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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 53-63 |
| Number of pages | 11 |
| Journal | Mutation Research DNA Repair Reports |
| Volume | 193 |
| Issue number | 1 |
| DOIs | |
| State | Published - 1988 |
| Externally published | Yes |
Keywords
- (6-4)Photoproducts
- Cyclobutane dimers
- DNA excision repair
- Split-dose recovery
ASJC Scopus subject areas
- Medicine(all)