Stoll R, Faucounau N, Maraud R
Gen Comp Endocrinol. 1987 May;66(2):218-23. doi: 10.1016/0016-6480(87)90270-x.
The caudal deficiencies of the Müllerian ducts (MDs) induced in chick embryos after early treatment with testosterone propionate (TP), 17 beta-estradiol benzoate (EB), or dihydrotestosterone (DHT) are the consequence of agenesia, i.e., a stop in duct development occurring during the sexually indifferent stage. The present work shows that EB and DHT act on the MDs in binding cellular estrogen receptors. Indeed, the antiestrogenic drug, tamoxifen, which competes with estrogens at the receptor site level, significantly decreases the percentage and extent of these MD caudal deficiencies. The results also show that such receptors are already present at a time when MDs begin to grow from 4.5 to 5 days of embryonic life onward. On the other hand, tamoxifen does not significantly modify agenesia induced by TP.
用丙酸睾酮（TP）、苯甲酸雌二醇（EB）或双氢睾酮（DHT）早期处理鸡胚后诱导出的苗勒管（MD）尾部缺陷是发育不全的结果，即性未分化阶段导管发育停止。目前的研究表明，EB和DHT通过与细胞雌激素受体结合作用于MD。实际上，在受体位点水平与雌激素竞争的抗雌激素药物他莫昔芬，能显著降低这些MD尾部缺陷的百分比和程度。结果还表明，在胚胎生命4.5至5天MD开始生长时，此类受体就已存在。另一方面，他莫昔芬不会显著改变由TP诱导的发育不全。
