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

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

Research output: Contribution to journalArticle

44 Scopus citations

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 languageEnglish (US)
Pages (from-to)53-63
Number of pages11
JournalMutation Research DNA Repair Reports
Volume193
Issue number1
DOIs
StatePublished - 1988
Externally publishedYes

Keywords

  • (6-4)Photoproducts
  • Cyclobutane dimers
  • DNA excision repair
  • Split-dose recovery

ASJC Scopus subject areas

  • Medicine(all)

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