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J Biol Chem, Vol. 274, Issue 6, 3430-3438, February 5, 1999
From the Department of Environmental Health Sciences and Center for
Bioenvironmental Research, Tulane University School of Public Health
and Tropical Medicine, New Orleans, Louisiana 70112-2699
2,3,7,8-Tetrachlorodibenzo-p-dioxin
(TCDD) exerts its toxic action via the aryl hydrocarbon (Ah) receptor,
which induces a battery of xenobiotic-metabolizing enzymes, including
the cytochrome P450 isozyme, CYP1A1. TCDD-induced
7-ethoxycoumarin-O-deethylase activity was reduced 75% in
cultured human endometrial ECC-1 cells exposed to various
concentrations of 17
-estradiol for up to 72 h, with a
half-maximal effective concentration (EC50) of 0.9 nM. Reduced enzyme activity was correlated with decreased
CYP1A1 mRNA levels, and transcription. Exposure to TCDD plus
17-estradiol also reduced CYP1A1 activity in MCF-7 breast cancer
cells but not in Hep-3B human liver cells or HuE primary human
keratinocytes, suggesting that the effect was specific to
estrogen-regulated cells. Estrogen receptor antagonists
4-hydroxytamoxifen and
7
-[9-(4,4,5,5,5-pentafluoro-pentylsulfinyl)nonyl]estra-1,3,5(10)-triene3, 17-diol
restored TCDD-induced CYP1A1 transcription, steady-state mRNA levels, and enzymatic activity in ECC-1 cells. Gel mobility shift assay showed that 17-estradiol had little effect on Ah receptor binding to its DNA-responsive element. 17-Estradiol did not
alter the induction of another Ah receptor-regulated gene, CYP1B1, suggesting that altered Ah receptor binding to DNA
does not mediate reduced CYP1A1 transcription. Transfecting
ECC-1 cells with a general transcription factor involved in CYP1A1
induction, nuclear factor-1, reversed 17-estradiol antagonism of
dioxin induced-CYP1A1. The data suggest that 17-estradiol reduced
CYP1A1 expression at the transcriptional level by squelching available nuclear factor-1, a transcription factor that interacts with both Ah and estrogen receptors.
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