It was found that acute exposure to ionizing radiation at doses of 7.5 and 8 Gy leads to the development of bone marrow syndrome of acute radiation sickness in mice. On the 7th day after exposure at doses of 7.5 Gy and 8 Gy, the mortality rate of animals was 66.7%, on the 10th day 83.3 and 86.7%, and by the 14th day it reached 91.7 and 100%, respectively. Prophylactic exposure to electromagnetic radiation from a helium-neon laser modulated with preparations with the tissue of the hypothalamic structures of the brain, spleen and bone marrow of a newborn mouse (P1-4) before X-ray irradiation at doses of 7.5 and 8 Gy contributed to a decrease in the mortality of animals from acute radiation sickness during the first 14 days, which was 28.6 and 50%, respectively. However, with this method of protective action, by the 22nd day after the radiation damage of 7.5 Gy, the mortality rate reached 64.3%, and 8 Gy-90%. On the contrary, with a therapeutic and preventive method of exposure to electromagnetic radiation by a helium-neon laser modulated by drugs with tissue from hypothalamic structures of the brain, spleen and bone marrow of a newborn mouse (R1-4) after a radiation lesion at a dose of 7.5 Gy, the mortality on the 25th day was 23.3%, and 8 Gy 30% and remained at this level for more than 30 days. We believe that the increase in the resistance of mice to ionizing radiation and the different nature of the course of acute radiation sickness with preventive and therapeutic methods of exposure is due to several factors. On the one hand, it is the realization of antihypoxic, antioxidant effects when exposed to electromagnetic radiation modulated by drugs with tissue from hypothalamic structures of the brain, spleen and bone marrow of a newborn mouse. On the other hand, the effect of electromagnetic radiation modulated by the preparation of the bone marrow and spleen of a newborn mouse has a cytoprotective effect on the bone marrow cells of mice with acute radiation sickness. It is also possible that this effect contributes to adequate neuroimmune regulation in the development of acute radiation sickness in mice.