Lung cell oxidant injury: decrease in oxidant mediated cytotoxicity by N-acetylcysteine.
Lung cell damage mediate by polymorphonuclear leukocyte (PMN) reactive oxygen metabolites has been suggested as a pathophysiologic mechanism in a variety of acute and chronic pulmonary disease states, while oxidant injury may be a non-specific cytotoxic mechanism. Reducing agents therefore represent one therapeutic direction for decreasing lung cell injury in several clinical circumstances. N-Acetylcysteine (NAC) is a known antioxidant which can be distributed in soluble form to multiple intrapulmonary sites. We have therefore examined a possible role for NAC against oxidant injury in a controlled in vitro model for oxygen metabolite cytotoxicity. Our data suggest that extracellular NAC is able to protect lung cells against PMN mediated oxidant injury. Pre-exposure of lung cells to NAC results in decreased susceptibility to oxidant damage by increasing intracellular antioxidant defense systems. An increase in extracellular and/or intracellular resistance to toxic oxygen metabolites by NAC may be one approach to the prevention of in vivo lung oxidant injury.
D000111:Acetylcysteine / Q000494:pharmacology*; D002478:Cells, Cultured; D003602:Cytotoxicity, Immunologic; D006801:Humans; D066298:In Vitro Techniques; D008168:Lung / Q000166:cytology* / Q000276:immunology; D009504:Neutrophils / Q000378:metabolism; D010100:Oxygen / Q000633:toxicity*
D010100:Oxygen; D000111:Acetylcysteine