Submitted September 6, 1997.
A concept postulating that aging is a specific biological function that promotes the progressive evolution of sexually reproducing species is reviewed. Death caused by aging clears the population of ancestors and frees space for progeny carrying new useful traits. Like any other important function, aging is mediated by several molecular mechanisms working simultaneously. At least three such mechanisms have been postulated thus far: 1) telomere shortening due to suppression of telomerase at early stages of embryogenesis; 2) age-related activation of a mechanism that induces the synthesis of heat shock proteins in response to denaturing stimuli; and 3) incomplete suppression of generation of reactive oxygen species (ROS) with inadequate scavenging of already existing ROS. None of these phenomena can kill the organism, but only weaken it, which becomes crucial under certain extreme conditions. This mechanism of age-induced death can be compensated for (within certain time limits) by several positive traits that greatly increase the evolutionary potential of species capable of performing this function. Similarly to apoptosis (programmed cell death), the programmed death of the body can be called "phenoptosis". Aging presumably belongs to the category of "soft" (extended in time and allowing a certain degree of compensation) phenoptosis, in contrast to "acute" phenoptosis; the death of salmon females immediately after spawning is a good example of the latter.
KEY WORDS: telomere, telomerase, heat-shock proteins, superoxide, mitochondria, aging, apoptosis.