Cytogenetic Damage Induced by Acrylamide and Glycidamide in Mammalian Cells: Correlation with Specific Glycidamide-DNA Adducts

Acrylamide (AA) is a suspected human carcinogen generated in carbohydrate-rich foodstuffs upon heating. Glycidamide (GA), formed via epoxidation, presumably mediated by cytochrome P450 2E1, is thought to be the active metabolite playing a central role in AA genotoxicity. In this work we investigated DNA dam-age induced by AA and GA in mammalian cells, using V79 Chinese hamster cells. For this purpose, we evaluated two cytogenetic end points, chromosomal aberrations (CAs) and sister chromatid ex-changes (SCEs), as well as the levels of specific GA-DNA adducts, namely, N7-(2-carbamoyl-2-hydroxyethyl)guanine (N7-GA-Gua) and N3-(2-carbamoyl-2-hydroxyethyl)adenine (N3-GA-Ade) using high-performance liquid chromatographycoupledwith tandemmass spectrometry. GAwasmore cytotoxic and clastogenic than AA. Both AAandGAinducedCAs (breaks andgaps) anddecreased themitotic index. GA induced SCEs in a dose-responsive manner; with AA