[Problems of radiobiology and p53 protein]

The data about the structure and the mechanisms of participation of p53 protein in regulation of the cell cycle checkpoints, DNA repair and apoptosis in normal conditions and after ionizing irradiation are considered. The double strand break of DNA, as a signal of radiation damage, lead to binding of ATM protein with DNA, to appearance of the protein kinase activity at the ATM protein, that after phosphorylation of p53 protein lead to its stabilization and activation. It is noted, that the p53 protein is an integrator of environmental lesion signals, which triggers the transcription, that activate or inhibite the synthesis of protein factors leading to cell cycle arrest in the checkpoints, to increase of DNA repair or to apoptosis. The data evidenced the participation of p53 protein in radioresistance formation are considered: p53 protein after mutation changes loses the control over the cell cycle, DNA repair and apoptosis, and that leads both to the radioresistance increase and to the possibility of the radiation-induced defects retention in progeny of the irradiated cells and organisms. Potential prospective research directions in radiobiology in connection with the data on the molecular biology of p53 gene and protein (the problems of norm, radiosensitivity/radioresistance, drug research for prophylaxe and treatment of radiation injury, low dose effect including by high density irradiation) are reviewed.