Neonatal exposure to 17α-ethynyl estradiol affects ovarian gene expression and disrupts reproductive cycles in female rats
Neonatal exposure to 17α-ethynyl estradiol affects ovarian gene expression and disrupts reproductive cycles in female rats
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DOI：
10.1016/j.reprotox.2014.03.001
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发表时间：
2014-07-01
影响因子：
3.3
通讯作者：
Watanabe, Gen
中科院分区：
文献类型：
--
作者：
Nozawa, Kaori;Nagaoka, Kentaro;Watanabe, Gen
新生儿暴露于合成雌激素导致雌性大鼠迟发性生殖功能障碍。低剂量组在PND 171 -190期间和高剂量组在PND 126 -145期间暴露于17 α-乙炔基雌二醇（EE，低：20和高：2000 μ g/kg）诱导异常动情周期。在正常发情周期PND 90时，高剂量组动物的血清LH峰消失，卵巢激素水平降低。基因表达分析表明，编码促黄体生成素/绒毛膜促性腺激素受体（LHCGR）的mRNA水平在EE处理的卵巢高于对照卵巢，LHCGR蛋白共定位于卵巢的间质区与骨化相关蛋白。在PND 1，卵巢LHCGRmRNA水平在EE治疗组大鼠高于对照组大鼠，并直接诱导LHCGR表达EE在体外观察。我们的研究结果表明，新生儿暴露于EE诱导不规则的LHCGR表达在未成熟的卵巢，这可能会影响发生迟发性生殖功能障碍的成年动物。(C)2014爱思唯尔公司All rights reserved.
Neonatal exposure to synthetic estrogen causes delayed reproductive dysfunction in female rats. Exposure to 17 alpha-ethynyl estradiol (EE, low: 20 and high: 2000 mu g/kg) induced an abnormal estrous cycle during PND171-190 in low-dose and PND126-145 in high-dose group. At PND90 within normal estrous cycle, high-dose animals showed lack of LH surge and low of ovarian hormones in serum level. Gene expression analysis demonstrated that level of mRNA encoding luteinizing hormone/chorionic gonadotropin receptor (LHCGR) was higher in EE-treated ovaries than in control ovaries, and LHCGR protein colocalized with apoptosis-related proteins in the interstitial area of the ovary. At PND1, ovarian LHCGR mRNA levels were higher in EE-treated rats than in control rats, and direct induction of LHCGR expression by EE was observed in vitro. Our results indicate that neonatal exposure to EE induces irregular LHCGR expression in the immature ovary, which may influence the occurrence of delayed reproductive dysfunction in adult animals. (C) 2014 Elsevier Inc. All rights reserved.