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ToxSci Advance Access published online on December 22, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfh045
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
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Received August 13, 2003; accepted November 17, 2003
© 2003 Society of Toxicology

Endocrine Toxicology

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

K. P. Lai 1, M. H. Wong 1, and Chris K. C. Wong 1*

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

* To whom correspondence should be addressed. 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 EROD activities in H4IIE cell by pico-molar level of TCDD treatment. In this study, we examined the hormonal modulation of TCDD elicited AhR-mediated biochemical responses. Lipid soluble hormones, 17{beta}-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 the cotreatment with the estrogen receptor antagonist, 4-hydroxytamoxifen or ICI 182780. Taking a step further to dissect the possible mechanisms involved, with the aid of CHX, Dex-mediated potentiation was found to depend on the posttranscriptional process. Dex pretreatment study implicated 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.


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