ABSTRACT
A number of studies have shown an increased oxidant burden and consequently increased makers of oxidative stress in the airspaces, breath, blood, and urine of smokers and patients with chronic obstructive pulmonary disease (COPD). The presence of oxidative stress has important consequences for the pathogenesis of COPD. These include oxidative inactivation of antiproteinases, airspace epithelial injury, increased sequestration of neutrophils in the pulmonary microvasculature, and gene expression of pro-inflammatory mediators. Oxidative stress may thus have a role in enhancing the inflammation, which occurs in smokers and patients with COPD, through the activation of redox-sensitive transcriptions factors such as NF-kB and AP-1, which regulate the genes for pro-inflammatory mediators as well as protective antioxidant gene expression.
