Abstract

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.