Kaufman E R, Davidson R L
Proc Natl Acad Sci U S A. 1978 Oct;75(10):4982-6. doi: 10.1073/pnas.75.10.4982.
Studies were undertaken to determine how a line of mutant Syrian hamster melanoma cells (HAB-2E) that displays unlimited growth potential when all of the thymine residues in nuclear DNA are replaced by bromouracil (BrUra) could avoid the deleterious effects of bromodeoxyuridine (BrdUrd) mutagenicity. It was found that BrdUrd could be mutagenic to these cells. However, there was a nonlinear relationship between mutagenicity and the amount of BrUra in the DNA of the HAB-2E cells. With these cells, mutagenicity apparently is determined by the concentration of BrdUrd to which the cells are exposed rather than the amount of BrUra in DNA. These results were obtained with both the induction of ouabain resistance and thioguanine resistance as markers for mutagenesis. The dependence of BrdUrd mutagenicity on BrdUrd concentration was also observed for the parental melanoma cells.
开展了多项研究,以确定当核DNA中所有胸腺嘧啶残基被溴尿嘧啶(BrUra)取代时表现出无限生长潜能的叙利亚仓鼠黑色素瘤细胞系(HAB - 2E)如何避免溴脱氧尿苷(BrdUrd)致突变性的有害影响。研究发现,BrdUrd对这些细胞具有致突变性。然而,HAB - 2E细胞DNA中致突变性与BrUra含量之间存在非线性关系。对于这些细胞,致突变性显然由细胞所接触的BrdUrd浓度决定,而非DNA中BrUra的含量。这些结果是通过诱导哇巴因抗性和硫鸟嘌呤抗性作为诱变标记获得的。在亲代黑色素瘤细胞中也观察到了BrdUrd致突变性对BrdUrd浓度的依赖性。