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首页> 外文期刊>Congenital anomalies >Exposure to diethylstilbestrol during fetal stage disrupts male external genitalia development mediated by its specific hazardous effects rather than its estrogen action
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Exposure to diethylstilbestrol during fetal stage disrupts male external genitalia development mediated by its specific hazardous effects rather than its estrogen action

机译：在胎儿阶段暴露于二乙基胱螺母破坏由其特定危险作用而不是雌激素作用介导的男性外部生殖器发育

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In recent years, the number of onset of hypospadias, which is a representative disorder of external genitalia formation in boys, has been increasing year after year. It is suspected to be in relationship to endocrine disruptors which have androgenic/anti‐androgenic action because androgen signaling is well known to be important for external genitalia formation. In addition, a synthetic estrogen, diethylstilbestrol (DES), caused external genitalia disorders in human newborn male babies, hence it is also suspected that disruption of estrogenic signaling in the critical period of external genitalia formation causes external genitalia disorder. However, it remains unclear whether estrogenic signaling is also involved in external genitalia formation. In our current study, to assess the effect of DES on external genitalia formation, DES (100 μg/kg per day) was administered to pregnant mice from embryonic day 14.5 to 16.5. At embryonic day 18.0, the pregnant mice were sacrificed and the fetuses were collected for analysis of the external genitalia. The anogenital distance (AGD) and the size of the genital tubercle were measured under a semi‐automatic stereoscopic microscope and the formation of urethral plate in the external genitalia was observed by using hematoxylin‐eosin stained sections. These parameters have been already identified as indexes of external genital formation by a previous report using an anti‐androgenic agent. An androgen receptor full antagonist, Flutamide used as a positive control caused prominent reduction in all indices of AGD, genital tubercle and urethral plate in the experimental condition. On the other hand, in the DES treatment group, shortening of AGD and trivialization of external genitalia were observed, but no abnormality was found in the urethral plate formation. Furthermore, in order to verify whether some external genitalia disorders caused by DES is caused by its estrogenic action, we prepared ArE‐TG mice, which produces excessive estrogens in the placenta during the fetal stage. Pregnant mice obtained by mating ArE‐TG mice with wild type mice were dissected at pregnancy day 18.0 and analyzed for fetal external genitalia as in DES. In the ArE‐TG fetus, there was no particular abnormality as found in DES for external genitalia formation. These results suggested that some external genitalia disorders induced by DES in embryonic stage is not due to estrogenic signaling.
机译：近年来，腹期下患病的发病次数，这是男孩外部生殖器形成的代表性障碍，一年后一直在增加。怀疑是与具有雄激素/抗雄激素作用的内分泌破坏剂的关系，因为雄激素信号众所周知，对于外部生殖器形成是重要的。此外，合成雌激素，二乙基胱然而，仍然不清楚雌激素信号是否也参与外部生殖器形成。在我们目前的研究中，为了评估DES对外部生殖器形成的影响，将DES（每天100μg/ kg）从胚胎第14.5天施用至孕妇小鼠至16.5。在胚胎第18.0天，处死怀孕小鼠并收集胎儿以分析外部生殖器。在半自动立体显微镜下测量胃部距离（AgD）和生殖器结节的尺寸，并通过使用苏木精 - 嗜素染色部分观察到外部生殖器中的尿道板的形成。通过使用抗雄激素剂的先前报告已经鉴定为外部生殖器形成的索引已经鉴定为外部生殖器形成的指标。雄激素受体全拮抗剂，氟胺用于阳性对照导致实验条件下的所有agd，生殖结节和尿道板的所有索引突出。另一方面，在DES治疗组中，观察到外部生殖器的缩短和外部生殖器的差异化，但在尿道板形成中没有发现异常。此外，为了验证由DES引起的一些外部生殖器疾病是由其雌激素作用引起的，我们制备的是-TG小鼠，其在胎儿期间在胎盘中产生过量的雌激素。通过配合的妊娠小鼠在妊娠第18.0天中解剖用野生型小鼠获得的孕鼠，并为胎儿外部生殖器分析。在IS-TG胎儿中，在外部生殖器形成中没有特别的异常。这些结果表明，胚胎阶段的DES诱导的一些外部生殖器紊乱不是由于雌激素信号传导。

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