[The redox homeostasis system in radiation-induced genomic instability].

The participation of the redox homeostasis system in the formation of the radiation-induced genome instability and new data of literature, that give a direct evidence the presence of this instability in vivo, is considered. The O2.-, H2O2 and NO. role as signal molecules, that triggered the cascade of active responses to change of redox status of the cells, are discussed. These compounds are mediators, that triggered the expression of specific genes. The reactive oxygen species (ROS) reorganize the membrane physico-chemical system of cell metabolism regulation. The composition, structure and function of cell membranes are changed, the membrane-bound proteins are modified. The data about changes in ROS generation system, including NO, that lead to genome instability after ionizing irradiation even in low doses, are analyzed. It is noted, that the radiation-induced genome instability and ROS production increase may be observed both in direct irradiated cells and their progeny and in the cells, that are not find oneself in ionization tracks, and their progeny. There are evidences that the genome instability of irradiated cell progeny is maintained by the increased ROS production. One of the mechanisms of genome instability transduction is carried out over "bystander effect", triggered by ROS.