DIFFERENTIAL-EFFECTS OF LUMINOL, NICKEL, AND ARSENITE ON THE REJOINING OF ULTRAVIOLET-LIGHT AND ALKYLATION-INDUCED DNA BREAKS

When Chinese hamster ovary cells were treated with ultraviolet (UV) li ght or methyl methane-sulfonate (MMS), a large number of DNA strand br eaks could be detected by alkaline elution. These strand breaks gradua lly disappeared if the treated cells were allowed to recover in a drug -free medium. The presence of nickel or arsenite during the recovery i ncubation retarded the disappearance of UV-induced strand breaks, wher eas the disappearance of MMS-induced strand breaks was retarded by the presence of arsenite or of luminol, a new inhibitor for poly(ADP-ribo se) synthetase. Luminol, however, had no apparent effect on the repair of UV-induced DNA strand breaks, and nickel had no effect on the repa ir of MMS-induced DNA strand breaks. When UV- or MMS-treated cells (Ar aC) plus hydroxyurea (HU), a large amount of low molecular weight DNA was detected by alkaline sucrose sedimentation. The molecular weight o f these DNAs increased if the cells were further incubated in a drug-f ree medium. This rejoining of breaks in cells pretreated with UV plus AraC and HU was inhibited by nickel and by arsenite, but not by lumino l. The rejoining of breaks in cells pretreated with MMS plus AraC and HU was inhibited by luminol and by arsenite, but not by nickel. These results suggest that different enzymes may be used in DNA resynthesis and/or ligation during the repairing of UV- and MMS-induced DNA strand breaks, and that nickel, luminol, and arsenite may have differential inhibitory effects on these enzymes. (C) 1994 Wiley-Liss, Inc.