Disease relevance of N-ethyl-N-methyl-nitrous amide

• At low doses, N-nitrosomethylethylamine (NMEA) selectively produces liver tumors in rats, whereas beta-trideuterated NMEA also includes esophageal carcinomas under these conditions [1].

High impact information on N-ethyl-N-methyl-nitrous amide

• Bioactivation of N-nitrosomethylethylamine can be initiated by hydroxylation of either the methyl or ethyl moiety leading to an ethylating or methylating intermediate, respectively [2].
• Methylation versus ethylation of DNA in target and nontarget tissues of Fischer 344 rats treated with N-nitrosomethylethylamine [2].
• Dimethylnitrosamine, diethylnitrosamine, and methylethylnitrosamine were metabolized by microsomes from noninduced male Fischer rat liver, and the aldehydes produced by these reactions were examined [3].
• Beta-deuteration of N-nitrosoethylmethylamine causes a shift in DNA methylation from rat liver to esophagus [4].
• While N-nitrosoethylmethylamine (NEMA) is carcinogenic primarily for the liver, its beta-trideuterated derivative, N-nitroso( [2-D3]ethyl)methylamine (NEMA-d3), also produces a high incidence of tumors in the esophagus [4].

Biological context of N-ethyl-N-methyl-nitrous amide

• Single-dose toxicokinetics of N-nitrosomethylethylamine and N-nitrosomethyl (2,2,2-trideuterioethyl)amine in the rat [5].

Anatomical context of N-ethyl-N-methyl-nitrous amide

• The metabolism of benzo[a]pyrene, aflatoxin B1, N-nitrosodimethylamine, N-nitrosoethylmethylamine, and N-nitrosopyrrolidine has been studied in cultures of normal human and rat urinary bladder epithelial cells [6].
• The present results do not indicate that hepatocytes take an 'intermediate' position between existing in vitro and in vivo activation systems, although they do suggest that these mouse hepatocyte preparations activate the nitrosamines DMNA and MENA in a quantitatively or qualitatively different way than do mouse-liver homogenates [7].

Associations of N-ethyl-N-methyl-nitrous amide with other chemical compounds

• Highest levels of hepatic DNA methylation were found with N-nitrosodimethylamine (C1) and N-nitrosomethylethylamine (C2), the most potent hepatocarcinogens in this series [8].
• Although the mouse hepatocytes retained their activating capacity longer than S9 preparations did during incubation at 37 degrees C, the latter gave much higher yields of mutants with 10 mM (DMNA, MENA, DMH) and 5 mM (CP) of 4 out of the 5 compounds [7].
• All the N-nitrosamine compounds tested increased the activity of glutathione reductase except ethylmethylnitrosamine had no effect [9].
• Detection of metabolites of N-nitrosopyrrolidine and N-nitrosoethylmethylamine in cultures of human bladder epithelial cells of normal origin [10].
• In vitro binding of the tobacco-specific nitrosamines, methylethylnitrosamine (MEN) and nitrosonornicotine (NNN), to exogenous DNA and guanosine was studies in a rat liver microsome-catalyzed system [11].

Gene context of N-ethyl-N-methyl-nitrous amide

• P-450ac also catalyzed the oxygenation of N-nitrosomethylethylamine and aniline and the activity was enhanced slightly by cytochrome b5 [12].
• P450ac was also active in the metabolism of N-nitrosoethylmethylamine (NEMA), but was less active than phenobarbital-inducible cytochrome P450 (P450b) in the metabolism of N-nitrosobutylmethylamine (NBMA), especially in catalysing the debutylation reaction [13].

References