Role of oxidant–antioxidant imbalance in the pathogenesis of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a common respiratory condition involving the airways and characterized by airflow limitation. Antioxidants are substances that may protect cells from the damage caused by unstable molecules known as free radicals. Antioxidants interact with and stabilize free radicals and may prevent some of the damage free radicals might otherwise cause. Under physiological conditions a balance exists between the amount of reactive oxygen species (ROS) produced in normal cellular metabolism and the endogenous antioxidant defense. An imbalance between the antioxidant capacity and the production of reactive oxygen species leads to oxidative stress, which is associated with the pathogenesis of several human diseases. An oxidant/antioxidant imbalance has been proposed as having a key role in the pathogenesis of COPD. The lung is directly exposed to high levels of oxygen, and therefore has to have efficient antioxidant mechanisms. To examine the role of altered levels of oxidant–antioxidants in disease severity of COPD and correlate it with the degree of airflow obstruction in the Egyptian population. Eighty subjects with COPD, 20 healthy smokers, and 20 healthy nonsmokers participated in this study. The investigation included determination of the lung function and the measurements of plasma superoxide dismutase activity (SOD), glutathione content (GSH) reduced form, glutathione peroxidase activity (GSH-Px), catalase activity (CAT), lipid peroxidase (LP), and nitric oxide (NO). The mean concentration of nitric oxide (NO) was significantly higher in the control subjects (smokers and nonsmokers) compared with the COPD group (p=0.001, 0.0001) respectively. Also the mean concentration of nitric oxide (NO) was significantly higher in control nonsmoker group compared to control smoker group (p=0.002). The mean concentration of lipid peroxidase (LP) was significantly higher in COPD patients compared with control subjects (smokers and nonsmokers), (p=0.0001, 0.0001) respectively. The mean concentration of glutathione (GSH) was significantly higher in the control subjects (smokers and nonsmokers) compared with COPD patients (p=0.001, 0.001) respectively. There is no significant difference in the concentration of glutathione-peroxidase (GSH-Px) in all study participants (COPD patients, control smokers, control nonsmokers). The mean concentration of catalase (CAT) was significantly higher in control nonsmokers, compared to COPD patients and