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Abstract:   (402 Views)

Background: Excessive synthesis of thyroid hormone in hyperthyroidism is related to the imbalance of oxidative status in living organisms. Melatonin mediates its effects either directly through scavenging free radicals or indirectly through the activation of melatonin receptors (MT1 and MT2). The present study investigated the involvement of melatonin receptors in the melatonin-mediated attenuation of hyperthyroidism-induced oxidative stress in the spleen of laboratory mice.
Methods: The hyperthyroidism was induced by L-thyroxine (0.6µg/g B. wt.) supplementation. The experimental mice were supplemented with melatonin (25 µg/100g B. wt.) subcutaneously. Oxidative stress, and melatonin receptor expression in the spleen tissues, and circulatory levels of thyroid hormone were determined.
Results: L-thyroxine treatment caused a significant increase in serum T3 and T4 levels. Melatonin supplementation caused a significant decrease in serum T3 and T4 levels in L-thyroxine-treated mice. L-thyroxine treatment increased MDA levels and suppressed catalase and SOD enzyme activities. Melatonin treatment caused suppression of MDA levels and an increase in SOD and catalase activities. L-thyroxine treatment caused significant suppression in MT1 receptor expression and a significant increase in MT2 receptor expression. Melatonin supplementation significantly induced the MT2 receptor protein expression in the spleen tissues of experimental mice.  
Conclusion: This study suggests that alterations in MT2 melatonin receptor expression may be associated with melatonin-mediated attenuation of oxidative stress in the spleen tissues of hyperthyroid mice.

     

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