Thielmann H W, Edler L, Friemel S
J Cancer Res Clin Oncol. 1986;112(3):245-57. doi: 10.1007/BF00395919.
A total of 45 XP fibroblast strains from the Mannheim XP Collection (representatives of XP complementation groups A, C, D, E, F or G, I, and XP variants) were investigated for colony-forming ability (term: D0) after treatment with up to ten doses of the methylating carcinogen MeSO2OMe. As controls 16 fibroblast strains from normal donors were used. Except for 4 XP strains (1 from group C and 3 from group D) which, however, were borderline cases, none of the remaining 41 XP strains was found to be more sensitive than normal controls. This held true within the limits of an experimental accuracy (experimental variability of D0 values) of +/- 7%. When weighted means were calculated for XP complementation groups and compared with that of normal donors at a significance level of 5%, no significant difference was detected. In contrast, after exposure of 6 XP group D strains to MeNOUr, a weighted mean D0 value was obtained which was significantly decreased by 27%. Unscheduled DNA synthesis (term: G0 which serves as a measure of excision repair) after exposure to MeNOUr was quantitatively the same (experimental variability: +/- 8%) both in the group of normal strains and in most of the XP complementation groups. Exceptions were group E and group F (or G) which had higher, and group I which had lower repair. Analogous G0 values measured after exposure to MeSO2OMe (experimental variability: +/- 13%), however, differed from that of the control strains: they were lower in XP complementation groups A, D, E, F (or G), and I. However, groups A, E, F (or G), and I including only 3 individual strains or less may be considered to be possibly ill-represented. Yet, group D including 11 XP strains did show reduction of the mean G0 value by 35%. From this it is concluded that there are repair defects in XP group D strains with regard to MeSO2OMe-induced adducts. These defects seem to be small.
对来自曼海姆着色性干皮病（XP）细胞株库的总共45株XP成纤维细胞株（代表XP互补组A、C、D、E、F或G、I以及XP变异型），在用高达十剂甲基化致癌物甲磺酸甲酯（MeSO2OMe）处理后，研究其集落形成能力（术语：D0）。作为对照，使用了16株来自正常供体的成纤维细胞株。除了4株XP细胞株（1株来自C组，3株来自D组），不过这几株属于临界情况外，其余41株XP细胞株中没有发现比正常对照更敏感的。在实验精度（D0值的实验变异性）为±7%的范围内，情况确实如此。当计算XP互补组的加权平均值并与正常供体的加权平均值在5%的显著性水平上进行比较时，未检测到显著差异。相比之下，6株XP D组细胞株暴露于甲基硝基亚硝基胍（MeNOUr）后，获得的加权平均D0值显著降低了27%。在正常细胞株组和大多数XP互补组中，暴露于MeNOUr后的非预定DNA合成（术语：G0，用作切除修复的指标）在数量上是相同（实验变异性：±8%）。例外的是E组和F（或G）组，它们的修复较高，而I组的修复较低。然而，暴露于MeSO2OMe后测得的类似G0值（实验变异性：±13%）与对照细胞株不同：在XP互补组A、D、E、F（或G）和I中较低。然而，A组、E组、F（或G）组和I组每组仅包含3株或更少的个体细胞株，可能被认为代表性不足。不过，包含11株XP细胞株的D组确实显示平均G0值降低了35%。由此得出结论，XP D组细胞株在MeSO2OMe诱导的加合物方面存在修复缺陷。这些缺陷似乎较小。
