De Weerd-Kastelein E A, Keijzer W, Rainaldi G, Bootsma D
Mutat Res. 1977 Nov;45(2):253-61. doi: 10.1016/0027-5107(77)90025-2.
The role of DNA repair mechanisms in the induction of sister chromatid exchanges (SCE) after exposure to ultraviolet radiation was investigated in xeroderma pigmentosum cells. Cells from different excision-deficient XP strains, representing the 5 complementation groups in XP, A, B, C, D and E, and from excision-proficient XP variant strains were irradiated with low doses of UVR (0-3.5 J/m2). The number of SCE was counted after two cycles in the presence of BUdR. In cells of the complementation groups A, B, C and D the number of SCE was significantly higher than in UV-exposed control cells. The frequencies of SCE in group E cells and in XP varient cells were not different from those in control cells. Treatment with caffeine (0-200 microgram/ml) did not result in a different response of variant cells compared with normal cells. A simple correlation between SCE frequency and residual excision-repair activity was not observed. The response of the excision-repair deficient cells suggest that unrepaired damage, produced by UVR is involved in the production of SCE.
在着色性干皮病细胞中研究了DNA修复机制在紫外线辐射后诱导姐妹染色单体交换（SCE）中的作用。来自不同切除缺陷型XP菌株（代表XP中的5个互补组，即A、B、C、D和E组）以及切除功能正常的XP变异株的细胞，用低剂量的紫外线辐射（0 - 3.5 J/m2）进行照射。在存在溴脱氧尿苷（BUdR）的情况下经过两个细胞周期后，对SCE的数量进行计数。在互补组A、B、C和D的细胞中，SCE的数量显著高于紫外线照射的对照细胞。E组细胞和XP变异细胞中SCE的频率与对照细胞中的频率没有差异。用咖啡因（0 - 200微克/毫升）处理后，变异细胞与正常细胞相比没有产生不同的反应。未观察到SCE频率与残余切除修复活性之间的简单相关性。切除修复缺陷细胞的反应表明，紫外线辐射产生的未修复损伤参与了SCE的产生。
