Skip Navigation


ToxSci Advance Access originally published online on December 22, 2003
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
78/1/41    most recent
kfh045v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (12)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Lai, K. P.
Right arrow Articles by Wong, C. K. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lai, K. P.
Right arrow Articles by Wong, C. K. C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

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.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Drug Metab. Dispos.Home page
K. A. Bielefeld, C. Lee, and D. S. Riddick
Regulation of Aryl Hydrocarbon Receptor Expression and Function by Glucocorticoids in Mouse Hepatoma Cells
Drug Metab. Dispos., March 1, 2008; 36(3): 543 - 551.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
S. Shin, N. Wakabayashi, V. Misra, S. Biswal, G. H. Lee, E. S. Agoston, M. Yamamoto, and T. W. Kensler
NRF2 Modulates Aryl Hydrocarbon Receptor Signaling: Influence on Adipogenesis
Mol. Cell. Biol., October 15, 2007; 27(20): 7188 - 7197.
[Abstract] [Full Text] [PDF]

Home page
 Toxicol SciHome page
E. Sonneveld, A. Jonas, O. C. Meijer, A. Brouwer, and B. van der Burg
Glucocorticoid-Enhanced Expression of Dioxin Target Genes through Regulation of the Rat Aryl Hydrocarbon Receptor
Toxicol. Sci., October 1, 2007; 99(2): 455 - 469.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Pharmacol.Home page
W. Hu, C. Sorrentino, M. S. Denison, K. Kolaja, and M. R. Fielden
Induction of Cyp1a1 Is a Nonspecific Biomarker of Aryl Hydrocarbon Receptor Activation: Results of Large Scale Screening of Pharmaceuticals and Toxicants in Vivo and in Vitro
Mol. Pharmacol., June 1, 2007; 71(6): 1475 - 1486.
[Abstract] [Full Text] [PDF]

Home page
 Hum Exp ToxicolHome page
V. C Dhulipala, W. V Welshons, and C. S Reddy
Cell cycle proteins in normal and chemically induced abnormal secondary palate development: a review
Human and Experimental Toxicology, November 1, 2006; 25(11): 675 - 682.
[Abstract] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.