The metabolism of N-nitrosodiethanolamine (NDELA) was studied to assess whether the formation of the β-oxidated metabolites N-(2-hydroxyethyl)N-(formylmethyl)nitrosamine (EFMN) and N-(2-hydroxyethyl)-N-(carboxy-methyl)nitrosamine (ECMN) is involved in the mechanism of tumor induction in various animal species with different susceptibility to NDELA carcinogenicity. In vitro studies using liver S9 fractions from rats, hamster, B6C3F1 and CD-1 mice and rabbits showed that all the animal species metabolize NDELA through the β-oxidation pathway, although to different extents. Urinary excretion of NDELA and its metabolite ECMN in rats, hamsters and mice after 5 mg·kg-1 NDELA i.p. confirmed these findings. The results suggest there is no correlation between carcinogenesis by NDELA and its β-oxidation. The possibility that ECMN formation might represent a detoxifying metabolic pathway for NDELA is discussed.
- Animal species
- gas chromatography-thermal energy analysis
- In vitro-in vivo metabolism
- trimethylsilyl derivative
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