The programmed death phenomena, aging, and the Samurai law of biology.
Analysis of the programmed death phenomena from mitochondria (mitoptosis) to whole organisms (phenoptosis) clearly shows that suicide programs are inherent at various levels of organization of living systems. Such programs perform very important functions, purifying (i) cells from damaged (or unwanted for other reasons) organelles, (ii) tissues from unwanted cells, (iii) organisms from organs transiently appearing during ontogenesis, and (iv) communities of organisms from unwanted individuals. Defence against reactive oxygen species (ROS) is probably one of primary evolutionary functions of programmed death mechanisms. So far, it seems that ROS play a key role in the mito-, apo-, organo- and phenoptoses. Here a concept is described which tries to unite Weismann's concept of aging as an adaptive programmed death mechanism and the alternative point of view considering aging as an inevitable result of accumulation in an organism of occasional injuries. It is suggested that injury accumulation is monitored by special system sending a death signal to actuate a phenoptotic program when the number of injuries reaches some critical level. The system in question is organized in such a way that the lethal case appears to be a result of phenoptosis long before occasional injuries make the functioning of the organism impossible. This strategy is supposed to prevent the appearance of asocial monsters capable to ruining kin, community and entire population. These relationships are regarded as an example of the Samurai law of biology: 'It is better to die than to be wrong'. It is stressed that for humans these cruel regulations look like an atavism that should be overcome to prolong the human life span.
Skulachev
V P
VP
Department of Bioenergetics, A.N. Belozersky Institute of Physico-Chemical Biology, Moscow State University, Moscow 119899, Russia. skulach@genebee.msu.su
D000375:Aging / Q000473:pathology*; D000818:Animals; D017209:Apoptosis; D006801:Humans; D008928:Mitochondria / Q000473:pathology; D008954:Models, Biological