ADVERSE EFFECTS OF NEONATAL HYPOTHYROIDISM ON WISTAR RAT SPERMATOGENESIS

Abstract

The effect of neonatal hypothyroidism on spermatogenesis was studied in Wistar rats of different age groups. Hypothyroidism was induced in newborn male rats from day one postpartum up to day 60 postpartum by daily administration of 0.05% methimazole (MMI) to the nursing mothers or directly through drinking water. The animals were killed at days 10, 15, 30, 40, and 60 postpartum, blood plasma was collected, and testes, epididymides, prostates, and seminal vesicles were separated and weighed. Testes were fixed in formalin for histological studies. Plasma testosterone (T), estradiol (E₂), and sex hormone binding globulin (SHBG) were measured by radioimmunoassay. Hypothyroidism significantly reduced seminiferous tubule and lumen diameter. Control rats showed active spermatogenesis whereas in hypothyroid rats, the proliferation and differentiation of germ cells were arrested and their number was decreased. Plasma T, E₂, and SHBG levels were significantly decreased at all ages for hypothyroid rats. The absolute weight of testes was decreased irrespective of age (except day 10 postpartum), however ventral, dorsolateral prostate, and epididymis weights were decreased at 30, 40, and 60 days postpartum. Coagulating gland weight was decreased in all age groups of hypothyroid rats. Hypothyroid rats of day 40 and 60 postpartum showed a decrease in absolute seminal vesicle weight. Relative testicular weights of hypothyroid rats decreased by postpartum day 15, 30, 40, and 60 whereas the opposite effect was observed by postpartum day 10. Relative organ weights were increased in epididymides (day 15 and 30 postpartum), seminal vesicles (day 30 and 40 postpartum), and dorsolateral prostates (day 15, 30, and 40 postpartum) and decreased in 10 and 60 day old hypothyroid rat. Ventral prostate relative weight was decreased in 40 and 60 day old rats. The coagulating gland weight was decreased in 10, 15, and 60 days postpartum and an opposite effect was observed in 30 and 40 days hypothyroid rats. The present study clearly indicates that hypothyroidism adversely affects spermatogenesis; it also indicates that thyroid hormones are essential for normal spermatogenesis. Their effect may either be direct or indirect.

ACKNOWLEDGMENTS

The authors are thankful to Prof. E. Nieschlag, Director, Institute of Reproductive Medicine, University of Münster, Germany and Dr. C. Munroe, and Dr. B. Lesely, University of California, Davis, CA, USA for their gift of testosterone and estradiol antibodies, respectively. Our sincere thanks to Diagnostic Systems Laboratories Inc., Texas, USA for the gift of SHBG RIA kit. We thank Dr. Adedayo Adeeko, Ms. Sarah Ali-Khan, Ms. Ekaterina Zubkova and Ms. Shayesta Seenundun for critical reading of this manuscript.