Repair of (6-4)photoproducts correlates with split-dose recovery in UV-irradiated normal and hypersensitive rodent cells

Mutation Research/DNA Repair Reports Pub Date : 1988-01-01 DOI:10.1016/0167-8817(88)90007-7

David L. Mitchell , Ronald M. Humphrey , Gerald M. Adair , Larry H. Thompson , Judith M. Clarkson

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引用次数: 44

Abstract

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 defectiev in the UV-sensitive cells. In contrast, only 20-–60% of antibody-binding sites specific for cylcobutane 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 pf (6-4)photoproducts accounts for split-dose recovery. In addition, we conclude thtat a consequences of DNA repair in CHO cells is modification rather that reemoval of cylobutane dimers.

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(6-4)光产物的修复与紫外线照射下正常和超敏感啮齿动物细胞的分剂量恢复相关

用中国仓鼠卵巢细胞和两种紫外线敏感衍生物来确定DNA切除修复对分剂量恢复的重要性。在野生型细胞中，当每隔2小时给药时，观察到75%的最大理论回收率。两种超敏细胞系几乎没有明显的恢复。利用(6-4)光产物和环丁烷二聚体特异性放射免疫测定，测定了紫外线照射下代表5个互补基团的修复缺陷细胞修复这2个光产物的能力。(6-4)光产物特异性抗体结合位点的去除在6小时内完成80%，并且在紫外线敏感细胞中存在缺陷。相比之下，只有20- 60%的环丁烷二聚体特异性抗体结合位点在辐照后18小时被去除，并且在正常和缺陷细胞系中去除的程度相同。我们得出的结论是，修复pf(6-4)光产物占分剂量恢复。此外，我们得出结论，CHO细胞DNA修复的结果是修饰而不是去除环丁烷二聚体。

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Mutation Research/DNA Repair Reports

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