Fornace A J, Seres D S
Radiat Res. 1983 Jan;93(1):107-11.
In this investigation, xeroderma pigmentosum (XP) fibroblasts, XP12BE, were uv-irradiated and then incubated with cytosine arabinoside and hydroxyurea for 4 hr to inhibit the polymerase step of DNA excision repair. By alkaline elution, DNA single-strand breaks (SSB) were detected in XP cells with this regimen with an efficiency of 0.1-0.2 SSB per 10(9) daltons of DNA per J m-2. There was an approximately linear relation between the SSB frequency and uv dose over a range of 0.2 to 25 J m-2. This effect was approximately two orders of magnitude greater in excision-proficient normal human fibroblasts than in XP cells. These results support the conclusion that a low residual level of DNA excision repair occurs in XP group A cells and that the SSB generated during this repair can be accumulated with this polymerase inhibitor.
在本研究中,对着色性干皮病(XP)成纤维细胞XP12BE进行紫外线照射,然后与阿糖胞苷和羟基脲一起孵育4小时,以抑制DNA切除修复的聚合酶步骤。通过碱性洗脱,用该方案在XP细胞中检测到DNA单链断裂(SSB),效率为每焦耳每平方米0.1-0.2个SSB/10⁹道尔顿DNA。在0.2至25焦耳每平方米的范围内,SSB频率与紫外线剂量之间存在近似线性关系。在切除功能正常的正常人成纤维细胞中,这种效应比在XP细胞中大约大两个数量级。这些结果支持以下结论:在XP A组细胞中发生低水平的DNA切除修复残留,并且在这种修复过程中产生的SSB可以被这种聚合酶抑制剂积累。