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首页> 外文期刊>Scientific reports. >Downregulation of testosterone production through luteinizing hormone receptor regulation in male rats exposed to 17α-ethynylestradiol
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Downregulation of testosterone production through luteinizing hormone receptor regulation in male rats exposed to 17α-ethynylestradiol

机译：通过暴露于17α-乙炔雌二醇的雄性大鼠的旋粉体激素受体调节，睾酮产生的下调。

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The pharmaceutical 17α-ethynylestradiol (EE2) is considered as an endocrine-disrupting chemical that interferes with male reproduction and hormonal activation. In this study, we investigated the molecular mechanism underlying EE2-regulatory testosterone release in vitro and in vivo. The results show that EE2 treatment decreased testosterone release from rat Leydig cells. Treatment of rats with EE2 reduced plasma testosterone levels and decreased the sensitivity of human chorionic gonadotropin (hCG). EE2 reduced luteinizing hormone receptor (LHR) expression associated with decreased cAMP generation by downregulation of adenylyl cyclase activity and decreased intracellular calcium-mediated pathways. The expression levels of StAR and P450scc were decreased in Leydig cells by treatment of rats with EE2 for 7 days. The sperm motility in the vas deferens and epididymis was reduced, but the histopathological features of the testis and the total sperm number of the vas deferens were not affected. Moreover, the serum dihydrotestosterone (DHT) level was decreased by treatment with EE2. The prostate gland and seminal vesicle atrophied significantly, and their expression level of 5α-reductase type II was reduced after EE2 exposure. Taken together, these results demonstrate an underlying mechanism of EE2 to downregulate testosterone production in Leydig cells, explaining the damaging effects of EE2 on male reproduction.
机译：药物17α-乙炔雌二醇（EE2）被认为是一种干扰雄性繁殖和荷尔蒙激活的内分泌破坏化学品。在这项研究中，我们研究了EE2-调节睾酮的分子机制在体外和体内释放出来。结果表明，EE2治疗降低了大鼠Leydig细胞的睾酮释放。对血浆睾酮水平降低的大鼠对大鼠的治疗，降低人绒毛膜促性腺激素（HCG）的敏感性。 EE2通过下调腺苷环酶活性和细胞内钙介导的途径减少了与营养的降低相关的叶氏素激素受体（LHR）表达。通过将EE2的大鼠进行7天，在Leydig细胞中降低了星和P450SCC的表达水平。输精管和附睾中的精子活力降低，但睾丸的组织病理学特征和输精管的总精子数不受影响。此外，通过用EE2治疗降低了血清二氢睾酮（DHT）水平。 ee2暴露后，前列腺和精益解的萎缩性明显，其表达水平为5α-还原酶II型。总之，这些结果证明了EE2的潜在机制，使睾酮产生在Leydig细胞中，解释了EE2对男性繁殖的破坏作用。

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