Skulachev V P
Department of Bioenergetics, A. N. Belozersky Institute of Physico-Chemical Biology, Moscow State University, Russia.
IUBMB Life. 2000 May;49(5):365-73. doi: 10.1080/152165400410209.
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 system 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.
线粒体参与细胞自杀信号放大这一事实激发了人们对其机制及相关现象的兴趣。线粒体似乎拥有一个自主系统,使其能够自我毁灭。这种线粒体凋亡由活性氧(ROS)介导,导致线粒体内膜通透性转换孔(PTP)开放。线粒体凋亡可从细胞的线粒体群体中清除产生过量ROS的细胞器。大量的线粒体凋亡可导致凋亡(程序性细胞死亡),这是因为促凋亡蛋白从线粒体膜间隙释放,该机制可从组织中清除产生过量ROS的细胞及其他不需要的细胞。生物体可利用大规模凋亡在个体发育过程中消除某些器官(器官凋亡)。在成年生物体中,对生命至关重要的器官发生器官凋亡可能会导致个体的程序性死亡(表型衰老)。这种机制可能会从群体中清除因例如严重感染(败血症休克)而变得危险的个体。据推测,衰老代表一种与ROS相关的缓慢表型衰老,它会清除基因组受损的个体,并赋予那些成功更好地保护其基因组免受损伤的个体繁殖优势。