Yusuf Aydemir1, Özlem Aydemir2, Aysun Şengül3, Adil Can Güngen4, Hikmet Çoban5, Canatan Taşdemir5, Hasan Düzenli5, Abidin Şehitoğulları6. 1. Sakarya University, Department of Pulmonology, Sakarya/Turkey. Electronic address: dryaydemir@yahoo.com. 2. Sakarya University, Department of Microbiology, Sakarya/Turkey. 3. Derince Education and Reseach Hospital, Department of Pulmonology, Kocaeli/Turkey. 4. İstinye University, Department of Pulmonology, Sakarya/Turkey. 5. Sakarya University, Department of Pulmonology, Sakarya/Turkey. 6. Sakarya University, Department of Chest Surgery, Sakarya/Turkey.
Abstract
BACKGROUND/AIM: Oxidative stress plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Smoking is the leading source of oxidants in lungs. However, it is currently unknown why some individuals are more resistant to the detrimental effects of smoking and do not develop COPD. The aim in this study is to measure and compare the oxidant/antioxidant balance between in non-COPD individuals who smoke and COPD patients who smoke. MATERIALS AND METHODS: Included in the study were 137 patients with COPD and 102 healthy individuals. Participants were divided into groups as COPD patients (former and current smokers), non-COPD individuals who smoke and non-smokers healthy persons. In the following stage, the total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI) levels were measured in serum for all participants. RESULTS: In the current-smoker COPD group, the level of oxidant status were significantly higher than the former-smoker COPD group (p < 0.001). Similarly, oxidant levels were significantly high in current-smoker healthy group than never smoker healthy group. According to these results TOS was associated with especially smoking status rather than COPD. Antioxidant status were similar between former-smoker COPD group and current-smoker COPD group. The antioxidant levels were found significantly low in current-smoker COPD patients, compared to the current-smoker non-COPD individuals (p = 0.007). Nevertheless, no significant difference was found in OSI levels between two groups. Briefly, high TOS and OSI values were correlated with only smoking, independently from COPD. CONCLUSION: It was concluded that there are complex pathogenetic mechanisms, including genetic and individual variations other than oxidant/antioxidant balance, involved in the development of smoking-related COPD. TOS and OSI values are not predictive parameters for the development of COPD, but high level of TAS in non-COPD smokers is promising for future studies.
BACKGROUND/AIM: Oxidative stress plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Smoking is the leading source of oxidants in lungs. However, it is currently unknown why some individuals are more resistant to the detrimental effects of smoking and do not develop COPD. The aim in this study is to measure and compare the oxidant/antioxidant balance between in non-COPD individuals who smoke and COPDpatients who smoke. MATERIALS AND METHODS: Included in the study were 137 patients with COPD and 102 healthy individuals. Participants were divided into groups as COPDpatients (former and current smokers), non-COPD individuals who smoke and non-smokers healthy persons. In the following stage, the total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI) levels were measured in serum for all participants. RESULTS: In the current-smoker COPD group, the level of oxidant status were significantly higher than the former-smoker COPD group (p < 0.001). Similarly, oxidant levels were significantly high in current-smoker healthy group than never smoker healthy group. According to these results TOS was associated with especially smoking status rather than COPD. Antioxidant status were similar between former-smoker COPD group and current-smoker COPD group. The antioxidant levels were found significantly low in current-smoker COPDpatients, compared to the current-smoker non-COPD individuals (p = 0.007). Nevertheless, no significant difference was found in OSI levels between two groups. Briefly, high TOS and OSI values were correlated with only smoking, independently from COPD. CONCLUSION: It was concluded that there are complex pathogenetic mechanisms, including genetic and individual variations other than oxidant/antioxidant balance, involved in the development of smoking-related COPD. TOS and OSI values are not predictive parameters for the development of COPD, but high level of TAS in non-COPD smokers is promising for future studies.