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Objective. Determination of the peculiarities of ultrastructural changes and metabolism of reactive forms of oxy& gen and nitrogen in the tissues of the myocardium, aorta and portal vein of the radiosensitive BALB/c mice due long&term exposure to the complex of radionuclides of Chоrnobyl fallout (ejection) and low&intensity low&dose γ& irradiation. Materials and methods. Experimental studies were performed on 60 mice&female radiosensitive lines BALB/c with a body weight of 20-22 g, which were divided into 3 groups: I group (control) & animals age 6-9 months which were born and lived their lives in Kyiv vivarium under conditions natural radioactive background; ІІ - animals age 6 months, which were born and lived in the Chornobyl exclusion zone throughout their lives; ІІІ - animals, which from 3 months of age for 6 months were constantly located in cages with flat ionizing radiation sources and exposed to external γ&irradiation in a total dose of 0.43 Sv. Animals of II and III groups were kept in the vivarium of the Institute for Safety Problems of Nuclear Power Plants of the National Academy of Sciences of Ukraine (Chornobyl). Mice of the BALB/c lines are sensitive to radiation: for males LD 50/30 < 5.7 Gy, for females - 5.85 Gy. Results and conclusions. The peculiarities of structural and functional changes in the organs of the cardiovascular system (CVS) and mechanisms of the development of oxidative and nitrosatitative stress due long&term exposure to the complex of radionuclides of the Chornobyl fallout (ejection) and low&intensity low&dose γ&radiation based on the study of ultrastructural organization and metabolism of reactive oxygen species (ROS) and nitrogen (NRS) of the atri& al cardiomyocytes (CMC), the aortic endothelium and portal vein of the BALB/c mice. Found that the permanent expo& sure to low doses of radiation changes occur, including the dominant mechanism is to run a CMC apoptosis and endothelial cells of the aorta and portal vein. It is shown that the development of oxidative stress accompanied by increased activity of ROS metabolism that occurs due to activation of nucleotide and lipid superoxide generators. Found that under these conditions the development of nitrosative stress is due to the activation of inducible NO syn& thesis enzyme iNOS and inhibit its synthesis constitutive eNOS enzyme. High levels of simultaneous generation of superoxide and NO, bindting, lead to the formation of toxic peroxynitrite, which initiates the process of apoptosis. [ABSTRACT FROM AUTHOR]