Possible Causes of Variability of the Adaptive Response in Human Lymphocytes

Abstract

Mutagenesis research has been focused for a long period on the interaction between mutagens (mostly X-rays) and the cell structure modified by them. Subsequently, the emphasis was shifted to mutation as a cellular process in which the primary lesion was extensively modified by enzymatic DNA-repair systems constitutively present in the cell (Auerbach 1976). Finally, over the past 15 years, considerable interest has been focused on inducible cellular functions (possibly DNA repair activities) occurring in the cell after exposure to very low doses of mutagens, probably through DNA lesions (for reviews, see Walker 1985; Elespuru 1987). DNA-damage-inducible processes are probably part of a set of general biological phenomena by means of which the cells and the organism respond to various types of stress (Luckey 1980; McClintock 1984; Lindquist 1986; Morgan et al. 1986). When stress is represented by a mutagenic agent one of the most interesting responses is the adaptive response (AR; Samson and Cairns 1977). The mechanisms underlying the AR are reasonably well known in prokaryotes in which they were discovered (Sekiguchi and Nakabeppu 1987; Rebeck et al. 1988). In plant (Rieger et al. 1982; Heindorff et al. 1987) and animal cells (Samson and Schwartz 1980, 1983) investigation is focused mainly on the reduction of the yield of induced chromatid aberrations by various pretreatment procedures (clastogenic adaptation).