Mitchell D L, Humphrey R M, Adair G M, Thompson L H, Clarkson J M
University of Texas System Cancer Center, Science Park-Research Division, Smithville 78957.
Mutat Res. 1988 Jan;193(1):53-63. doi: 10.1016/0167-8817(88)90007-7.
Chinese hamster ovary cells and two UV-hypersensitive derivatives were used to determine the importance of DNA excision repair for split-dose recovery. In the wild-type cells 75% of the maximum theoretical recovery was observed when the fractions were delivered at 2-h intervals. Very little recovery was evident in the two hypersensitive cell lines. Using radioimmunoassays specific for (6-4)photoproducts and cyclobutane dimers, the ability of UV-irradiated repair-deficient cells representing 5 complementation groups to repair these 2 photoproducts was determined. Removal of antibody-binding sites specific for (6-4)photoproducts was 80% complete in 6 h and was defective in the UV-sensitive cells. In contrast, only 20-60% of antibody-binding sites specific for cyclobutane dimers were removed 18 h post-irradiation, and the extent of removal was the same in normal and defective cell lines. We conclude that repair of (6-4)photoproducts accounts for split-dose recovery. In addition, we conclude that a consequence of DNA repair in CHO cells is modification rather than removal of cyclobutane dimers.
利用中国仓鼠卵巢细胞和两种紫外线敏感衍生物来确定DNA切除修复对分次剂量恢复的重要性。在野生型细胞中，当分次剂量以2小时的间隔给予时，观察到最大理论恢复率的75%。在这两种敏感细胞系中，几乎没有明显的恢复。使用针对（6-4）光产物和环丁烷二聚体的放射免疫测定法，测定了代表5个互补组的紫外线照射修复缺陷细胞修复这两种光产物的能力。（6-4）光产物特异性抗体结合位点在6小时内80%被去除，且在紫外线敏感细胞中存在缺陷。相比之下，环丁烷二聚体特异性抗体结合位点在照射后18小时仅20%-60%被去除，且正常细胞系和缺陷细胞系的去除程度相同。我们得出结论，（6-4）光产物的修复导致分次剂量恢复。此外，我们得出结论，中国仓鼠卵巢细胞中DNA修复的一个结果是环丁烷二聚体的修饰而非去除。
