[Role of oxidative stress in respiratory diseases and its monitoring]

Together with inflammation and subsequent remodeling of airways, an imbalance between oxidative and anti-oxidative agents is generated during the development of numerous pulmonary diseases. This process seems to be involved in both the pathogenesis and chronification of asthma, chronic obstructive pulmonary disease (COPD), SOAS, interstitial lung diseases and cystic fibrosis. Reactive oxygen species including superoxide anion, hidroxyl radicals and hydrogen peroxide (H2O2) are synthetised as a response of inflammatory cells and are responsible of the oxidation of nucleic acids, proteins and membrane lipids, leading to cell damage and enhanced inflammation. Until recently, it was difficult to quantify the airway production of reactive oxidative species (ROS). In fact, it has been only in the last few years when it has been possible to determine indirectly the levels of ROS in expired air and in tissue of asthmatic patients. The analysis of exhaled air is a single, reproducible and non-invasive technique which is useful in the study of volatile and non-volatile gases generated in different conditions. The determination of exhaled nitric oxide and carbon monoxide (CO) has a great usefulness in the assessment of asthma. Nitric oxide seems to be closely related to the physiopathology of asthma and COPD. In fact, it is correlated with the levels of sputum eosinophils and with the response to the treatment with steroids. Yet a correlation with the degree of airflow obstruction and the seriousness of the process has not been found. Exhaled CO is another indirect marker of inflammation and it is increased in asthma, COPD, cystic fibrosis and bronchectases. Even though numerous studies have shown its usefulness as a marker of inflammation and in the response to corticosteroids, its clinical application has limitations. In particular, it is not a specific and exclusive marker of oxidative stress and its levels are highly influenced by tobacco smoke. On the other hand, the association between exhaled CO and FEV1 is not clear and no relationship has been proved so far with the improvement of pulmonary function after steroid therapy and with the decrease of maximum expiratory flow at relapses. In this Review, we describe the advances in the knowledge of oxidative stress as a decisive factor in the pathogenesis of prevalent pulmonary diseases, as well as the methods allowing its analysis and monitoring.