Epigallocatechin-3-gallate does not affect the activity of enzymes involved in metabolic activation and cellular excretion of benzo[a]pyrene in human colon carcinoma cells.

Benzo[a]pyrene (B[a]P) and related procarcinogens found in cigarette smoke and roasted foodstuff require metabolic activation to build mutagenic DNA adducts that may cause tumor diseases like colorectal cancer. The major B[a]P-activating enzymes belong to the cytochrome-P450 (CYP)-1 family and are regulated by the aryl hydrocarbon receptor (AhR). Previous studies have indicated that an inhibition of AhR is accompanied with a reduced metabolic activation of B[a]P and therefore may act protective against carcinogenesis.

Species-specific differential AhR expression protects human neural progenitor cells against developmental neurotoxicity of PAHs.

Background: Because of their lipophilicity, persistent organic pollutants (POPs) cross the human placenta, possibly affecting central nervous system development. Most POPs are known aryl hydrocarbon receptor (AhR) ligands and activators of AhR signaling. Therefore, AhR activation has been suggested to cause developmental neurotoxicity (DNT).

Regulation of dioxin receptor function by different beta-carboline alkaloids.

The dioxin receptor, also known as arylhydrocarbon receptor (AhR), is a ligand-activated transcription factor that mediates the toxicity of dioxins and related environmental contaminants. In addition, there is a growing list of natural compounds, mainly plant polyphenols that can modulate AhR function and downstream signaling with quite unknown consequences for cellular function. We investigate the potential of four different beta-carboline alkaloids to stimulate AhR signaling in human hepatoma cells and keratinocytes.

Luteolin enhances the bioavailability of benzo(a)pyrene in human colon carcinoma cells.

We investigated the effect of luteolin, a plant-derived flavonoid, on benzo(a)pyrene (B(a)P)-stimulated drug metabolism and transport in human colon carcinoma cells. While luteolin treatment inhibited B(a)P-induced expression and activity of arylhydrocarbon receptor-dependent cytochrome P450 enzymes, the overall activity of UDP-glucuronosyltransferases and sulfotransferases was not affected by luteolin, indicating that luteolin affects phase-I but not phase-II function. Luteolin exposure decreased apical transport of B(a)P metabolites due to its interaction with the transporter breast cancer resistance protein.

Growth factors, cytokines and their receptors as downstream targets of arylhydrocarbon receptor (AhR) signaling pathways.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental pollutant, which causes a variety of severe health effects, e.g. immunosuppression, hepatotoxicity, and carcinogenesis.

Analysis of the transcriptional regulation and molecular function of the aryl hydrocarbon receptor repressor in human cell lines.

The aryl hydrocarbon receptor repressor (AhRR) is a member of the aryl hydrocarbon receptor (AhR) signaling cascade, which mediates dioxin toxicity and is involved in regulation of cell growth and differentiation. The AhRR was described as a feedback modulator, which counteracts AhR-dependent gene expression. We investigated the molecular mechanisms of transcriptional regulation of the human AhRR by cloning its regulatory DNA region located in intron I of the AhRR.