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Dimethylnitrosamine genotoxicity: does N-acetyltransferase activity play a role?
P D Josephy1, H L Lord, V A Snieckus
1Guelph-Waterloo Centre for Graduate Work in Chemistry, Department of Chemistry and Biochemistry, University of Guelph, Ontario, Canada.
Carcinogenesis
|March 1, 1994
Summary
Dimethylnitrosamine (DMN) genotoxicity was assessed using bacterial assays. Results indicate that acetyl CoA:arylamine N-acetyltransferase (NAT) activity is not a major factor in DMN
Area of Science:
- Toxicology
- Genetics
- Biochemistry
Background:
- Dimethylnitrosamine (DMN) is a known carcinogenic nitrosamine.
- The role of metabolic activation in DMN genotoxicity is under investigation.
Purpose of the Study:
- To evaluate the genotoxicity of DMN using bacterial test systems.
- To determine the involvement of acetyl CoA:arylamine N-acetyltransferase (NAT) in DMN's metabolic activation.
Main Methods:
- Assessed DMN genotoxicity via umu operon induction (lacZ gene fusion) and Ames mutagenicity assay.
- Utilized three Salmonella typhimurium strains with varying NAT enzyme expression levels.
Main Results:
- No increased sensitivity to DMN was observed in a strain overexpressing NAT.
- The study contradicts previous reports on NAT's role in DMN genotoxicity.
Conclusions:
- Metabolic activation by NAT does not appear to be a significant contributor to DMN genotoxicity.
- Further research may be needed to elucidate other metabolic pathways involved in DMN's carcinogenic effects.