Etiology of ovarian dysfunction in chronic murine toxoplasmosis
Etiology of ovarian dysfunction in chronic murine toxoplasmosis
复制标题
DOI：
10.1007/bf00931615
复制
发表时间：
2004
影响因子：
2
通讯作者：
W. Stahl;J. Dias;G. Turek;Y. Kaneda
中科院分区：
文献类型：
--
作者：
W. Stahl;J. Dias;G. Turek;Y. Kaneda
慢性感染弓形虫的 Nya:NYLAR 小鼠会出现卵巢功能障碍。为了区分原发性卵巢功能衰竭和垂体促性腺激素不足，我们（a）监测卵巢对孕马血清促性腺激素（PMSG）和人绒毛膜促性腺激素（hCG）的反应性，（b）通过单侧卵巢切除（ULO）后发生的卵巢代偿性肥大（OCH）的程度评估内源性垂体促性腺激素的能力。 PMSG 刺激旺盛的卵泡发生和雌激素合成，但不刺激排卵。 PMSG 在 16 小时内诱导“超数排卵”后 3 天给予 HCG。这些观察结果表明，垂体中不存在关键的排卵前内源性黄体生成素 (LH) 激增。此外，ULO 不会导致对侧卵巢代偿性肥大，这是卵泡刺激素 (FSH) 不足的迹象。我们假设，响应寄生虫而外周释放的细胞因子到达下丘脑并引发一系列抑制促性腺激素释放激素（GnRH）脉冲式释放的事件，导致随后垂体-卵巢轴受损。
Ovarian dysfunction develops in Nya:NYLAR mice chronically infected withToxoplasma gondii. To differentiate between primary ovarian failure and pituitary gonadotropin insufficiency, we (a) monitored ovarian responsiveness to pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotropin (hCG) and (b) assessed endogenous pituitary gonadotropin capacity by the degree of ovarian compensatory hypertrophy (OCH) developing after unilateral ovariectomy (ULO). PMSG stimulated vigorous folliculogenesis and estrogen synthesis, but not ovulation. HCG given 3 days after PMSG induced “superovulation” within 16 h. These observations indicate the absence of the critical preovulatory surge of endogenous luteinizing hormone (LH) from the pituitary. In addition, ULO did not result in compensatory hypertrophy of the contralateral ovary, an indication of follicle-stimulating hormone (FSH) insufficiency. We hypothesize that cytokines released peripherally in response to the parasite reached the hypothalamus and initiated a sequence of events that inhibited the pulsatile release of gonadotropin-releasing hormone (GnRH), leading to the subsequent impairment of the pituitary-ovarian axis.