Best C J, McKenna P G, McKelvey-Martin V J
Cancer and Ageing Research Group, School of Biomedical Sciences, University of Ulster at Coleraine, Londonderry, Northern Ireland, UK.
Br J Biomed Sci. 1997 Dec;54(4):267-72.
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.
在本研究中，研究了胸苷激酶缺乏对人淋巴母细胞系Raji对甲磺酸甲酯和丝裂霉素C反应的影响。通过细胞存活情况以及对次黄嘌呤-鸟嘌呤磷酸核糖转移酶缺乏的突变情况来衡量诱变敏感性。与野生型细胞相比，在用每种诱变剂处理后，胸苷激酶缺陷的Raji细胞存活能力下降，突变频率增加。这表明这可能是由于脱氧核糖核苷三磷酸供应与切除修复过程失衡所致。还讨论了O6-甲基鸟嘌呤-DNA甲基转移酶在这些诱变剂引起的DNA损伤修复中的作用。
