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 e ven 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 i n the course of ontogenesis and then disappearing by means of apoptosis of the organ-composing cells). Following the same logic, one may put a questio n about programmed death of an organism as a mechanism of purification of a kin, community of organisms, or population from individuals who became unw anted for this kin, etc. A putative mechanism of such kind is proposed to b e coined "phenoptosis" by analogy with apoptosis and mitoptosis. In a unice llular organism (the bacterium Escherichia coli), three different biochemic al 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 infect ion among E. coli cells. Purification of a population from infected individ uals looks like an evolutionary invention useful for a species. Such an inv ention has high chances to be also employed by multicellular organisms. Mos t probably, septic shock in animals and humans serves as an analog of the p hage-induced bacterial phenoptosis. It is hypothesized that the stress-indu ced ischemic diseases of brain and heart as well as carcinogenesis if they are induced by repeated stresses also represent phenoptoses that, in contra st to sepsis, are age-dependent. There are interrelations of programmed dea th phenomena at various levels of complexity of the living systems. Thus, e xtensive mitoptosis in a cell leads to apoptotic death of this cell and ext ensive apoptosis in an organ of vital importance results in phenoptotic dea th of an individual. In line with this logic, some cases are already descri bed when inhibition of apoptosis strongly improves the postischemic state o f the organism.