Effects of chlordecone on progesterone receptors in immature and adult rats.
Effects of chlordecone on progesterone receptors in immature and adult rats.
复制标题
十氯酮对未成熟和成年大鼠孕酮受体的影响。
DOI：
10.1016/0041-008x(89)90298-6
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发表时间：
1989
影响因子：
3.8
通讯作者：
Uphouse,L
中科院分区：
文献类型：
--
作者：
Eckols,K;Williams,J;Uphouse,L
在用25微克雌二醇或75毫克/千克十氯酮处理CDF-344雌性大鼠后，研究了氯化农药十氯酮诱导中枢神经系统（下丘脑和视前区）以及脑垂体和子宫孕酮受体的能力。在成年卵巢切除大鼠和完整的未成年大鼠，雌二醇增加孕激素受体的神经和子宫组织。这与十氯酮的效果形成对比。对大鼠进行十氯酮处理后，未成年大鼠子宫内的孕酮受体出现变化，但切除卵巢的成年大鼠子宫内的孕酮受体则没有变化。两个年龄组的中枢神经系统和脑垂体孕酮受体在十氯酮治疗后都没有增加。这些结果表明，杀虫剂未能模拟雌激素依赖性事件的实质性后果的中枢神经系统调节女性生殖功能。对这些发现进行了讨论，认为十氯酮有可能减弱雌二醇对中枢神经系统的影响，而不是模仿雌二醇的作用。除了十氯酮对孕酮受体的影响外，还研究了十氯酮与雌二醇合用时的影响。对十氯酮和雌二醇的三种时间组合进行了研究，这三种组合对性行为产生不同的影响。目的是确定十氯酮对性行为的抑制是否是由于雌二醇减少了中枢神经系统孕酮受体的生成。在上述三种处理条件下，十氯酮均未减弱雌二醇对中枢神经系统孕酮受体的升高作用。总的来说，这些研究表明，十氯酮无法模拟雌二醇与中枢神经系统雌二醇受体之间的相互作用所产生的明确且功能上重要的影响。然而，他们还表明，杀虫剂对中枢神经系统雌二醇事件的抑制并不依赖于其对雌二醇对中枢神经系统孕酮受体的诱导的减弱。
The ability of the chlorinated pesticide chlordecone to induce the CNS (hypothalamus and preoptic area) plus pituitary and uterine progesterone receptors was examined in CDF-344 female rats following treatment with 25 μg estradiol or with 75 mg/kg chlordecone. In adult ovariectomized rats and in intact immature rats, estradiol increased progesterone receptors in neural and uterine tissues. This was in contrast to the effect of chlordecone. Chlordecone treatment of rats induced progesterone receptors in uterus of immature rats, but not in uterus of ovariectomized adult rats. In neither age group were CNS plus pituitary progesterone receptors increased following chlordecone treatment. These results suggest that the pesticide fails to mimic an estradiol-dependent event of substantial consequence to the CNS regulation of female reproductive functioning. These findings are discussed in terms of the possibility that chlordecone may, rather than mimicking, have the potential to attenuate estradiol's CNS effects. In addition to the effects of chlordecone on progesterone receptors, the effects of chlordecone in combination with estradiol were examined. Three temporal combinations between chlordecone and estradiol, which produce different effects on sexual behavior, were examined. The objective was to determine if chlordecone's inhibition of sexual behavior may have resulted from an attenuation of estradiol's production of CNS progesterone receptors. Chlordecone did not attenuate estradiol's elevation of CNS progesterone receptors under any of the three treatment conditions. Collectively, these studies demonstrate that chlordecone fails to mimic a well-defined and functionally significant effect of estradiol's interaction with the CNS estradiol receptor. However, they also suggest that the pesticide's inhibition of CNS estradiol events does not depend upon its attenuation of estradiol's induction of the CNS progesterone receptor.