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Eckols K, Williams J, Uphouse L: Effects of chlordecone on progesterone receptors in immature and adult rats. Toxicol Appl Pharmacol. 1989 Sep 15;100(3):506-16.
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 micrograms 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. |
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