Mechanism of reaction, tissue distribution, and inhibition of arylhydroxamic acid acyltransferase.

摘要: The enzyme of rat liver that can transform N -hydroxy- -2-fluorenylacetamide into a reactive derivative capable introducing fluorenylamine groups nucleic acids has been shown to be sulfhydryl-dependent with molecular weight approximately 28,000. A 30-fold purification the from 105,000 × g supernatants achieved by precipitation ammonium sulfate and gel filtration on Sephadex G-100. Evidence this mechanism activation involves transfer -acetyl group oxygen hydroxylamine came experiments showed O -methylation prevented hydroxamic acid. Distribution studies demonstrated considerable acyltransferase activity in kidney, stomach, small intestine, colon; lung spleen were less active; blood, brain, muscle essentially without activity. Tissue distribution protein utilizing techniques disclosed responsible for was inseparable transfers acetyl 4-aminoazobenzene. Acyltransferase-catalyzed -2-fluorenylpropionamide not restricted acetylated derivatives. Hepatic acyltransferase-catalyzed formation fluorenylamine-substituted acid inhibited both arylamines arylacetamides. This inhibition, considered previous reports inhibition hepatocarcinogenesis acetanilide p -hydroxyacetanilide, suggest arylhydroxamic may involved tumors.