Wade M H, Trosko J E
Mutat Res. 1983 Aug;112(4):231-43. doi: 10.1016/0167-8817(83)90009-3.
The effect of pyrimidine dimers on cytotoxicity, DNA repair and mutagenesis was studied in cells, derived from the rat kangaroo, which possess photoreactivating capabilities. A significant enhancement in colony-forming ability was achieved after UV irradiation in exponentially growing cells if photoreactivating light treatment followed the UV irradiation. If photoreactivation treatment was delayed 24 h after UV irradiation, no significant increase in survival was observed. Assays of pyrimidine dimers, unscheduled DNA synthesis, and survival in contact-inhibited cells all confirmed a minor role of dark excision repair and a major role of photoreactivation. Photoreactivation decreased the frequency of mutations to 6-thioguanine resistance to a greater extent than the alteration seen in survival. Approximately 1.6 times the dose must be given to get equal killing in photoreactivated cells, whereas 4 times the dose must be given to obtain equal mutation frequencies in light-treated cells. This suggests that the removal of dimers is more effective in mutant reduction than enhancement of survival.
