We have previously demonstrated that neonatal and transient neonatal
hypothyroidism modulates Leydig, Sertoli, and germ cell numbers, sex
steroids and
androgen binding protein concentration. The present study was undertaken to study the effect of neonatal onset
hypothyroidism on Leydig and peritubular myoid cell numbers, plasma and testicular interstitial fluid (TIF) sex
steroid concentration at different age groups of Wistar rats.
Hypothyroidism was induced by giving 0.05%
methimazole (MMI) to lactating mothers or directly to the male pups from day 1 postpartum through days 10, 15, 30, 40 and 60 postpartum. To confirm
hypothyroidism, plasma
thyroid hormones and TSH were assayed. Plasma and TIF
testosterone,
progesterone,
dihydrotestosterone (DHT) and
estradiol were assayed by radioimmunoassay. Leydig cell number in hypothyroid rats were less than the age-matched controls. The diameter of Leydig cells in hypothyroid rats was smaller than the controls but 10 days old hypothyroids alone had larger than control rats. A significant decrease of peritubular myoid cell number was observed in 30, 40 and 60 days hypothyroid rats and increased in 10 and 15 days
hypothyroidism. Hypothyroid rats had elevated level of plasma LH and decreased GH (except day 10 postpartum). Plasma PRL level was increased in 10 and 15 days hypothyroid rats and an opposite effect was observed in 40 and 60 days
hypothyroidism. Plasma
testosterone, DHT and
estradiol were decreased in all hypothyroid rats. However, plasma
progesterone level in hypothyroid rats was significantly higher at days 10, 30, and 40 postpartum and an opposite effect was seen in 15 and 60 days experimental groups. TIF
testosterone and
progesterone titre showed a consistent decrease in hypothyroid rats irrespective of the duration. In hypothyroid rats, TIF DHT levels decreased significantly in days 10, 40 and 60 postpartum. However, it increased in days 15 and 30 postpartum. Except at day 10 postpartum, the level of TIF
estradiol in hypothyroid rats was significantly less than their age matched controls. Our data clearly indicate that neonatal onset
hypothyroidism adversely affect Leydig cell proliferation along with impaired steroidogenesis.