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

Authors
Citation
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
Citations number
47
Categorie Soggetti
Biochemistry & Biophysics
Journal title
IUBMB LIFE
ISSN journal
15216543 → ACNP
Volume
49
Issue
5
Year of publication
2000
Pages
365 - 373
Database
ISI
SICI code
1521-6543(200005)49:5<365:MITPDP>2.0.ZU;2-2
Abstract
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.