Hepatic glutathione transferase activity induced by polycyclic aromatic compounds. Lack of correlation with the murine Ah locus.

Abstract

Hepatic cytosolic glutathione transferase activity with 1-chloro-2,4-dinitrobenzene as substrate was induced by 3-methylcholanthrene or β-naphthoflavone in C57BL/6N inbred mice and in (C57BL/6N)(DBA/2N)F1 but not in DBA/2N inbred mice. High doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin induced the transferase activity in both C57BL/6N and DBA/2N mice. The glutathione transferase activity with benzo[a]pyrene 4,5-oxide as substrate was induced by 3-methylcholanthrene in C57BL/6N but not DBA/2N mice. The transferase activity with styrene 7,8-oxide as substrate was different from either of the above activities in that about twofold induction by 3-methylcholanthrene occurred in both C57BL/6N and DBA/2N mice. Among progeny from the (C57BL/6N)(DBA/2N)F1 x DBA/2N backcross, however, no association was found between the transferase induction process by 3-methylcholanthrene and the presence of the Ah receptor [i.e., inducible aryl hydrocarbon (benzo[a]pyrene) hydroxylase activity]. It is therefore concluded that induction of glutathione transferase activity by polycyclic aromatic compounds is mediated by a gene(s) distinct from the Ah regulatory genes. These data emphasize the importance of examining progeny from the appropriate backcross before making conclusions about the genetic linkage of any two expressed traits.