Improper iodine intake is a major concern in public health. Chronic intake of low iodine affects gonadal functions of man and animals; however, such effects of excess iodine in male reproduction, specially on testicular morphology, testicular steroidogenic enzyme activities, sperm morphology, sperm viability, and sperm count including male hormonal profiles in reference to iodine status and thyroid hormone profiles are yet to be explored. With this background, adult male rats of 120 ± 10 gm Bw of 90 ± 5 days were divided broadly in two groups depending on the duration of the treatment for 30 and 60 days, respectively. Both the groups consisted of control animals. Excess iodine (100EI), i.e., 100 times more than its recommended level but within its tolerable ranges, was administered through gavage regularly to the first group of experimental animals for 30 and 60 days, respectively, and excessive iodine (500EI), i.e., 500 times more than its recommended level and above tolerable range in the same way and for the same durations, was administered to the other group of experimental animals. Overall results revealed that regular consumption of iodine in excess impairs reproductive functions in adult male rats depending on the dose and duration of its exposure through different mechanisms. Excess iodine accumulates in the testis which results in generation of reactive oxygen species (ROS) as evidenced by higher lipid peroxidation level as well as an imbalance in the pro-/antioxidant status inhibiting the activity of ∆(5) 3β- hydroxysteroid dehydrogenase (HSD) and 17β-HSD resulting to reduced synthesis of testosterone that causes structural and functional changes of the testis. Secondly, persistent generation of ROS in testis as a result of prolonged excess iodine exposure affects hypothalamo-pituitary-adrenal axis that stimulates synthesis and secretion of corticosterone which inhibits LH release that downregulates testosterone synthesis causing further testicular disruption. Thirdly, excess iodine when administered above its tolerable ranges for prolonged duration acts on thyroid itself developing a state of biochemical hypothyroidism (as evident by low T3) which further potentiate the disrupting effect of excess iodine on male gonads by reducing circulating testosterone level.

Objective: L-thyroxine is used for control and prevention of many thyroidal diseases, though it may cause damages in thyroid hormone-sensitive organs, namely, liver and kidney. Reports on the protective effects of any antioxidants in L-thyroxine induced oxidative stress are scanty. Thus, L-thyroxine induced oxidative stress and its prevention by Vitamin E supplementation have been studied in the present investigation.Methods: Adult, male Wister rats were divided into four groups of six animals each, and L-thyroxine (T4) (0.3 mg/kg body weight) was administered intraperitoneally in the treated group. Similarly, L-thyroxine (T4), at the above-mentioned dose, and Vitamin E acetate (100 mg/kg of body weight/ day orally) coadministered simultaneously (T4+VE) in the next group. Third group was administered only with Vitamin E, and the remaining group kept as control. Treatment continued regularly for 15 and 30 days. Animals were sacrificed after completion of treatment. Lipid peroxidation (LPO) level, superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) activities were assayed in liver and kidney along with their histology. Obtained results were interpreted statistically against their respective control groups.Results: Body weight was significantly decreased, and relative kidney weight was increased after L-thyroxine administration as compared to control (p<0.05). LPO level, SOD and catalase activities were significantly enhanced in L-thyroxine treated groups, whereas GPx activity was decreased. However, LPO level and the activities of those enzymes along with body weight and organ weights were almost restored their normal in L-thyroxine and Vitamin E coadministered group treated for 15 days and 30 days, respectively.Conclusion: Exogenously administered L-thyroxine causes oxidative stress in liver and kidney that in turn generates reactive oxygen species resulting cell damages. Vitamin E acetate supplementation reduces these adverse effects on liver and kidney and thus acts as a beneficial health management agent.