Mitochondria in the programmed death phenomena; A principle of biology: "It is better to die than to be wrong"

被引:96
作者
Skulachev, VP [1 ]
机构
[1] Moscow MV Lomonosov State Univ, A N Belozersky Inst Physicochem Biol, Dept Bioenerget, Moscow 119899, Russia
关键词
aging; apoptosis; programmed death of mitochondria; reactive oxygen species;
D O I
10.1080/152165400410209
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
The very fact that mitochondria participate in amplification of the cell suicide signals has stimulated interest in the mechanism of this and related phenomena. It seems probable that mitochondria possess an autonomic sa stem that allows them to commit suicide. This mitoptosis is mediated by reactive oxygen species (ROS), causing opening of the permeability transition pores (PTP) in the inner mitochondrial membrane, Mitoptosis can purify the mitochondrial population in a cell from the ROS-overproducing organelles. Massive mitoptosis can result in apoptosis (programmed cell death) because of the release of proapoptotic proteins from the mitochondrial intermembrane space, a mechanism purifying tissues from the ROS-overproducing and other unwanted cells. Large-scale apoptosis can be used by organisms to eliminate some organs during ontogenesis (organoptosis). In adult organisms, organoptosis of organs of vital importance may entail a programmed death of individuals (phenoptosis), This mechanism might purify kins, communities, and populations from individuals becoming dangerous because of, for example, heavy infection (septic shock), It is hypothesized that aging represents a slow ROS-linked phenoptosis that eliminates individuals with damaged genomes and gives reproductive advantage to those who succeeded in a better preservation of their genomes from damage.
引用
收藏
页码:365 / 373
页数:9
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