Inhibition of UV-induced DNA repair at different steps by quinacrine and anthralin

Abstract

Inhibition of DNA repair can result in accumulation of unrepaired and partially repaired lesions in DNA. Such lesions are important, not only for their primary disruption of information fidelity, but because they may serve as inducers for repair pathways which may be error prone. Inhibition of UV repair by quinacrine and anthralin (50μM each) was detected in 3H thymidine-labeled mouse L1210 cells by sedimentation of nucleoids on neutral sucrose gradients. Quinacrine delayed strand-nicking (and presumably lesion removal) following uv irradiation and anthralin exerted its strongest effects on some other repair step(s) subsequent to strand-incision with accumulation of strand disruptions. Since anthralin is a potent tumor promoter, it will be interesting to examine other promoters to see if they also cause accumulation of repair ‘intermediates’ which could act as inducers of error prone repair.