Gamma interferon induction depresses murine hepatic promutagen/procarcinogen activation

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Abstract
In vivo induction of gamma interferon (IFN-γ) by sensitization of mice with Mycobacterium bovis strain BCG and subsequent challenge with tuberculin depressed the ability of liver homogenates from treated animals to metabolically activate promutagens. The Ames Salmonella typhimurium revertant assay was used for analyses of metabolic conversion of promutagens by liver homogenates. Relative to the mutant frequencies determined with control liver bomogenates, induction of IFN-γ depressed the abilities of homogeoates from treated animals to activate N-acetylaminofluorene (AAF), aflatoxin B 1 (AFB 1 ), and benzo[a]pyrene (BP) by 55%, 44% and 95%, respectively. Within 18–24 h of Aroclor 1254 treatment, liver P-450 content had increased 43%, and the relative mutant yields per unit protein for all three promutagens had approximately doubled. In vivo induction of IFN-γ suppressed the Aroclor 1254-dependeot increases in mutagenesis by AAF (63%), AFB 1 (90%), and BP (reduced to a level 23% below non-Araclor 1254 treatment). In all cases, the levels of depression of promutagen activation qualitatively correlated with cytochrome P-450 content and the induction of IFN-γ.

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