The present study was conducted to study the effect of hypothyroidism on the prenatal and postnatal development of the testis, spermatogenesis and the study of the effect of thyroxine replacement on the hypothyroid rat testis. The purpose of this study was to know the role of thyroid hormones in the development and maturation of the testis and the mechanism by which thyroxine exerts its effect on the testis.
In this study twenty pergnant female rats and forty newborn male rats were used and were divided into two groups. Prenatal group (twenty pregnant rats) in which the pregnant rats received 0.05% solution of propylthiouracil in their drinking water daily starting at 8th day of gestation up to 18th and 21st days of gestation.
Postnatal groups were divided into, control group, postnatal treated group and replacement group:
- Postnatal control group fifteen newborn male rats received water only.
- Treated postnatal group (fifteen male rats) received 0.05 % solution of propylthiouracil in the drinking water of lactating mother starting from the day of birth up to 20 days then in the drinking water of the male rats up to 15, 30, 60 days of age, each of five rats.
- Replacement group (ten male rats). The lactating rats received 0.05% solution of PTU starting from the day of the birth up to the age of 20 days then in the drinking water of the male rats. At the same time the male rats received thyroxine injection from the day of birth every second day up to 60 days
From all groups the preganant mothers were opened and fetuses removed and opened below umbilicus and cutted to demonstrate the testes in the prenatal group and prepared for light microscope. The male rats were opened and testes then prepared for light and electron microscope in postnatal control, treated and replacement groups.
It was found that in the fetuses there were no changes in the testes between the control and treated rats.
In the postnatal treated rats the weight of the male rats and the testes showed reduction than in control, while no change in replacement group. By light and electron microscope, the seminiferous tubules showed defects in the spermatogenesis and spermatogonia and no sperms could be seen in the postnatal treated rats. In replacement rats there were normal spermatogenesis and sperms could be seen. The Sertoli cells in the postnatal treated rats were still immature while in replacement group normal maturation of Sertoli cells occurred. The basal laminae were thickened in the postnatal treated rats while they were normal in the replacement group. The Leydig cells showed delay in their differentiation than those of control.
In conclusion, this study can support the idea that hypothyroidism in the fetal life don’t affect the development of the testis and hypothyroidism in neonatal life lead to infertility and defects in spermatogenesis and abnormalities in spermatogenic cells and Sertoli cells. Also this study support that thyroxine replacement in hypothyroidism can antagonize the effects of hypothyroidism on the testis and lead to normal maturation of both spermatogenic cells and Sertoli cells which at the end lead to normal spermatogenesis and fertility.
From all the previous findings and data this study advise to diagnose hypothyroidism early in life and rapid use of thyroxine to reverse the hazard of hypothyroidism and also recommend to try the effect of hypothyroidism on adult rat testes.
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