Oxidant injury of cells.
H2O2 compromises a multitude of cellular functions the combination of which leads to cell death. DNA is an important target for oxidant-induced injury. The formation of DNA strand breaks leads to activation of poly-ADP-ribose polymerase (24) which in turn causes depletion of NAD and ATP, followed by Ca++ influx and eventually by cell lysis. Inhibitors of poly-ADP-ribose polymerase prevented cell lysis, but not DNA damage. A similar sequence of events has been described for cell injury following DNA damage induced by gamma-irradiation and alkylating agents, and was proposed to be a suicide mechanism for cells with irreversibly damaged DNA. Sublethal doses of H2O2 will delay cell division, but not necessarily prevent it.
D000818:Animals; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004249:DNA Damage; D005347:Fibroblasts / Q000187:drug effects; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D008214:Lymphocytes / Q000187:drug effects*; D008264:Macrophages / Q000187:drug effects*; D008954:Models, Biological; D010084:Oxidation-Reduction; D000067856:Poly(ADP-ribose) Polymerase Inhibitors
D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D006861:Hydrogen Peroxide