Estrogenic activity of the insecticide chlordecone (Kepone) and interaction with uterine estrogen receptors.

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Abstract
Reproductive disorders (i.e., sterility as judged by oligospermia and hypomotile sperm) were observed in male employees at a chlordecone (Kepone) manufacturing plant and were associated with exposure to high levels of this chlorinated insecticide. The chlorinated insecticide chlordecone interacts with the estrogen receptor system in the rat uterus in vitro and in vivo. It competes with estradiol for binding to the cytoplasmic receptor in vitro and also induces nuclear accumulation of estrogen receptor sites in uteri in vitro. When injected into immature rats, chlordecone translocates estrogen receptor sites to the uterine nucleus, increases uterine weight, and stimulates the synthesis of the progesterone receptor, an estrogen receptor-mediated process. Its slow onset of action, but prolonged duration of interaction with estrogen receptor, stimulation of uterine weight gain and progesterone receptor synthesis indicates that, although it has an affinity for receptor only 0.01-0.04% that of estradiol, its considerable estrogenic activity may likely be derived from its long half-life and bioaccumulative character.