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Glucocorticoid Receptor Functions in HeLa Cells Are Perturbed by 2,3,8,9-tetrachlorodibenzo-p-dioxin (TCDD)

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We used 2,3,8,9-tetrachlorodibenzo-p-dioxin (TCDD) and dexamethasone (DEX) to examine their effects on aryl hydrocarbon receptor (AhR) and glucocorticoid receptor (GR) in HeLa cells. TCDD (5 nM), DEX (100 nM) and their combination down-regulated GR after 24 h. DEX reversed AhR mRNA increase and AhR protein decrease caused by TCDD. Since AhR-GR cross-talk occurs in cell-type and species-specific manner, the presented data may serve as the basis in the understanding of mechanisms underlying mutual interactions between AhR and GR.





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Keywords: Receptors; aryl hydrocarbon; drug-metabolizing enzymes; glucocorticoid

Document Type: Research Article

Publication date: December 1, 2007

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  • Drug Metabolism Letters publishes short papers on major advances in all areas of drug metabolism and disposition. The emphasis will be on publishing quality papers very rapidly. Letters will be processed rapidly by taking full advantage of the Internet technology for both the submission and review of manuscripts. The journal covers the following areas:

    In vitro systems including CYP-450; enzyme induction and inhibition; drug-drug interactions and enzyme kinetics; pharmacokinetics, toxicokinetics, species scaling and extrapolations; P-glycoprotein and transport carriers; target organ toxicity and interindividual variability; drug metabolism and disposition studies; extrahepatic metabolism; phase I and phase II metabolism; recent developments for the identification of drug metabolites, reactive intermediate and glutathione conjugates.
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