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ToxSci Advance Access originally published online on December 22, 2003
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Toxicological Sciences 78, 41-49 (2004)
Copyright © 2004 by the Society of Toxicology

REGULAR ARTICLE

Modulation of AhR-Mediated CYP1A1 mRNA and EROD Activities by 17ß-Estradiol and Dexamethasone in TCDD-Induced H411E Cells

K. P. Lai, M. H. Wong and Chris K. C. Wong1

Institute for Natural Resources and Environmental Management, and Department of Biology, Hong Kong Baptist University, Hong Kong, PR China

1 To whom correspondence should be addressed at Department of Biology, Hong Kong Baptist University, Kowloon Tong, Hong Kong. Fax: (852)-3411-5995. E-mail: ckcwong{at}hkbu.edu.hk.

ABSTRACT

TCDD elicits a variety of species- and organ-specific pathological consequences. The differential toxicities are thought to relate to the de novo modulation of TCDD action by endogenous hormones. Previous studies from this laboratory demonstrated a dose- and time-dependent induction of CYP1A1 expression and 7-ethoxyresorufin-O-deethylase (EROD) activities in H4IIE cells by picomolar levels of TCDD treatment. In this study, we examined the hormonal modulation of TCDD-elicited AhR-mediated biochemical responses. Lipid-soluble hormones, 17ß-estradiol (E2), diethylstilbestrol (DES), testosterone (T), 5{alpha}-dihydrotestosterone (DHT), dexamethasone (DEX), and T3, were studied for their possible interactions with the TCDD-mediated effects. Our results showed that CYP1A1 expression and EROD activities induced by TCDD were potentiated or suppressed, respectively, by DEX or E2/DES treatment. Other tested hormones, however, had no significant effect. Using a receptor antagonist (RU486), DEX-mediated potentiation of TCDD-elicited EROD activity was completely abolished. E2-mediated suppression, however, was not affected by cotreatment with the estrogen receptor antagonists, 4-hydroxytamoxifen or ICI 182780. Taking a step further to dissect the possible mechanisms involved, with the aid of cycloheximide (CHX), DEX-mediated potentiation was found to depend on the posttranscriptional process. The DEX pretreatment study indicated that the potentiation was a time-dependent process. In contrast, E2-mediated suppression did not rely on the synthesis of protein factors. Presumably it might hinder the formation of the activated TCDD/AhR complex and so the subsequent binding on DRE.

Key Words: CYP1A1 mRNA; EROD; 17ß-estradiol; dexamethasone; H411E cells.


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