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Vol. 61, Issue 6, 1393-1403, June 2002
Department of Environmental Toxicology, University of California,
Davis, California
We have used human ovarian carcinoma BG-1 cells to determine which
steps in the pathway of estrogen signaling are disrupted by the aryl
hydrocarbon receptor (AhR) ligand
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). We report
that inhibition of estrogen signaling occurs between 7 and 18 h
after TCDD treatment and that this effect is not caused by a decrease
in estradiol concentration. TCDD decreased estrogen receptor (ER)
levels in cells grown in standard medium; however, in estrogen-stripped
medium, ER (but not AhR) levels were dramatically reduced (~7-fold)
but were not decreased further by TCDD. Because the absolute level of
estradiol inducibility and inhibition by TCDD was similar in either
medium, decreases in ER are not responsible for the antiestrogenic
effect. The AhR also did not bind to the estrogen-responsive element
(ERE) in vitro, and ERE binding by nuclear ER complexes was not
decreased by TCDD, indicating that the effect of TCDD does not involve
direct competition between the AhR and ER for DNA binding. However,
inhibition of protein synthesis by cycloheximide blocked the
TCDD-induced inhibition of ER-dependent gene expression. Overall, our
results are consistent with the action of a TCDD-induced protein at a step(s) after ER-DNA binding, most likely at the level of gene transcription.
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