REPAIR OF TRANS-PT(II)DIAMMINEDICHLORIDE DNA PROTEIN CROSSLINKS IN NORMAL AND EXCISION-DEFICIENT HUMAN-CELLS
REPAIR OF TRANS-PT(II)DIAMMINEDICHLORIDE DNA PROTEIN CROSSLINKS IN NORMAL AND EXCISION-DEFICIENT HUMAN-CELLS
复制标题
DOI：
10.1016/0027-5107(82)90291-3
复制
发表时间：
1982-01-01
期刊：
影响因子：
--
通讯作者：
SERES, DS
中科院分区：
文献类型：
--
作者：
FORNACE, AJ;SERES, DS
在这项调查中，持续的DNA-蛋白质交联（DPC）诱导的反式铂在正常和切除缺陷性着色性干皮病（XP）A组成纤维细胞。在暴露于50 μ M trans-Pt 2小时后，DPC水平在两种细胞类型中增加了数小时，但到12小时时，它在正常细胞中显著减少。到18小时，它大约是正常细胞中最大值的一半，但在XP细胞中几乎没有下降。当细胞与trans-Pt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细胞中达到低得多的水平。这些单链断裂可能是在切除修复过程中产生的，并且在频率上与相同时间间隔内正常细胞中去除的DPC数量大致相当。通过集落存活，trans-Pt对XP细胞的毒性更大。DPC在正常细胞中被明显识别，并通过切除修复途径进行修复。
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 .mu.M 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. DPC were evidently recognized in normal cells and repaired by the excision repair pathway.