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Introduction. The attention of researchers has been drawn to the study of molecular mechanisms of drug-induced liver damages, in recent years. It is well known that the regeneration of the liver structure and function in the case of its damage can be carried out due to proliferation, polyploidization and hypertrophy of hepatocytes [1, р. 148]. Mature hepatocytes have been shown to have a higher Hayflick limit than other somatic cells and to exhibit more than 100 replicative cycles. Unipotency of hepatocytes is associated with a polyploid set of chromosomes that are normally stable in the G0 resting phase, however after loss of the parenchyma, they may return to the G1 phase of the cell cycle, followed by DNA synthesis and mitosis. Further proliferative activity may be insignificant or very pronounced, depending on the conditions in which regeneration occurs [4, р. 285]. Polyploidy, on the one hand, can be considered as a sign of severe damage to

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