Neonatal exposure to T3 disrupts male reproductive functions by altering redox homeostasis in immature testis of rats.

Abstract

T3 is the active hormone, produced by peripheral deiodination of thyroxine. Exposure to excess thyroid hormones leads to hypermetabolic state and thus generates oxidative stress which seems to be involved in hyperthyroidism-induced testicular pathophysiology. We investigated the effects of T3 administration on the testis during development throughout sexual maturation in rats. Male pups were divided into two groups. T3 group was administered 80µg/kg body weight intraperitoneal T3 injections daily for 21days from the 1st postnatal day, while the control group was administered saline intraperitoneal injections. The pups were sacrificed at pnd 10, 20 and 30. T3 treatment resulted in a significant decrease in body weight at all ages tested and an increase in testis weight during the treatment period. The treatment produced imbalance in their testicular redox status, reflected by a significant increase in the amount of thiobarbituric acid-reactive substances and protein carbonyl content in the testicular homogenates of 20-day-old rats. We observed a significant increase in antioxidant system activities γ-glutamyl transferase, glucose-6-phosphate dehydrogenase, catalase and superoxide dismutase, reduced glutathione content and lactate dehydrogenase activity. Histological examination showed altered seminiferous tubules, degenerated germ cells and decreased height of the germinal epithelium. Chronic neonatal exposure to T3 resulted in redox state alterations which contribute to testicular impairment.