title: Mitochondria in the programmed death phenomena; a principle of biology: "it is better to die than to be wrong".
abstract: 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.
authors.affiliation: Department of Bioenergetics, A. N. Belozersky Institute of Physico-Chemical Biology, Moscow State University, Russia. skulach@genebee.msu.su
authors.forename: V P
authors.initials: VP
authors.lastname: Skulachev
mesh_terms: D000375:Aging; D000818:Animals; D017209:Apoptosis; D001419:Bacteria / Q000166:cytology; D006801:Humans; D008928:Mitochondria / Q000502:physiology*; D010101:Oxygen Consumption; D010766:Phosphorylation; D017382:Reactive Oxygen Species; D012156:Reticulocytes / Q000473:pathology; D012772:Shock, Septic; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015003:Yeasts / Q000166:cytology
chemical_list: D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha