3-N-Nitroso-N-methylaminopyridine

3-N-Nitroso-N-methylaminopyridine (1-10 mM; 20 min) is metabolized by liver microsomes from phenobarbital-pretreated male BD VI rats, with its metabolism proceeding mainly through inactivation pathways (denitrosation, N-oxidation) and only minimal activation-demethylation activity^[1].
3-Nitroso-N-methylaminopyridine (10-50 mM; 1-4 h) directly induces VAL^R and NAL^R forward mutations in E. coli K-12/343/113 cells without requiring mammalian metabolic activation^[2].
3-Nitroso-N-methylaminopyridine (10-50 mM; 4 h) does not induce VAL^R forward mutations in Escherichia coli K-12/343/113 cells when incubated with Aroclor-induced rat liver S-9 fractions^[2].
3-Nitroso-N-methylaminopyridine (10-50 mM; 1-4 h, 60-240 min) does not induce VAL^R forward mutations in Escherichia coli K-12/343/113 cells when incubated with Aroclor-induced rat liver microsomal fractions^[2].
The direct mutagenic activity of 3-Nitroso-N-methylaminopyridine (30 mM; 4 h) in Escherichia coli K-12/343/113 cells is completely abolished upon co-incubation with Aroclor-induced rat liver S-100 fraction^[2].
3-Nitroso-N-methylaminopyridine (1.5-12 mM; 15 min) reacts directly with cysteine in a concentration-dependent manner without requiring metabolic activation by Escherichia coli K-12/343/113 cells^[2].
3-Nitroso-N-methylaminopyridine (30 mM; 4 h) does not induce significant VAL^R or NAL^R forward mutations in Escherichia coli K-12/343/113 cells when incubated with uninduced mouse liver S-9 or microsomal fractions^[2].
3-N-Nitroso-N-methylaminopyridine shows no mutagenic activity in Salmonella typhimurium TA100^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.