Deacetylation to 2-aminofluorene as a major initial reaction in the microsomal metabolism of 2-acetylaminofluorene to mutagenic products in preparations from rabbit lung and liver.

摘要: Abstract The rabbit pulmonary and hepatic microsomal pathways for the metabolism of 2-acetylaminofluorene (AAF) 2-aminofluorene (AF) to mutagenic products were investigated by means high performance liquid chromatography Salmonella mutagenicity assay. Mutagenic activity approached a maximum with increasing concentrations AAF incubated preparations ; preparations, was proportional concentration over range examined. activities AF exhibited typical saturation kinetics both preparations. Approximately 7 times more than N -hydroxy-2-acetylaminofluorene (N-hydroxy-AAF) formed in incubations (0.5 mm) When formation AF, but not N-hydroxy-AAF, detected. inclusion paraoxon blocked did lead recovery any N-hydroxy-AAF. We conclude that from rabbits is initiated primarily, if entirely, deacetylation AF. limited deacetylase which, like activity, exhibits linear relationship AAF. On basis rates N-hydroxy-AAF their activities, we estimate about 60% dependent upon subsequent oxidation formed.