which include polychlorinated biphenyls (PCBs), dibenzofuSpecies-Specific Recombinant Cell Lines as Bioassay Systems rans (PCDFs), and dibenzo-p-dioxins (PCDDs) as well as for the Detection of 2,3,7,8-Tetrachlorodibenzo-p-dioxin-like many other subclasses of PCDHs (Giesy et al., 1994a). These known to bioaccumulate and biomagnify in the food chain Exposure to specific polychlorinated diaromatic hydrocarbons (Ballschmitter et al., 1989; Tanabe et al., 1987; Webster and (PCDH), such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, di- Commoner, 1994; Giesy et al., 1994a,b). Exposure to and oxin), produces a wide variety of species-and tissue-specific toxic bioaccumulation of PCDHs has been observed to produce a and biological effects. Many of these responses are mediated by variety of species-and tissue-specific effects, such as tumor of PCDHs involve costly and time-consuming traditional instrumental analysis methods, such as gas chromatography Polychlorinated diaromatic hydrocarbons (PCDHs) 2 are a (GC) separation and mass spectrometry (MS). The identifidiverse group of widespread environmental contaminants, cation and quantification of these compounds is complicated by the fact that techniques and standards for identifying many of the congeners and isomers do not exist. In addition,

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The Ah receptor (AhR) is a ligand‐dependent transcription factor that mediates biological and toxicological actions of halogenated aromatic hydrocarbons such as 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin. Although much is known about the biochemical and molecular mechanisms of AhR action, little is known about the factors and events that control expression of the AhR gene itself. The 5′‐flanking region of the murine AhR gene was characterized and deletion analysis demonstrated that regulatory elements necessary for full constitutive promoter activity are contained within a fragment encompassing −184 to +380 of the AhR gene. The murine AhR gene promoter is a GC‐rich, TATA‐less promoter that contains at least five putative Sp1‐like binding sites. Transient transfection experiments not only identified a region between −1431 and −721 that represses constitutive promoter activity by 2‐ to 3‐fold, but also demonstrate that basal AhR promoter activity occurs in a cell‐ and species‐specific manner. n‐Butyrate, a nonspecific histone deacetylase inhibitor, increased AhR promoter activity 8‐fold, suggesting a role for histone acetylation in AhR gene promoter activity. Overall, this study defines upstream regulatory regions important for constitutive AhR gene expression and identifies a novel activator of AhR gene expression. © 1999 John Wiley & Sons, Inc. J Biochem Toxicol 14: 1–10, 2000