Vp. Skulachev, Mitochondria in the programmed death phenomena; A principle of biology: "It is better to die than to be wrong", IUBMB LIFE, 49(5), 2000, pp. 365-373
The very fact that mitochondria participate in amplification of the cell su
icide 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 reactiv
e oxygen species (ROS), causing opening of the permeability transition pore
s (PTP) in the inner mitochondrial membrane, Mitoptosis can purify the mito
chondrial population in a cell from the ROS-overproducing organelles. Massi
ve mitoptosis can result in apoptosis (programmed cell death) because of th
e release of proapoptotic proteins from the mitochondrial intermembrane spa
ce, a mechanism purifying tissues from the ROS-overproducing and other unwa
nted cells. Large-scale apoptosis can be used by organisms to eliminate som
e organs during ontogenesis (organoptosis). In adult organisms, organoptosi
s of organs of vital importance may entail a programmed death of individual
s (phenoptosis), This mechanism might purify kins, communities, and populat
ions from individuals becoming dangerous because of, for example, heavy inf
ection (septic shock), It is hypothesized that aging represents a slow ROS-
linked phenoptosis that eliminates individuals with damaged genomes and giv
es reproductive advantage to those who succeeded in a better preservation o
f their genomes from damage.