MolPharm xPharm- The Comprehensive Pharmacology Reference

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

Molecular Pharmacology Fast Forward
First published on February 18, 2005; DOI: 10.1124/mol.105.010983

0026-895X/05/6705-1393-1398$20.00
Mol Pharmacol 67:1393-1398, 2005

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
mol.105.010983v1
67/5/1393    most recent
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Pande, K.
Right arrow Articles by Bradfield, C. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pande, K.
Right arrow Articles by Bradfield, C. A.
ACCELERATED COMMUNICATION

Aspects of Dioxin Toxicity Are Mediated by Interleukin 1-Like Cytokines

Kalyan Pande, Susan M. Moran, and Christopher A. Bradfield

McArdle Laboratory for Cancer Research, University of Wisconsin Medical School, Madison, Wisconsin

Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) results in a broad spectrum of toxic effects. Most, if not all, of these responses are dependent upon the binding of dioxin to the aryl hydrocarbon receptor. Given their common roles in chemically induced toxicity, we asked whether interleukin 1 (IL1)-like cytokines play a role in acute aspects of the dioxin response. To test this idea, we employed a "triple-null" mouse model that lacks the two receptors for the tumor necrosis factors-{alpha} and -{beta} and the receptor for the IL1-{alpha} and IL1-{beta} cytokines. When triple null mice were treated with dioxin, there was significant attenuation in the levels of serum alanine aminotransferase, signifying reduced hepatocellular damage. In addition, the triple-null mice were protected from dioxin-induced liver inflammation. Loss of receptors for the IL1-like cytokines was not protective for all aspects of dioxin toxicity. Endpoints such as thymic involution, Cyp1a2 induction, hepatomegaly, and hydropic degeneration remain unchanged in this model.

Received January 6, 2005; accepted February 18, 2005

Address correspondence to: Christopher A. Bradfield, McArdle Laboratory for Cancer Research, 1400 University Avenue, Madison, WI 53706-1599. E-mail: bradfield{at}oncology.wisc.edu




This article has been cited by other articles:


Home page
 J. Immunol.Home page
L. Z. Shi, N. G. Faith, Y. Nakayama, M. Suresh, H. Steinberg, and C. J. Czuprynski
The Aryl Hydrocarbon Receptor Is Required for Optimal Resistance to Listeria monocytogenes Infection in Mice
J. Immunol., November 15, 2007; 179(10): 6952 - 6962.
[Abstract] [Full Text] [PDF]

Home page
 Toxicol SciHome page
L. Umannova, J. Zatloukalova, M. Machala, P. Krcmar, Z. Majkova, B. Hennig, A. Kozubik, and J. Vondracek
Tumor Necrosis Factor-{alpha} Modulates Effects of Aryl Hydrocarbon Receptor Ligands on Cell Proliferation and Expression of Cytochrome P450 Enzymes in Rat Liver "Stem-Like" Cells
Toxicol. Sci., September 1, 2007; 99(1): 79 - 89.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
J. A. Walisser, E. Glover, K. Pande, A. L. Liss, and C. A. Bradfield
Aryl hydrocarbon receptor-dependent liver development and hepatotoxicity are mediated by different cell types
PNAS, December 6, 2005; 102(49): 17858 - 17863.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 2005 by the American Society for Pharmacology and Experimental Therapeutics