Best C J, McKelvey-Martin V J, McKenna P G
Department of Biological and Biomedical Sciences, University of Ulster at Coleraine, N. Ireland, UK.
Mutat Res. 1994 Sep 1;309(2):235-42. doi: 10.1016/0027-5107(94)90097-3.
In this study the effect of thymidine kinase (TK) deficiency on mutagen sensitivity was examined in the human lymphoblastoid cell line Raji. Wild-type and TK-deficient Raji cells were treated with a range of concentrations of ethyl methanesulphonate (EMS) and a range of doses of ultraviolet (UV) light, then examined for mutagen sensitivity as measured by cell survival and mutation to HGPRT deficiency. Dose-dependent responses were observed and TK-deficient cells exhibited decreased survivals and increased mutant frequencies relative to wild-type cells. TK-deficient Raji cells are also deficient in O6-methylguanine-DNA-methyltransferase. This may partially account for their sensitivity to EMS but does not account for the results obtained with UV. It is therefore likely that an additional factor, such as alterations in supply of deoxyribonucleoside triphosphates, may affect the mutagen sensitivity of Raji cells.
在本研究中，在人淋巴母细胞系Raji中检测了胸苷激酶（TK）缺乏对诱变敏感性的影响。用一系列浓度的甲磺酸乙酯（EMS）和一系列剂量的紫外线（UV）处理野生型和TK缺陷型Raji细胞，然后通过细胞存活和对次黄嘌呤鸟嘌呤磷酸核糖转移酶（HGPRT）缺乏的突变来检测诱变敏感性。观察到剂量依赖性反应，相对于野生型细胞，TK缺陷型细胞的存活率降低，突变频率增加。TK缺陷型Raji细胞也缺乏O6-甲基鸟嘌呤-DNA甲基转移酶。这可能部分解释了它们对EMS的敏感性，但不能解释用UV获得的结果。因此，很可能还有一个额外的因素，如脱氧核糖核苷三磷酸供应的改变，可能会影响Raji细胞的诱变敏感性。
