Аннотация:DNA double-strand breaks (DSB) are the key type of DNA damage that determines the cellular response to IR exposure. The number of DSB, their repair kinetics and accuracy depend on several parameters, including total absorbed dose, particle energy, structure of the sample under study, etc. Among these factors, dose rate also plays an important role, but further investigation is necessary to determine the nature of this dependence. In this work, we use immunofluorescent analysis of DNA repair proteins (H2AX, ATM and Rad51) in order to identify major differences between the effects of acute (400 mGy min-1 ) and continuous (4 mGy min- 1 ) modes of exposure to low-LET irradiation on DSB induction and repair. There are several pathways of DSB repair. The major ones are classical non-homologous end joining (c-NHEJ), alternative non-homologous end joining (a-NHEJ), and homologous recombination (HR). These three mechanisms have different kinetics and induced error probability. These two properties determine the time-delayed effects on the irradiated cells. Our theoretical and experimental results show that the contribution of each pathway highly depends on the dose rate of irradiation. These results should significantly contribute to the development of new radiotherapy modes in cancer treatment and to the improvement of radiation hygiene rules.