Experimental thyrotoxicosis in rats is accompanied by the increase of serum alanine aminotransferase (AlA), aspartate aminotransferase (AsA), creatine kinase-MB (CK-MB) activities and content of primary products of lipid peroxidation - conjugated dienes - in liver, heart and blood. This suggests impairments in these organs accompanying free radical processes intensification. Administration of melatonin decreased AlA, AsA and CK-MB activities and CD level decreased. Thyrotoxicosis increased catalase activity in liver, heart and blood. Exogenous melatonin decreased specific activity of catalase in blood and in heart in comparison with animals subjected to hyperthyroidism. However, some increase of catalase specific activity (~15%) was observed in liver. α-Tocopherol content, raising in rat tissues in thyrotoxicosis development conditions, decreased after melatonin treatment. Thus, exogenous melatonin is capable to reduce lipid peroxidation intensity at thyrotoxicosis and to act as an adoptogen, regulating free radical homeostasis.