Stoll R, Faucounau N, Maraud R
Laboratoire d'Histologie et Embryologie, U.E.R. Médicale 1, Université Bordeaux II, France.
Gen Comp Endocrinol. 1990 Oct;80(1):101-6. doi: 10.1016/0016-6480(90)90153-d.
Treatment of genetically female chick embryos with norethindrone (NET), a progesterone-like steroid chemically related to testosterone, caused two types of Müllerian duct (MD) deficiencies. The first consisted in an absence of the caudal part of the ducts owing to their partial agenesia occurring between Days 5 and 7 of embryonic life. This is nonspecific since it was observed after a treatment with almost all steroidal sex hormones. In particular, this was obtained with estradiol which also increases the frequency and extent of agenesia caused by the NET, as reported here. The second type of deficiency appeared between Days 12 and 14 and was due to a regression destroying the more or less large part of the MDs having escaped agenesia, i.e., for most of the cephalic half. This resulted from the influence of the anti-Müllerian hormone originating from the ovary and normally inhibited by the ovarian estrogens. This protective action of endogenous estrogens was inhibited by the NET, but an additional treatment with estradiol removed this inhibition and prevented duct regression. Our results suggest that estrogen protects the duct from the regression induced indirectly by NET, by acting both at gonad and MD levels.
用炔诺酮(NET)对基因上为雌性的鸡胚胎进行处理,炔诺酮是一种与睾酮化学相关的孕酮样类固醇,导致了两种类型的苗勒管(MD)缺陷。第一种表现为由于胚胎生命第5天至第7天之间部分发育不全,导致苗勒管尾部缺失。这并不具有特异性,因为在用几乎所有甾体性激素处理后都观察到了这种情况。特别是,用雌二醇也能得到这种情况,正如本文所报道的,雌二醇还会增加由炔诺酮引起的发育不全的频率和程度。第二种缺陷出现在第12天至第14天之间,是由于一种退化作用破坏了在一定程度上逃过发育不全的苗勒管的大部分,即大部分头侧半部。这是由于来自卵巢的抗苗勒管激素的影响,而这种激素通常受到卵巢雌激素的抑制。内源性雌激素的这种保护作用被炔诺酮抑制,但额外给予雌二醇可消除这种抑制并防止管道退化。我们的结果表明,雌激素通过在性腺和苗勒管水平发挥作用,保护苗勒管免受炔诺酮间接诱导的退化。