Genotoxic effects of acrylamide and glycidamide in mouse lymphoma cells.
作者： Nan Mei , Jiaxiang Hu , Mona I. Churchwell , Lei Guo , Martha M. Moore
DOI: 10.1016/J.FCT.2007.09.093
关键词:
摘要: In addition to occupational exposures acrylamide (AA), concerns about AA health risks for the general population have been recently raised due finding of in food. this study, we evaluated genotoxicity and its metabolite glycidamide (GA) L5178Y/Tk(+/-) mouse lymphoma cells. The cells were treated with 2-18 mM or 0.125-4 GA 4 h without metabolic activation. DNA adducts, mutant frequencies types mutations examined. Within dose range tested, induced adducts adenine guanine [N3-(2-carbamoyl-2-hydroxyethyl)-adenine N7-(2-carbamoyl-2-hydroxyethyl)-guanine] a linear dose-dependent manner. levels consistently 60-fold higher across than those adenine. contrast, no GA-derived found any concentrations AA, consistent lack conversion GA. However, frequency was significantly increased by at 12 higher. mutagenic starting 2mM dose, suggesting that is much more AA. increasing GA, mainly an increase proportion small colony mutants. To elucidate underlying mechanism, examined loss heterozygosity (LOH) four microsatellite loci spanning entire chromosome 11 mutants Compared mutations, whose LOH extended D11Mit22 D11Mit74, alteration larger half chromosome. Statistical analysis mutational spectra revealed significant difference between treatments (P=0.018). These results suggest although both generate through clastogenic mode action cells, induces via adduct mechanism whereas not involving formation adducts.
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