The murine aromatic hydrocarbon responsiveness locus: A comparison of receptor levels and several inducible enzyme activities among recombinant inbred lines

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Abstract
The aromatic hydrocarbon responsiveness (Ah) locus has been correlated with genetic differences in the risk of drug toxicity, teratogenesis, chemical carcinogenesis, and mutagenesis. Hepatic cytosolic Ah receptor levels, 2‐amino‐5‐chlorobenzoxazole (zoxazolamine) paralysis time following β‐naphthoflavone treatment and aryl hydrocarbon hydroxylase (AHH),3 acetanilide 4‐hydroxylase (Ac4H), and NAD(P)H:menadione oxidoreductase (NMOR);4 induction by 3‐methylcholanthrene were studied in (a) the progenitors C57BL/6J (Ahb/Ahb) and DBA/2J (Ahd/Ahd) and 25 BXD recombinant inbred lines, (b) the progenitors C57BL/6N and C3H/HeN and 14 B6NXC3N recombinant inbred lines, and (c) the progenitors C57BL/6J and C3H/HeJ and 12 BXH recombinant inbred lines. The Ahb phenotype exhibits >5 femtomole receptor/mg of cytosolic protein, ≤15 minutes zoxaxolamine paralysis time, and twofold to 15‐fold induction of these three hepatic enzyme activities; the Ahd phenotype exhibits ≤2 fmol receptor/mg protein, >15 minutes zoxazolamine paralysis time, and Ahd phenotype mouse. These data underline the complexity of this genetic system when genes from C57BL/6 and DBA/2 are combined and particularly when genes from C57BL/6 and C3H/He inbred mouse strains are combined.

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