Phenoptosis: programmed death of an organism.
Programmed cell death (apoptosis) is well-established in many multicellular organisms. Apoptosis purifies a tissue from cells that became useless or even harmful for the organism. Similar phenomena are already described also at subcellular level (suicide of mitochondria, i.e., mitoptosis) as well as at supracellular level (degradation of some organs temporarily appearing in the course of ontogenesis and then disappearing by means of apoptosis of the organ-composing cells). Following the same logic, one may put a question about programmed death of an organism as a mechanism of purification of a kin, community of organisms, or population from individuals who became unwanted for this kin, etc. A putative mechanism of such kind is proposed to be coined "phenoptosis" by analogy with apoptosis and mitoptosis. In a unicellular organism (the bacterium Escherichia coli), three different biochemical mechanisms of programmed death are identified. All of them are actuated by the appearance of phages inside the bacterial cell. This may be regarded as a precedent of phenoptosis which prevents expansion of the phage infection among E. coli cells. Purification of a population from infected individuals looks like an evolutionary invention useful for a species. Such an invention has high chances to be also employed by multicellular organisms. Most probably, septic shock in animals and humans serves as an analog of the phage-induced bacterial phenoptosis. It is hypothesized that the stress-induced ischemic diseases of brain and heart as well as carcinogenesis if they are induced by repeated stresses also represent phenoptoses that, in contrast to sepsis, are age-dependent. There are interrelations of programmed death phenomena at various levels of complexity of the living systems. Thus, extensive mitoptosis in a cell leads to apoptotic death of this cell and extensive apoptosis in an organ of vital importance results in phenoptotic death of an individual. In line with this logic, some cases are already described when inhibition of apoptosis strongly improves the postischemic state of the organism.
Skulachev
V P
VP
Department of Bioenergetics, Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, 119899, Russia. skulach@head.genebee.msu.su.
D000375:Aging / Q000473:pathology; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002545:Brain Ischemia / Q000473:pathology; D003643:Death; D004926:Escherichia coli / Q000166:cytology / Q000502:physiology / Q000821:virology; D006801:Humans; D008954:Models, Biological; D017202:Myocardial Ischemia / Q000473:pathology; D009369:Neoplasms / Q000473:pathology; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000209:etiology / Q000378:metabolism; D012772:Shock, Septic / Q000382:microbiology / Q000503:physiopathology
D017382:Reactive Oxygen Species