Melatonin enhances antioxidant defenses but could not ameliorate the reproductive disorders in induced hyperthyroidism model in male rats

Abstract

The present study was carried out to clarify the effect of different doses of melatonin on some reproductive hormones, serum total antioxidant, histopathological examination, lipid peroxidation, and antioxidant parameters in liver, kidney, heart, and testis tissues in induced-hyperthyroidism (HT) male rat model. A total of 75 mature male Wistar rats were equally allocated into five groups; control groups were daily I/P injected with distilled water containing 4 M ammonium hydroxide in methanol and 1% absolute ethanol; on hyperthyroidism model group, rats received daily I/P injection of L-thyroxine (0.2 mg/kg body weight). In melatonin-treated groups, rats were injected with the same dose of L-thyroxine followed by I/P injection of melatonin (1, 5, or 10 mg/kg, respectively) for 21 days. The hyperthyroidism group showed significant increase in serum thyroxine (T4), triiodothyronine (T3), and testosterone levels and a significant decrease in the levels of thyroid stimulating hormone (TSH), follicle stimulating hormone (FSH), luteinizing hormone (LH), and serum total antioxidants capacity, with a significant decrease in superoxide dismutase (SOD) activity and glutathione reductase (GSH) content with a significant increase in malondialdehyde (MDA) concentration in all examined tissues. While, melatonin co-treatment to HT groups partially counteracted the effect of hyperthyroidism by decreasing serum T4 and T3 levels and increasing serum TSH. In addition, melatonin could decrease serum levels of FSH, LH, and testosterone, as well as it could increase serum total antioxidants capacity, SOD activity, and GSH content and decreased MDA concentration in all examined tissues. Additionally, melatonin could amend the histopathological alterations in the examined tissues of hyperthyroid rats but not the testicular tissue. It is concluded that melatonin has a protective role against the hyperthyroidism-induced oxidative damage but cannot ameliorate the reproductive disorders in male rat model.