The timeliness of the work is due to the prevalence of magnesium deficiency associated with the use of drugs that contribute to the excretion of magnesium from the body. The aim of the work is to elucidate the cell-mediated reaction of the thymus to magnesium deficiency caused by the administration of furosemide. Magnesium deficiency was modeled by intraperitoneal administration of furosemide to experimental rats. The amount of magnesium and sodium in the blood and thymus tissue was determined by inductively coupled plasma atomic emission spectrometry, the cell composition of the thymus was evaluated on histological sections. It is shown that at furosemide load the amount of magnesium decreases in the blood, but increases in the tissue of the thymus gland. The areas of the structural zones of the thymus (subcapsular zone, cortex, medulla), their percentage; cortical/medullary ratio were calculated. Cell density, lymphocyte count large, medium and small lymphocytes, reticular epithelial cells, macrophages, mast cells, apoptotic cells, thymic corpuscle were counted in each structural zone per unit area (100 μ2). In experimental animals the amount of magnesium in the blood decreases, but in the thymus tissue increases, there is leukocytosis and lymphocytosis, eosinophilia. Revealed histo- and cytostructural morphological rearrangements indicate a change in the functional activity of the gland. It was shown that the furosemide-induce deficiency of magnesium the area of the medulla increases, the number of macrophages and apoptotic elements increases; without affecting on the mast cells, but their secretory activity increases. There are size thymic corpuscle and the number of cells in them increases. Thus, the furosemide load is accompanied by magnesium imbalance, proinflammatory changes induce, is accompanied by a proapoptotic action and stimulates the starting of a macrophage reaction and degranulation of mastocytes in the thymus.