Impact of smoking on redox homeostasis and 8-OHdG levels in COPD patients: a cross-sectional comparative study

Chronic obstructive pulmonary disease (COPD) is a chronic and progressive condition that develops due to a genetic predisposition, with the dysfunction of antioxidants and anti-protease systems triggered by factors such as smoking. In this study, we aimed to determine the effects of smoking on serum 8-hydroxy-2′ deoxyguanosine (8-OHdG) as a marker of oxidative DNA damage, malondialdehyde (MDA) to indicate lipid peroxidation, protein carbonyl (PCO) as a marker of protein damage, and paraoxonase (PON)1 levels as a measure of antioxidant activity involved in maintaining cellular redox balance in COPD patients. We conducted a cross-sectional study involving 141 patients with COPD (70 smokers, 71 non-smokers) and 140 healthy controls (70 smokers, 70 non-smokers) recruited from the Acibadem Mehmet Ali Aydinlar University outpatient clinic. In the COPD-smokers group, significantly higher serum levels of 8-OHdG, MDA, and PCO, and a lower PON1 activity were found. A strong negative correlation was observed between 8-OHdG levels and both FEV1 and FEV1/FVC, as well as between 8-OHdG and PON1 activity in this group. ROC analysis demonstrated strong predictive power for 8-OHdG in the COPD-smokers group. However, given the study's cross-sectional design and limited adjustment for confounders, these findings should be interpreted cautiously. These findings emphasize the critical importance of smoking cessation and antioxidant-targeted strategies in the clinical management of COPD. A systemic oxidant-antioxidant imbalance leads to impairment in the cellular redox homeostasis in patients with COPD and smokers. This study revealed that increased oxidative damage and reduced antioxidant defense in smoking COPD patients are associated with disease severity.