Bioenergetic aspects of apoptosis, necrosis and mitoptosis

被引:315
作者
Skulachev, VP
机构
[1] Moscow MV Lomonosov State Univ, Belozersky Inst Physicochem Biol, Dept Bioenerget, Moscow 119992, Russia
[2] Moscow MV Lomonosov State Univ, Sch Bioengn & Bioinformat, Moscow 119992, Russia
关键词
apoptosis; bioenergetics; mitochondria; mitoptosis; necrosis; reactive oxygen species;
D O I
10.1007/s10495-006-5881-9
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
In this review I summarize interrelations between bioenergelc processes and such programmed death phenomena as cell suicide (apoptosis and necrosis) and mitochondrial suicide (miloptosis). The following conclusions are made. (I) ATP and rather often mitochondrial hyperpolarization (i.e. an increase in membrane potential, Delta Psi) are required for certain steps of apoptosis and necrosis. (II) Apoptosis, even if it is accompanied by Delta Psi and [ATP] Increases at its early stage, finally results in a Delta Psi collapse and ATP decrease. (III) Moderate (about threw-fold) lowering of [ATP] for short and long periods of time induces apoptosis and necrosis, respectively. In some types of apoptosis and necrosis, the cell death is mediated by a Delta Psi-dependent overproduction of ROS by the initial (Complex I) and the middle (Complex III) spans of the respiratory chain. ROS initiate mitoptosis which is postulated to rid the intracellular population of mitochondria from those that are ROS overproducing. Massive mitoptosis can result in cell death due to release to cytosol of the cell death proteins normally hidden in the mitochondrial Intermembrane space.
引用
收藏
页码:473 / 485
页数:13
相关论文
共 105 条
[41]   Characterization of superoxide production sites in isolated rat brain and skeletal muscle mitochondria [J].
Kudin, AP ;
Debska-Vielhaber, G ;
Kunz, WS .
BIOMEDICINE & PHARMACOTHERAPY, 2005, 59 (04) :163-168
[42]   Characterization of superoxide-producing sites in isolated brain mitochondria [J].
Kudin, AP ;
Bimpong-Buta, NYB ;
Vielhaber, S ;
Elger, CE ;
Kunz, WS .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (06) :4127-4135
[43]   Mitochondrial fusion in human cells is efficient, requires the inner membrane potential, and is mediated by mitofusins [J].
Legros, F ;
Lombès, A ;
Frachon, P ;
Rojo, M .
MOLECULAR BIOLOGY OF THE CELL, 2002, 13 (12) :4343-4354
[44]   JNK phosphorylation of Bim-related members of the Bcl2 family induces Bax-dependent apoptosis [J].
Lei, K ;
Davis, RJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (05) :2432-2437
[45]   Intracellular adenosine triphosphate (ATP) concentration: A switch in the decision between apoptosis and necrosis [J].
Leist, M ;
Single, B ;
Castoldi, AF ;
Kuhnle, S ;
Nicotera, P .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 185 (08) :1481-1486
[46]   Perspective - Selective mitochondrial autophagy, or mitophagy, as a targeted defense against oxidative stress, mitochondrial dysfunction, and aging [J].
Lemasters, JJ .
REJUVENATION RESEARCH, 2005, 8 (01) :3-5
[47]  
Levy M.R., 1973, P227
[48]   p53 regulates mitochondrial membrane potential through reactive oxygen species and induces cytochrome c-independent apoptosis blocked by Bcl-2 [J].
Li, PF ;
Dietz, R ;
von Harsdorf, R .
EMBO JOURNAL, 1999, 18 (21) :6027-6036
[49]   MECHANISM OF COUPLING OF OXIDATIVE PHOSPHORYLATION AND MEMBRANE POTENTIAL OF MITOCHONDRIA [J].
LIBERMAN, EA ;
TOPALY, VP ;
TSOFINA, LM ;
JASAITIS, AA ;
SKULACHEV, VP .
NATURE, 1969, 222 (5198) :1076-+
[50]   Role of JNK activation in apoptosis: A double-edged sword [J].
Liu, J ;
Lin, AN .
CELL RESEARCH, 2005, 15 (01) :36-42