Fornace A J, Seres D S
Mutat Res. 1982 Jun;94(2):277-84. doi: 10.1016/0027-5107(82)90291-3.
In this investigation the persistence of DNA-protein crosslinks (DPC) induced by trans-Pt was determined in normal and excision-deficient xeroderma pigmentosum (XP) group A fibroblasts. After exposure to 50 microM trans-Pt for 2 h, the level of DPC increased in both cell types for several hours but by 12 h it was significantly less in normal cells. By 18 h it was approximately half the maximal value in normal cells but had decreased little in XP cells. When cells were incubated with trans-Pt and polymerase inhibitor, DNA single-strand breaks accumulated in normal but to a much lower level in XP cells. These single-strand breaks were presumably produced during excision repair and were roughly comparable in frequency to the number of DPC removed in normal cells during the same interval. By colony survival, trans-Pt was more toxic to XP cells. These results indicate that DPC were recognized in normal cells and repaired by the excision repair pathway.
在本研究中，测定了反式铂诱导的DNA-蛋白质交联（DPC）在正常和切除缺陷型色素性干皮病（XP）A组成纤维细胞中的持久性。暴露于50微摩尔反式铂2小时后，两种细胞类型中的DPC水平均在数小时内升高，但到12小时时，正常细胞中的DPC水平显著降低。到18小时时，其约为正常细胞中最大值的一半，但在XP细胞中降低很少。当细胞与反式铂和聚合酶抑制剂一起孵育时，DNA单链断裂在正常细胞中积累，但在XP细胞中积累水平低得多。这些单链断裂大概是在切除修复过程中产生的，其频率与同一时间段内正常细胞中去除的DPC数量大致相当。通过集落存活实验，反式铂对XP细胞毒性更大。这些结果表明，DPC在正常细胞中被识别并通过切除修复途径进行修复。
