Abstract

Accumulation of various types of unrepaired damage of the genome because of increasing production of reactive oxygen species and decreasing efficiency of the antioxidant defense system and repair systems can cause age-related diseases and emergence of phenotypic signs of senescence. This should lead to increasing vulnerability and to mortality monotonously increasing with age independently of the position of the species on the evolutionary tree. In this light, the survival, mortality, and fertility curves for 45 animal and plant species and one alga published by the Max Planck Institute for Demographic Research (Germany/Denmark) are of special interest (Jones, O. R., et al. (2014) Nature, 505, 169-173). We divided all species treated in that study into four groups according to the ratio of mortality at the terminal age (which corresponds to 5% survival) and average mortality during the entire studied period. For animals of group IV (long-lived and senescent), including humans, the Jones method makes it possible to trace mortality during the entire life cycle. The same applies to short-lived animals (e.g. nematodes or the tundra vole), whether they display the Gompertz type of senescence or not. However, in long-lived species with a less pronounced increase in mortality with age (e.g. the freshwater crocodile, hermit crab, or Scots pine), as well as in animals of average lifespan that reach the terminal age earlier than they could have enough time to become senescent, the Jones method is capable of characterizing only a small part of the life cycle and does not allow judging how senescence manifests itself at late stages of the life cycle. Thus, it is known that old trees display signs of biological senescence rather clearly; although Jones et al. consider them non-senescent organisms because less than 5% of sexually mature individuals survive to display the first manifestations of these characters. We have concluded that the classification proposed by Jones et al. makes it possible to approximately divide animals and plants only by their levels of the Gompertz type of senescence (i.e. actuarial senescence), whereas susceptibility to biological senescence can be estimated only when principally different models are applied.

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