Effects of the beta-isomer of hexachlorocyclohexane on estrogen-sensitive human mammary tumor cells.
The effects of the beta-isomer of hexachlorocyclohexane (beta-HCH) on the induction of the cytosolic progesterone receptor ( PgRc), on the redistribution of the estrogen receptor ( ER), and its affinity for ER were investigated in the estrogen-sensitive human mammary tumor cell line MCF-7. The effects of beta-HCH were compared to those of estradiol-17 beta ( E2) and 2,4,6-trichlorophenol (TCP), a major urinary metabolite of beta-HCH in rats. beta-HCH in concentrations higher than 1 microM caused induction of PgRc whereas TCP was essentially without effect up to a cytotoxic concentration of 100 microM. Furthermore, beta-HCH (10 microM) caused redistribution of ER, i.e., decrease of cytosolic ER concentration and increase of nuclear ER concentration, in a way similar to E2. In contrast to this, beta-HCH up to a molar excess of 6 X 10(4) (concentration 30 microM) caused no significant displacement of [3H]E2 from ER indicating that beta-HCH has no substantial affinity for ER. It is concluded that beta-HCH has estrogenic properties which are at variance with the failure to demonstrate binding of beta-HCH to ER.[1]References
- Effects of the beta-isomer of hexachlorocyclohexane on estrogen-sensitive human mammary tumor cells. Coosen, R., van Velsen, F.L. Toxicol. Appl. Pharmacol. (1989) [Pubmed]
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