The importance of the underlying local and systemic oxidative stress and
inflammation in
chronic obstructive pulmonary disease (
COPD) has long been established. In view of the lack of
therapy that might inhibit the progress of the disease, there is an urgent need for a successful therapeutic approach that, through affecting the
pathological processes, will influence the subsequent issues in
COPD management such as lung function, airway clearance, dyspnoea, exacerbation, and quality of life.
N-acetylcysteine (NAC) is a
mucolytic and
antioxidant drug that may also influence several inflammatory pathways. It provides the sulfhydryl groups and acts both as a precursor of
reduced glutathione and as a direct
reactive oxygen species (ROS) scavenger, hence regulating the redox status in the cells. The changed redox status may, in turn, influence the
inflammation-controlling pathways. Moreover, as a
mucolytic drug, it may, by means of decreasing viscosity of the sputum, clean the bronchi leading to a decrease in dyspnoea and improved lung function. Nevertheless, as successful as it is in the in vitro studies and in vivo studies with high dosage, its actions at the dosages used in
COPD management are debatable. It seems to influence exacerbation rate and limit the number of hospitalization days, however, with little or no influence on the lung function parameters. Despite these considerations and in view of the present lack of effective
therapies to inhibit
disease progression in
COPD, NAC and its derivatives with their multiple molecular modes of action remain promising medication once doses and route of administration are optimized.