| Male reproductive system can secrete lots of estrogen, which conducts its biological effects through combination with estrogen receptors. Estrogen is important to the development and function of male reproductive system, default or overexposure of estrogen has deleterious effects on male fertility, but now more mechanisms of estrogen action in male reproductive system are still unknown. It is urgent to know which point and how it could act on male reproductive system, and certain that male reproductive health of human and animals is impaired or not by the growing estrogen and chemicals having estrogenic activity in environment. The study was aimed to illuminate the mechanisms underlying the damaged male fertility of adult rats treated neonatally with estrogen. Rats were divided into 4 groups and treated respectively with 10μg, 500ng, 25ng ethinylestradiol and vehicle-corn oil on alternate days from postnatal days 2 to 12. The rats were killed in the adulthood, then the morphological changes of testis and epididymis, daily sperm production (DSP), the numbers of sperm in epididymis, the acrosin activity of sperm in deferent duct and the mRNA expression of acrosin in testis were detected. There were cryptorchidism, fluid retention in the testes and epididymal lumps in some rats of the 10μg group and the 25ng group. Although there was no great difference of body weight between the treated groups and control, the absolute testis and epididymis weight and the relative testis weight in the treated groups were significantly decreased. The epithelial height, tubular diameter and luminal diameter of stages Ⅶ and Ⅷ tubules in the 10μg and 500ng groups were significantly lower than in control and the 25ng group. DSP and the numbers of sperm in epididymis between the treated groups and control (p>0.05), But sperm content of epididymis in all treated groups were lower than control. Percent of sperm which acrosin was showed activity in 10μg, 500ng and 25ng groups were 54.72%, 64.93% and 73.78% respective, were lower than control (81.64%)(p<0.01). And mRNA expression of acrosin in testis of the treated groups was greatly reduced (p<0.05). Conclusion is that: 1) Neonatal exposure of male rats toethinylestradiol did not decreased their body weight, but the weight of the testes and epididymis declined, besides, there were some developmental disorders in the male reproductive system such as cryptorchidism, fluid retention in the testes, testicular and epididymal lumps. 2) Efficiency of spermatogenesis in the seminiferous tubules did not declined in the adulthood rats treated neonatally with ethinylestradiol, but the number of spermatozoa in the epididymis reduced, which was probably resulted from an enhanced rate of sperm transport through the epididymis caused by decreased androgen concentration and/or lower expression of androgen receptor in the epididymis. 3) Development of spermatids and/or spermatozoa in testis of the adult male rats was damaged after neonatal exposure to ethinylestradiol, so did the mature of spermatozoa in epididymis, which resulted in impairment of sperm fertility.
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