Mutagen sensitivity in thymidine kinase- and methyltransferase-deficient human lymphoblastoid cells.
In this study, the effect of thymidine kinase deficiency on the responses of the human lymphoblastoid cell line Raji to methyl methanesulphonate and mitomycin C was investigated. Mutagen sensitivity was measured in terms of cell survival and mutation to hypoxanthine-guanine phosphoribosyltransferase deficiency. Thymidine kinase-deficient Raji cells showed decreased survival and increased mutant frequency relative to wild-type cells following treatments with each of the mutagens used. It is suggested that this may be due to an imbalance in the supply of deoxyribonucleoside triphosphates to the excision repair process. The role of O6-methylguanine-DNA methyltransferase in the repair of DNA damage caused by these mutagens is also discussed.
Best
C J
CJ
Cancer and Ageing Research Group, School of Biomedical Sciences, University of Ulster at Coleraine, Londonderry, Northern Ireland, UK.
McKenna
P G
PG
McKelvey-Martin
V J
VJ
D002051:Burkitt Lymphoma / Q000201:enzymology* / Q000473:pathology; D002470:Cell Survival / Q000187:drug effects; D006801:Humans; D008780:Methyltransferases / Q000172:deficiency*; D009153:Mutagens / Q000494:pharmacology*; D013937:Thymidine Kinase / Q000172:deficiency*; D014407:Tumor Cells, Cultured / Q000187:drug effects
D009153:Mutagens; D008780:Methyltransferases; D013937:Thymidine Kinase