Abstract
Experimental thyrotoxicosis in rats is accompanied by the increase of serum alanine aminotransferase (AlAT), aspartate aminotransferase (AsAT), creatine phosphokinase-MB (CPK-MB) activities and the content of primary products of lipid peroxidation, conjugated dienes, in liver, heart and blood. This suggests impairments in functioning of these organs, which accompany intensification of free radical processes. Melatonin administration resulted in the decrease of AlAT, AsAT, CPK-MB and conjugated dienes; this indicates positive effect of melatonin in this pathology. Thyrotoxicosis is accompanied by the increase of catalase activity in rat liver, heart and serum. Exogenous melatonin decreased specific activity of serum and heart catalase by 22 and 43%, respectively, compared with rats subjected to hyperthyroidism. However, there was insignificant increase in specific activity of liver catalase (by ∼15%). Melatonin administration caused a decrease of α-tocopherol content increased in rat tissues under conditions of hyperthyroidism. Thus, exogenous melatonin is capable to reduce intensity of lipid peroxidation in hyperthyroidism and to act as an adaptogen, regulating free radical homeostasis in response to action of pathogenic factors on organism that is associated by concomitant reduction of mobilization of components of the antioxidant system.
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