Institut für Physiologische Chemie, Universitätsklinikum Essen, D-4300 Essen.
Brain Res. 1983 Jan 3;258(1):133-8. doi: 10.1016/0006-8993(83)91238-6.
Female rats were defeminized by neonatal treatment with estradiol-17beta benzoate, moxestrol (RU 2858), monohydroxytamoxifen ICI 79,280) or the dibenzoate esters of the catecholestrogens, 2-hydroxyestradiol-17beta and 4-hydroxyestradiol-17beta. When ovariectomized as adults and primed with estradiol-17beta benzoate all these rats demonstrated a deficient luteinizing hormone response to progesterone administration. However, estrogen responsiveness of progestin receptor induction was unimpaired in both the pituitary gland, the preoptic-hypothalamic brain and the uterus.
雌性大鼠在新生期用雌二醇-17β苯甲酸酯、莫昔妥尔(RU 2858)、单羟他莫昔芬(ICI 79280)或儿茶酚雌激素的二苯甲酸酯,2-羟基雌二醇-17β和 4-羟基雌二醇-17β处理后会出现去女性化。当这些大鼠在成年时被卵巢切除并被雌二醇-17β苯甲酸酯预刺激时,它们对孕酮的促黄体生成素反应都不足。然而,无论是在下丘脑-垂体前叶脑还是子宫,孕激素受体诱导的雌激素反应都没有受到影响。