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本研究首先用化学突变剂MNNG处理人胃癌细胞系(BGC 823),以提高突变率。然后用递增浓度的鸟便嘌呤类似物8-AG选择次黄嘌呤-鸟便嘌呤磷酸核糖转移酶(HGPRT)缺陷细胞,8-AG递增浓度为1～20μg/ml,历时半年。获得抗8-AG毒性的突变细胞,在HAT培养基中不能生存。经HGPRT酶的同位素法测定,发现野生型与突变型的BGC 823细胞有明显差别。本文还对缺陷型BGC 823的A、B、C、D、E、F株的应用进行了讨论。
In this study, the human gastric cancer cell line (BGC 823) was first treated with the chemical mutant MNNG to increase the mutation rate. Hypoxanthine-aigoine phosphoribosyl transferase (HGPRT)-deficient cells were then selected with increasing concentrations of the aconitine analog 8-AG at progressively 8-AG concentrations of 1-20 μg/ml for six months. Mutant cells resistant to 8-AG were obtained and could not survive in HAT medium. As determined by the isotope method of HGPRT enzyme, it was found that the wild-type and mutant BGC 823 cells were significantly different. This article also discusses the application of the defective BGC 823 A, B, C, D, E and F strains.