The effect of smoking cessation on the oxidative stress in patients with chronic obstructive pulmonary disease (COPD) was assessed. We recruited 73 smokers with COPD (study group), whose blood was analysed before smoking cessation, after the 1st, 2nd, and 3rd months of abstinence, 35 healthy nonsmokers (Control I), and 35 smokers with COPD (Control II). Blood was taken once in Control I and 4 times (every month) in Control II. In the study group conjugated dienes (CDs) level in plasma and erythrocytes before smoking cessation was 3 and 6.5 times higher than in Control I, respectively ( ), while thiobarbituric acid-reactive substances (TBARS) level was 89% ( ) and 51% higher ( ), respectively. Superoxide dismutase (SOD) activity was 40% higher ( ) while glutathione peroxidase (GPx) was 41% lower ( ) than in Control I. In Control II, the similar differences as compared to Control I were observed throughout the study. Smoking cessation resulted in decrease of CDs, TBARS, and SOD and GPx increase, with no changes in catalase and vitamins A and E. COPD is accompanied by oxidative stress. A three-month tobacco abstinence facilitated restoring the oxidant-antioxidant balance systemically, but it did not affect spirometric parameters. 1. Introduction Chronic obstructive pulmonary disease (COPD) is the most frequent chronic respiratory disease. It is currently the 4th most common cause of death in the USA and Europe, after cardiovascular diseases, cancer, and road traffic injuries. In light of the increasing number of smokers in the developing countries, particularly in China, COPD is prognosticated to become the 3rd most common cause of death globally by the year 2020 [1]. The main characteristic of COPD is a progressive, irreversible narrowing (obturation) of the bronchi that obstructs the air passage through the bronchi to the lungs. As a result, the lungs lose their elasticity. The disease has an inflammatory background, which is caused by the inhalation of harmful dust and gases [2]. Apart from inflammatory reactions, the domination of proteinases over antiproteinases [3] and oxidative stress [4] are also important factors in the pathogenesis of COPD. It has been proven that the incidence of COPD is strictly correlated with the addiction to smoking tobacco [1, 5, 6]. Toxic derivatives of the metabolism of oxygen present in tobacco smoke, the so-called reactive oxygen species (ROS), may be the cause of oxidative stress, which may be the background of the development of COPD, as hypothesized by some researchers [7]. Oxidative stress in cells and tissues is
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