A MODEL FOR THE STUDY OF ANDROGEN EFFECTS ON FOLLICULAR ATRESIA AND OVULATION
A MODEL FOR THE STUDY OF ANDROGEN EFFECTS ON FOLLICULAR ATRESIA AND OVULATION
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DOI：
10.1095/biolreprod27.4.903
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发表时间：
1982-01-01
影响因子：
3.6
通讯作者：
MAHESH, VB
中科院分区：
文献类型：
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作者：
BAGNELL, CA;MILLS, TM;MAHESH, VB
切除垂体（第24天）的未成熟雌性大鼠给予孕马血清促性腺激素（PMSG，32 IU）以启动卵泡生长，并给予人绒毛膜促性腺激素（hCG，10 IU）以诱导排卵，与在成年骑自行车大鼠中观察到的结果相当。不可芳香化的雄激素5 α的作用双氢睾酮（DHT）对卵巢卵泡数量和排卵的影响进行了评估。单次注射的DHT（2或4毫克/公斤体重）30小时后PMSG导致卵巢重量减少PMSG控制相比。这种卵巢重量的减少与卵泡闭锁的刺激和健康的初级、次级和三级卵泡数量的减少有关。将PMSG致敏的垂体切除大鼠暴露于1或4 mg/kg体重的DHT 24小时，结果为53.7 ± 0.05。3.8和66.7 . ±-。7.8闭锁卵泡;值显著高于（P < 0.05）32.2 ±。2.7在PMSG对照中观察到闭锁卵泡。这种DHT诱导的闭锁也与所有类型的健康卵泡减少相关。这些卵巢组织学的变化与DHT管理反映在体内的卵巢hCG的反应性的损失。双氢睾酮处理使输卵管中的卵子数量从14.9 ± 0.01个减少到14.9 ± 0.01个。1.2与PMSG单独给药至7.8 ±。1.2.共同管理的雌二醇（1或2毫克/公斤体重）防止闭锁效应的DHT测量的卵泡和恢复排卵PMSG水平的组织学外观。该模型允许检查由于类固醇治疗对生物学功能的卵巢变化，并通过测试卵泡对hCG的体内反应性来验证卵巢的组织学评估。DHT诱导卵泡闭锁和雄激素效应可以通过同时治疗雌二醇来预防，这表明雄激素诱导的闭锁可能涉及干扰卵巢中雌二醇的产生和/或作用。
Hypophysectomized (day 24), immature female rats were given pregnant mare''s serum gonadotropin (PMSG, 32 IU) to initiate follicular growth and human chorionic gonadotropin (hCG, 10 IU) to induce ovulation comparable to that observed in an adult, cycling rat. The effects of a nonaromatizable androgen, 5.alpha.-dihydrotestosterone (DHT), on the ovarian follicular population and ovulation were assessed. A single injection of DHT (2 or 4 mg/kg body wt) 30 h after PMSG resulted in decreased ovarian weight compared to PMSG controls. This ovarian weight reduction was associated with a stimulation of follicular atresia and reduction in the number of healthy primary, secondary and tertiary follicles. A 24 h exposure of the PMSG-primed hypophysectomized rat to 1 or 4 mg/kg body wt DHT resulted in 53.7 .+-. 3.8 and 66.7 .+-. 7.8 atretic follicles, respectively; values significantly higher (P < 0.05) than the 32.2 .+-. 2.7 atretic follicles observed in PMSG controls. This DHT-induced atresia was correlated with decreases in healthy follicles of all types as well. These changes in ovarian histology with DHT administration were reflected in a loss of in vivo responsiveness of the ovary to hCG. DHT treatment reduced the number of ova present in the oviducts from 14.9 .+-. 1.2 with PMSG alone to 7.8 .+-. 1.2. Co-administration of estradiol (1 or 2 mg/kg body wt) prevented the atretic effects of DHT as measured by histological appearance of the follicles and restoration of ovulation to PMSG levels. This model permits examination of ovarian changes due to steroid treatment on biological function and verification of histological assessment of the ovary by testing the in vivo responsiveness of follicles to hCG. DHT induces atresia of ovarian follicles and the androgen effect can be prevented by simultaneous treatment with estradiol, suggesting that androgen-induced atresia may involve interference in the production and/or action of estradiol in the ovary.