERIZES IN-VIVO WITH A CONSERVED HOMOLOG, BAX, THAT ACCELERATES PROGRAMMED CELL-DEATH [J].
OLTVAI, ZN ;
MILLIMAN, CL ;
KORSMEYER, SJ .
CELL, 1993, 74 (04) :609-619
[67]   Caspase-9, Bcl-XL, and Apaf-1 form a ternary complex [J].
Pan, GH ;
O'Rourke, K ;
Dixit, VM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (10) :5841-5845
[68]   Mitochondrial oxidative phosphorylation changes in the life span. Molecular aspects and physiopathological implications [J].
Papa, S .
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS, 1996, 1276 (02) :87-105
[69]   The overexpression of Bax produces cell death upon induction of the mitochondrial permeability transition [J].
Pastorino, JG ;
Chen, ST ;
Tafani, M ;
Snyder, JW ;
Farber, JL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (13) :7770-7775
[70]   Crosstalk between nuclear and mitochondrial genomes [J].
Poyton, RO ;
McEwen, JE .
ANNUAL REVIEW OF BIOCHEMISTRY, 1996, 65 :563-607