期刊
JOURNAL OF TOXICOLOGICAL SCIENCES
卷 41, 期 6, 页码 719-730出版社
JAPANESE SOC TOXICOLOGICAL SCIENCES
DOI: 10.2131/jts.41.719
关键词
Acrylamide; Glycidamide; Big Blue mice; Brain; Mutation frequency; Mutation spectrum
类别
资金
- China Scholarship Council
- National Center for Toxicological Research
- International Scientist Exchange Program (ISEP) at the U.S. Food and Drug Administration (FDA)
Potential health risks for humans from dietary exposure to acrylamide (AA) and its reactive epoxide metabolite, glycidamide (GA), exist because substantial amounts of AA are found in a variety of fried and baked starchy foods. AA is tumorigenic in rodents, and a large number of studies indicate that AA is genotoxic in multiple organs of mice and rats. Although AA is neurotoxic, there are no reports on AA-induced gene mutations in the mouse brain. Therefore, to investigate if gene mutation can be induced by AA or its metabolite GA, we screened brains for cli mutant frequency (MF) and scored for mutation types in previously treated male and female Big Blue mice with 0, 1.4 mM, and 7.0 mM AA or GA in drinking water for up to 4 weeks. High doses of AA and GA induced similar cII MFs in males and females but only the induced cII MF in males was significantly higher than the corresponding male control MF (p < 0.05). Molecular analysis of the cli mutants from males showed that AA and GA each induced at least a 2.5-fold increase in the incidence of G:C -> T:A, A:T -> T:A, and A:T -> C:G trans versions compared to the vehicle controls, with similar mutational spectra observed when comparing AA with GA treatment. These results suggest that the MFs and types of mutations induced by AA and GA in the brain are consistent with AA exerting its genotoxicity via metabolism to GA.
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