Cordeiro-Stone M, Boyer J C, Smith B A, Kaufmann W K
Carcinogenesis. 1986 Oct;7(10):1783-6. doi: 10.1093/carcin/7.10.1783.
Xeroderma pigmentosum (XP) variant cells are characterized by an abnormal pattern of replication of DNA damaged by 254 nm radiation (u.v.). To see whether benzo[a]pyrene-diol-epoxide-I (BPDE-I) elicits the same response, we have compared the effects of u.v. and BPDE-I on DNA replication in XP variant and normal skin fibroblasts. Doses of u.v. that only affected replicon initiation in normal cells, inhibited DNA strand growth in the XP variant. These results were confirmed by measurements of the rate of growth of single-stranded nascent DNA in cells synchronized at the beginning of the S phase. Identical analyses using BPDE-I, however, indicated that the two cell types were equally sensitive to the inhibitions of both replicon initiation and DNA strand growth. These results indicate that the XP variant phenotype cannot be recognized in vitro by the pattern of response of fibroblasts to the inhibition of DNA replication by BPDE-I.
着色性干皮病（XP）变异细胞的特征是，其被254纳米辐射（紫外线）损伤的DNA呈现异常的复制模式。为了观察苯并[a]芘二醇环氧化物-I（BPDE-I）是否引发相同反应，我们比较了紫外线和BPDE-I对XP变异皮肤成纤维细胞和正常皮肤成纤维细胞中DNA复制的影响。仅影响正常细胞中复制子起始的紫外线剂量，会抑制XP变异细胞中的DNA链生长。在S期开始时同步化的细胞中对单链新生DNA生长速率的测量结果证实了这些结果。然而，使用BPDE-I进行的相同分析表明，这两种细胞类型对复制子起始和DNA链生长的抑制同样敏感。这些结果表明，在体外无法通过成纤维细胞对BPDE-I抑制DNA复制的反应模式来识别XP变异表型。
