Developmental aspects of 2-acetamidofluorene metabolism and mutagenic activation in the chick.
1. Oxidative metabolism and mutagenic activation of 2-acetamidofluorene (AAF) in the Salmonella test system were studied with liver subfractions from untreated and beta-naphthoflavone (BNF)-pretreated chicks during the first 10 days after hatching. 2. Newly hatched chicks had high liver microsomal mono-oxygenase activities, and these were markedly increased by BNF-pretreatment. 3. The mutagenic activation of AAF with control liver subfractions was highest on day 1 after hatching and declined towards day 10. 4. BNF-pretreatment caused decreases in the mutagenicity of AAF at high protein concentrations in the test system, but led to increases in mutagenic activity when low protein concentrations were applied. 5. N-Hydroxy-2-acetylaminofluorene was activated to a mutagen by microsomal metabolism, and this reaction was blocked by the deacetylase inhibitor paraoxon. 6. SDS polyacrylamide gel electrophoresis of liver microsomes from BNF-pretreated chicks showed an increase in a band with mol. wt. of approx. 55,000. The increase in the 55,000 mol. wt. band following BNF-pretreatment was associated with increases in benzo[a]pyrene hydroxylase and AAF N-hydroxylase activities in the chick liver microsomes.
D015073:2-Acetylaminofluorene / Q000378:metabolism* / Q000633:toxicity; D000818:Animals; D001579:Benzopyrene Hydroxylase / Q000378:metabolism; D001711:Biotransformation; D002645:Chickens; D008099:Liver / Q000378:metabolism; D009153:Mutagens / Q000378:metabolism*
D009153:Mutagens; D015073:2-Acetylaminofluorene; D001579:Benzopyrene Hydroxylase