Repair of non-dimer DNA damages in ICB 2A frog cells exposed to solar-ultraviolet radiation in the UVB (290-320 nm) range

The purpose of the research described in this dissertation was to investigate the repair and cellular consequences of non-dimer DNA damages induced by solar-UV irradiation of cultured I CR 2A (Rana pipiens) frog cells. Because this cell line is proficient in enzymatic photoreactivation, it was possible to induce a relatively pure population of non-dimer DNA photoproducts by exposure of cells to the Mylar-filtered solar-UV wavelengths produced by a fluorescent sunlamp followed by treatment with photoreactivating light. With a modification of bromodeoxyuridine photolysis assay, it was found that the solar-UV-induced non-dimer DNA damages were repaired by a short-patch repair mechanism in which less than 20 nucleotides were inserted into a repaired region. Similar results were also obtained for γ-irradiated cells. In contrast, excision repair of 254 nm-induced dimers was accomplished by a long-patch process in which an average of about 180 nucleotides were inserted into the repaired sites. A mutant cell line, DRP 36, hypersensitive to non-dimer DNA damages, was isolated from I CR 2A cells. It was found that the DRP 36 cells performed a significantly lower level of excision repair following the induction of non-dimer DNA damages. The results are consistent with the conclusion that the DRP 36 cells are deficient in the repair of at least one type of solar-UV-induced non-dimer DNA lesion. These experiments indicate that solar-UV-induced non-dimer DNA photoproducts behave more like the photoproducts of γ-rays than those of far-UV radiation, which are primarily pyrimidine dimers