The functional-metabolic response peculiarities of the rat blood cells to isoniazid (one of the main antituberculosis medications) were studied. Isoniazid or its complex with pyridoxine were administrated orally for 3 months in therapeutic (5 mg/kg) and the toxic (100 mg/kg) doses (based on isoniazid). Isoniazid in toxic dose was found to inhibit the phagocytosis and the myeloperoxidase activity in neutrophils, the hydrolase activity in neutrophils and lymphocytes, but, at the same time, it activated dehydrogenase activity in lymphocytes. Pyridoxine modified the toxic effect of isoniazid on the metabolic processes (prevented the inhibition of phagocytosis and peroxidase activity in neutrophils, stimulated acid phosphatase activity in lymphocytes, decreased in the level of the lysosomal cationic proteins in neutrophils). It is suggested that the response of the blood cells to isoniazid, demonstrated in this work, was caused by the capacity of the medication to functionally activate the adrenal cortex, while the cellular-metabolic effects of pyridoxine could be associated with the modulation of glucocorticosteroid activity.