Abstract
Hepatic 9, 000×g supernatant (S9) fraction from 3-methylcholanthrene (MC)-treated rats showed a significantly low activity in the in vitro conversion of 2-acetylaminofluorene (AAF) to mutagen(s), while S9 fraction from untreated or phenobarbital (PB)-treated rats showed a remarkable activity. The S9 fraction from MC-treated rats actually suppressed the PB-S9 mediated AAF mutagenicity. Since the suppressive effect of MC-S9 was lost by the addition of 10-4 M α-naphthoflavone (α-NF), rat specific cytochrome P-448 may be responsible for this suppressive effect.
