The role for N-acetylcysteine in the management of COPD

Abstract

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.

Role of oxidative stress and serum lipid levels in stable chronic obstructive pulmonary disease

“…Treatment with NAC in humans changes the pulmonary oxidanteantioxidant imbalance. 29 Sadowska et al 30 showed that long-term oral administration of NAC reduces H 2 O 2 formation in the airways of COPD patients and that there is evidence of antioxidant action of the drug.…”

Clinical and pharmacological aspects of bath salt use: A review of the literature and case reports

“…The low efficiency of NAC shown in the BRONCUS trial might be explained by the relatively low dose (600 mg once daily) used in that study [95]. Other studies such as Idiopathic Pulmonary Fibrosis International Group Exploring N-Acetylcysteine I Annual (IFIGENIA) study have suggested that 600 mg twice daily is safe and more effective [100].…”

“…Some systematic reviews and meta-analyses have suggested that NAC prevents exacerbations and improves symptoms in Chronic obstructive pulmonary disease (COPD) patients [94][95][96][97][98] (Table 2), however, probably with little or no effect on the lung function parameters [96].…”

N-acetyl-l-cysteine (NAC) inhibit mucin synthesis and pro-inflammatory mediators in alveolar type II epithelial cells infected with influenza virus A and B and with respiratory syncytial virus (RSV)

“…This molecule reduces the number A c c e p t e d M a n u s c r i p t 5 and impact of COPD exacerbations [28] and also the inflammatory response in epithelial cells exposed to H5N1 influenza A virus [20]. Although anti-mucolitic effects of NAC are well established, little is known about its effects on the MUC5AC expression in virus models of infection.…”