Ascorbate-copper induced DNA lesions and repair in Escherichia coli K12 cells.
Multiple lines of evidence show that oxidation products of ascorbic acid (vitamin C) are capable of inducing a variety of genetic alterations in microbial and mammalian cells. We have studied the inactivation kinetics in repair proficient and deficient Escherichia coli K12 cells treated with oxidized solutions of ascorbic acid, in the presence of catalytic amounts of copper. Our results suggest that the repair pathways controlled by the recA and uvrA gene products (the latter in a recA strain) contribute to cell survival. However, the lack of beta-galactosidase induction, in the SOS chromotest, implies a role for the RecA protein other than SOS induction. Catalase and thiourea suppress the toxic effects of oxidized ascorbate solutions, confirming that H2O2 and hydroxyl radicals are intermediate agents in the damaging action. Single-strand breaks were detected in DNA from treated cells.
D001205:Ascorbic Acid / Q000378:metabolism / Q000633:toxicity*; D002374:Catalase / Q000494:pharmacology; D003300:Copper / Q000633:toxicity*; D004260:DNA Repair / Q000187:drug effects*; D004269:DNA, Bacterial; D004926:Escherichia coli / Q000187:drug effects*; D006861:Hydrogen Peroxide / Q000633:toxicity; D006878:Hydroxides; D017665:Hydroxyl Radical; D009154:Mutation; D010084:Oxidation-Reduction; D011938:Rec A Recombinases / Q000235:genetics; D013890:Thiourea / Q000494:pharmacology; D001616:beta-Galactosidase / Q000096:biosynthesis
D004269:DNA, Bacterial; D006878:Hydroxides; D017665:Hydroxyl Radical; D003300:Copper; D006861:Hydrogen Peroxide; D002374:Catalase; D011938:Rec A Recombinases; D001616:beta-Galactosidase; D013890:Thiourea; D001205:Ascorbic Acid