[Hypothesis of the mechanism of adaptive response induction in mammalian cells by low-dose irradiation].

The mechanism for radiation-induced adaptive response (RAR) in mammalian cells is presented in this paper. The start point of the RAR in the frame of this mechanism is the receptors for growth factors activation due to the increase in the microviscosity of plasma membrane subjected to oxidative damage. There are components of the mitogen-activated signal transduction pathway which take part in the subsequent processes. The main of them are protein kinase C (PK C), motogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK). They make posttranslation modification of the DNA metabolism enzymes and of the transcription factors p53 and c-Jun/AP-1. There are genes taking part in the excision repair and apoptosis among the c-Jun/AP-1 and the p53 targets. C-Jun/AP-1 and p53 can be direct participants at the stage of exision repair when DNA damage is recognized. Thus, the proposed scheme of events removes the contradiction between two hypotheses which explain the RAR: intracell DNA repair induction, either of cell selection in culture of mammalian cells.