PMID: 8937891Nov 1, 1996Paper

Strain-specific enhancement or inhibition of coumarin hepatotoxicity in mice following pretreatment with two different liver enzyme-inducing agents

Fundamental and Applied Toxicology : Official Journal of the Society of Toxicology
S CottrellC J Powell

Abstract

Human exposure to coumarin continues despite controversy over its hepatotoxic potential. Greater understanding of human reactions to coumarin may be achieved by studying murine interstrain differences. The metabolic basis of coumarin hepatotoxicity and its modulation by liver enzyme inducers, beta-naphthoflavone (beta NF) and aroclor 1254 (ARO), were investigated in C3H/He and DBA/2 mice. Coumarin (200 mg/kg) was hepatotoxic to both strains, resulting in 2- to 15-fold plasma aminotransferase elevations, mild subcapsular linear hepatocyte necrosis after 24 hr, and, in some C3H/He mice, centrilobular necrosis. In this strain, beta NF pretreatment caused a 2- to 3-fold further increase in plasma aminotransferases and produced periportal necrosis. In contrast, ARO-pretreated C3H/He mice tended to exhibit lower plasma aminotransferases and occasional midzonal damage. Neither pretreatment significantly altered coumarin hepatotoxicity in DBA/2 mice. In C3H/He mice, hepatic microsomal metabolism of [3-14C]-coumarin via the 3-hydroxylation pathway doubled following both beta NF and ARO treatment. The contrasting nonresponsiveness of DBA/2 mice suggested that this pathway is linked to the Ah locus, which is defective in this strain. ARO ...Continue Reading

Citations

Jul 27, 1999·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·B G Lake

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