Thyroid hormones are involved in the development of several tissues and organs and are essential for the normal growth and reproductive function. The aim of this study was to determine the effects of thyroid hormones on the development of testis and progression of spermatogenesis. Lactating mothers were treated with oral thyroxine (T4; 20 µg/100 g) for 20 days after parturition. The pups were decapitated at the age of 20, 40 and 60 days post partum. Neonatal hyperthyroidism resulted in a decrease in body and testis mass, an increase of free thyroxine and a decrease of testosterone concentrations in plasma of treated rats. The treatment was associated with a significant decrease of the diameter of seminiferous tubules and a slowdown in spermatogenesis, following a delay in the maturation of germ cells. We conclude that thyroid hormones affect the progression of postnatal spermatogenesis.

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 80 µg/kg body weight intraperitoneal T3 injections daily for 21 days 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.

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