Gantt R, Taylor W G, Camalier R F, Stephens E V
Cancer Res. 1984 May;44(5):1809-12.
DNA-protein cross-links are induced in mammalian cells by X-rays, ultraviolet light, fluorescent light, and numerous chemical carcinogens. Others have shown that these cross-links are repaired by normal cells but that excision repair-deficient xeroderma pigmentosum (XP) Group A cells, XP12BE, are deficient in repair of these bulky adducts. This paper compares the DNA-protein cross-link repair competency of another XP Group A strain, XP20S, with its more rapidly proliferating simian virus 40-transformed derivative line and with normal human skin fibroblasts. DNA-protein cross-links were induced with 20 microM transplatinum(II)diamminedichloride and assayed by the membrane alkaline elution procedure of Kohn. Treated and untreated cells are lysed on a polycarbonate membrane filter, and the coelution rates of the DNA at pH 12.2 are compared; DNA-protein cross-links retard elution of DNA. The repair competency of XP20S cells for trans-platinum(II)diamminedichloride-induced DNA-protein cross-links was similar to that of XP12BE cells, but the competency of the simian virus 40-transformed XP20S cells was nearly equal to that of normal human skin fibroblasts. These results suggest that either cell cycling compensates for the genetic deficiency present in the nucleotide excision process of XP Group A cells or that a process other than nucleotide excision can repair these lesions; this process requires cell cycling or activation by the virus.
X射线、紫外线、荧光以及众多化学致癌物可在哺乳动物细胞中诱导产生DNA-蛋白质交联。其他人已经表明，这些交联可被正常细胞修复，但切除修复缺陷的色素性干皮病（XP）A组细胞（XP12BE）在修复这些大分子加合物方面存在缺陷。本文比较了另一株XP A组细胞系XP20S及其增殖更快的猿猴病毒40转化衍生细胞系与正常人皮肤成纤维细胞的DNA-蛋白质交联修复能力。用20微摩尔的反式二氯二氨合铂（II）诱导产生DNA-蛋白质交联，并通过科恩的膜碱性洗脱程序进行检测。将处理过和未处理的细胞裂解在聚碳酸酯膜滤器上，比较pH值为12.2时DNA的共洗脱速率；DNA-蛋白质交联会延缓DNA的洗脱。XP20S细胞对反式二氯二氨合铂（II）诱导的DNA-蛋白质交联的修复能力与XP12BE细胞相似，但猿猴病毒40转化的XP20S细胞的修复能力几乎与正常人皮肤成纤维细胞相当。这些结果表明，要么细胞周期可弥补XP A组细胞核苷酸切除过程中存在的遗传缺陷，要么存在一种除核苷酸切除以外的过程来修复这些损伤；该过程需要细胞周期或病毒激活。
