Promotion of endometriosis by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats and mice: Time-dose dependence and species comparison
Promotion of endometriosis by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats and mice: Time-dose dependence and species comparison
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DOI：
10.1006/taap.1996.0106
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发表时间：
1996-05-01
影响因子：
3.8
通讯作者：
Birnbaum, L
中科院分区：
文献类型：
--
作者：
Cummings, AM;Metcalf, JL;Birnbaum, L
在子宫内膜异位症的疾病中，子宫内膜组织生长在子宫外，通常在腹膜腔中。子宫内膜异位症的啮齿动物模型允许一种再现疾病、评估化学物质的影响和研究机制的方法。在产生子宫内膜异位症的诱导手术前21天，雌性Sprague-Dawley大鼠和B6 C3 F1小鼠用0，3或10 μ g TCDD/kg，在手术时和手术后3、6和9周再次对动物进行治疗。在术后3、6、9和12周进行评价。在大鼠中，当每个剂量内的所有时间点合并时，TCDD产生了剂量依赖性的增生部位直径增加，并且在小鼠中，在9周和12周时，部位直径急剧增加。在大鼠但不是小鼠中，卵巢重量在9周和12周时降低，在这些时间持续阴道发情的发生率增加，卵巢的组织学评价显示在12周时排卵停止。在这两个物种中，胸腺萎缩，表明免疫功能障碍，肝肿大被观察到的后果，TCDD曝光。大鼠的体重减轻，但小鼠的体重没有减轻。组织学评价显示，对照大鼠纤维化，TCDD治疗大鼠的部位出现坏死和炎性变化，TCDD治疗小鼠的部位主要出现纤维化变化。在大鼠和小鼠之间观察到的差异涉及（a）对子宫内膜部位直径的影响程度（大鼠<小鼠），（B）测量对卵巢功能的影响（大鼠>小鼠），这可能是基于TCDD的部分抗雌激素性，以及（c）小鼠和大鼠对TCDD的免疫反应不同的证据表明，介导TCDD促进子宫内膜异位症的机制是复杂的并且在大鼠和小鼠中可能不同。小鼠可能是一个更好的模型，为未来的研究阐明这些机制。(C)出版社：Academic Press，Inc.
In the disease of endometriosis, endometrial tissue grows outside the uterus, usually in the peritoneal cavity, Rodent models of endometriosis allow a way to reproduce the disease, evaluate effects of chemicals, and study mechanisms, Twenty-one days prior to induction surgery which produces endometriosis, female Sprague-Dawley rats and B6C3F1 mice were pretreated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) at 0, 3 or 10 mu g TCDD/kg, Animals were treated again at the time of surgery and at 3, 6, and 9 weeks following surgery. Evaluations were made at 3, 6, 9, and 12 weeks postsurgery. TCDD produced a dose-dependent increase in endometriotic site diameter when all time points were pooled within each dose in rats and a dramatic increase in site diameter in mice at 9 and 12 weeks. In rats but not mice, ovarian weight was decreased at 9 and 12 weeks, the occurrence of persistent vaginal estrus was increased at these times, and histological evaluation of the ovaries revealed ovulatory arrest at 12 weeks. In both species, thymic atrophy, indicating immune dysfunction, and hepatomegaly were observed as consequences of TCDD exposure. Body weight was reduced in rats but not in mice. Histological evaluations of endometriotic sites revealed fibrosis in control rats, necrotic and inflammatory changes in the sites from TCDD-treated rats, and predominantly fibrotic changes in sites from TCDD-treated mice. Differences observed between the rat and the mouse with respect to (a) the magnitude of the effect on endometrial site diameter (rats < mice), (b) measured effects on ovarian function (rats > mice) that may be based on the partial antiestrogenicity of TCDD, and (c) evidence that mice and rats differ in their immune response to TCDD suggest that the mechanisms mediating TCDD's action to promote endometriosis are complex and may be different in rats and mice. The mouse may be a better model for future studies necessary to elucidate these mechanisms. (C) 1996 Academic Press, Inc.