作者: L M Hallberg , R el Zein , L Grossman , W W Au
关键词: Gene mutation 、 Reporter gene 、 Mutation 、 Genotoxicity 、 Molecular biology 、 Xeroderma pigmentosum 、 DNA repair 、 Host-Cell Reactivation 、 DNA damage 、 Biology
摘要: We hypothesize that chronic exposure to environmental toxicants can induce genetic damage causing DNA repair deficiencies and leading the postulated mutator phenotype of carcinogenesis. To test our hypothesis, a host cell reactivation (HCR) assay was used in which pCMVcat plasmids were damaged with UV light (175, 350 J/m{sup 2} light), inactivating chloramphenicol acetyltransferase reporter gene, then transfected into lymphocytes. Transfected lymphocytes therefore challenged plasmids, reactivating gene. Xeroderma pigmentosum (XP) Gaucher lines as positive negative controls for HCR assay. The line repaired normally but XP demonstrated lower activity. Additionally, activity heterozygous showed intermediate compared homozygous cells. measure effects benzene on 12 exposed 8 nonexposed workers from local plant. Plasmids 175 mean frequency 66% 58%, respectively, control 71% 62% workers. Conversely, more grouped reduced category than controls. These differences inmore » capacity between were, however, not statistically significant. lack significant groups may be due extremely low (<0.3 ppm), small population size, or genotoxicity at these concentrations. results are consistent parallel hprt gene mutation 26 refs., 4 figs., 2 tabs.« less