To demonstrate whether there are any pathways of nitrite formation from N-nitrosamines other than reductive denitrosation by cytochrome P-450 we performed the following experiments. An esterified alpha-hydroxylated nitrosamine was incubated in a microsomal system to test if nitrite generation is
With the use of rat liver preparations, the in vitro microsomal metabolism of methylethylnitrosamine, methyl-n-butylnitrosamine, and methyl(2-phenylethyl)nitrosamine labeled with deuterium in the methyl and alpha-methylene positions has been compared with that of the parent (unlabeled) compounds. All three forms of
We studied the metabolism of methyl-n-butyl-nitrosamine (MBN), a carcinogen for the rat esophagus and liver. The 2-, 3- and 4-hydroxy derivatives were identified as new metabolites of MBN. In studies on tissue slices freshly removed from MRC-Wistar rats, MBN metabolism
Metabolic activation may be a key step in determining the tissue specificity of carcinogenic nitrosamines. In previous work, we characterized P450IIE1 (an acetone/ethanol-inducible form of cytochrome P-450) as the major enzyme for the metabolic activation of N-nitrosodimethylamine. In this work
The organic solvents dimethylsulphoxide (DMSO), acetone, ethanol and dimethylformamide inhibited the mutagenic activity of the promutagens dimethylnitrosamine and methylbutylnitrosamine in a higher plant Arabidopsis thaliana. In contrast, the direct-acting mutagens N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and N-methyl-N-nitrosourea (MNU) were not affected by the
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