Oxidative stress in COPD: molecular background and clinical monitoring.

Chronic obstructive pulmonary disease (COPD) is a major and rapidly increasing health problem associated with a chronic inflammatory response, predominantly in small airways and lung parenchyma. Oxidative stress induced by reactive oxygen and nitrogen species (ROS and RNS) plays a central role in the pathophysiology of COPD. There is evidence that several molecules formed during oxidative processes may have the potential to serve as biomarkers of oxidative stress in the airways of patients with COPD. Among these molecules carbon monoxide, ethane and pentane can be measured in the exhaled air, while 8-isoprostane, malondialdehyde, 4- hydroxyhexenal, 4-hyroxynonenal, acrolein, hydrogen peroxide, nitrogen oxides and 3-nitrotyrosine can be detected in exhaled breath condensate and/or sputum supernatant. In this review the molecular background of these processes including the formation of ROS and RNS, the biosynthesis of essential ω-3 and ω-6 polyunsaturated fatty acids as building blocks of lipids in the cellular membranes and their enzymatic and non-enzymatic metabolism to eicosanoids and related compounds have been summarized. Moreover, the formation of oxidative stress markers studied most commonly in the context of COPD has been briefly discussed. The associations between biomarkers and clinical variables have also been highlighted in an attempt to illustrate the potential clinical applicability of these biomarker measurements.

[Treatment of chronic obstructive pulmonary disease with inhaled pharmacotherapy: role of corticosteroids]. / Krónikus obstruktív tüdobetegség kezelése inhalációs farmakoterápiával: a kortikoszteroidok szerepe.

Cigarette smoke-induced airway inflammation plays a central role in the pathophysiology of chronic obstructive pulmonary disease (COPD). It causes bronchial epithelial cell injury, which in turn initiates the recruitment of inflammatory cells and increases the production of cytokines, chemokines, proteases and other proinflammatory mediators followed by oxidative stress and protease/anti-protease imbalance impairing lung parenchymal elastic structures. Inhaled corticosteroids in combination with long-acting bronchodilators are generally recommended for the treatment of COPD. However, steroid responsiveness of patients with COPD is often poor, since oxidative stress may reduce the activity and expression of histone deacetylases, and therefore interfere with the anti-inflammatory action of corticosteroids. Recently, a number of studies has indicated that presence of sputum eosinophilia and/or elevated exhaled nitric oxide (NO) level may predict a better response to corticosteroid treatment in COPD patients. While sputum processing and its profiling is a time-consuming and technically demanding method, exhaled NO measurement is a simple and completely non-invasive tool, thus, the later could be more convenient for routine clinical use in the future.