It is known that irradiation stress induces late intracellular processes and adaptation. In this paper, we formulate the adaptation hypothesis. On its basis, we present statistical modeling of cellular distributions on the number of chromosomal abnormalities in root meristems of pea seeds that experienced low-dose-rate irradiation, high temperatures, and aging. The modeling shows that multiple appearances of chromosomal abnormalities can be explained as a result of primary or late processes caused by DNA damage, with or without cell selection, which can be described with geometrical or Poisson distributions, respectively. The connections between the late intercellular processes (the “bystander effects”) and late intracellular regulatory processes are considered. It is shown that combinations of low-dose-rate irradiation, high temperatures, and aging lead to synergistically increasing instabilities and decreasing seed survivals. Approaches to risk estimation of chromosomal instability are investigated in plant cells and in human blood lymphocytes. Risks of instability were estimated as values of distribution parameters dependent on radiation intensity in ecology and in generations of persons who experienced radioactive fallouts from nuclear tests. We conclude that statistical model of adaptation describes intraand intercellular processes of genetic instability coupled with selection, and that the risks of these processes can be calculated as model parameters.
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