Ascorbate/iron mediation of hydroxyl free radical damage to PBR322 plasmid DNA.
Plasmid PBR322 DNA has been exposed to hydroxyl free radicals generated from an ascorbate/Fe system. Hydroxyl free radical scavengers as well as the iron chelator desferroxamine and catalase inhibit the DNA nicking which occurs, but superoxide dismutase had no effect. The DNA nicking was temperature dependent, occurring more rapidly at higher temperatures. The rate of DNA nicking was accelerated by the addition of hydrogen peroxide. There was an early lag phase in DNA nicking, even though the rate of hydroxyl free radical generation, as assessed by salicylate hydroxylation, showed no lag phase. It is considered that the early hydroxyl free radical damage to DNA may be biologically very important in mutagenic and carcinogenic processes.
Schneider
J E
JE
Molecular Toxicology Research Group, Oklahoma Medical Research Foundation, Oklahoma City 73104.
Browning
M M
MM
Floyd
R A
RA
D001205:Ascorbic Acid / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D004249:DNA Damage; D004269:DNA, Bacterial; D004278:DNA, Superhelical / Q000187:drug effects; D005609:Free Radicals; D006358:Hot Temperature; D006861:Hydrogen Peroxide / Q000494:pharmacology; D006878:Hydroxides / Q000633:toxicity*; D017665:Hydroxyl Radical; D007501:Iron / Q000494:pharmacology*; D010100:Oxygen / Q000494:pharmacology; D010957:Plasmids; D013482:Superoxide Dismutase / Q000378:metabolism
D004269:DNA, Bacterial; D004278:DNA, Superhelical; D005609:Free Radicals; D006878:Hydroxides; D017665:Hydroxyl Radical; D006861:Hydrogen Peroxide; D007501:Iron; D002374:Catalase; D013482:Superoxide Dismutase; D001205:Ascorbic Acid; D010100:Oxygen