The role for N-acetylcysteine in the management of COPD.
Oxidative stress has been implicated in the pathogenesis and progression of COPD. Both reactive oxidant species from inhaled cigarette smoke and those endogenously formed by inflammatory cells constitute an increased intrapulmonary oxidant burden. Structural changes to essential components of the lung are caused by oxidative stress, contributing to irreversible damage of both parenchyma and airway walls. The antioxidant N-acetylcysteine (NAC), a glutathione precursor, has been applied in these patients to reduce symptoms, exacerbations, and the accelerated lung function decline. This article reviews the available experimental and clinical data on the antioxidative effects of NAC in COPD, with emphasis on the role of exhaled biomarkers.
Department of Pulmonary Diseases, Radboud University Nijmegen Medical Centre, The Netherlands. r.dekhuijzen@long.umcn.nl
P N R
PN
Dekhuijzen
W J C
WJ
van Beurden
D000111:Acetylcysteine / Q000627:therapeutic use*; D015415:Biomarkers / Q000378:metabolism; D045853:Exhalation; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D006801:Humans; D018384:Oxidative Stress; D029424:Pulmonary Disease, Chronic Obstructive / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology
D015415:Biomarkers; D016166:Free Radical Scavengers; D000111:Acetylcysteine