Repair of (6-4)photoproducts correlates with split-dose recovery in UV-irradiated normal and hypersensitive rodent cells.
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.
Mitchell
D L
DL
University of Texas System Cancer Center, Science Park-Research Division, Smithville 78957.
Humphrey
R M
RM
Adair
G M
GM
Thompson
L H
LH
Clarkson
J M
JM
D000818:Animals; D002460:Cell Line; D006224:Cricetinae; D004247:DNA / Q000528:radiation effects*; D004249:DNA Damage; D004260:DNA Repair; D004261:DNA Replication; D004307:Dose-Response Relationship, Radiation; D004706:Endodeoxyribonucleases / Q000378:metabolism; D007158:Immunologic Techniques; D009154:Mutation / Q000528:radiation effects*; D011740:Pyrimidine Dimers / Q000378:metabolism; D014466:Ultraviolet Rays
D011740:Pyrimidine Dimers; D004247:DNA; D004706:Endodeoxyribonucleases; C026044:deoxyribonuclease V