Abstract
The respiratory system is continuously exposed to endogenous and exogenous oxidants. Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation of the airways, leading to the destruction of lung parenchyma (emphysema) and declining pulmonary function. It is increasingly obvious that reactive oxygen species (ROS) and reactive nitrogen species (RNS) contribute to the progression and amplification of the inflammatory responses related to this disease. First, we described the association between cigarette smoking, the most representative exogenous oxidant, and COPD and then presented the multiple pathophysiological aspects of ROS and antioxidative defense systems in the development and progression of COPD. Second, the relationship between nitric oxide system (endothelial) dysfunction and oxidative stress has been discussed. Third, we have provided data on the use of these biomarkers in the pathogenetic mechanisms involved in COPD and its progression and presented an overview of oxidative stress biomarkers having clinical applications in respiratory medicine, including those in exhaled breath, as per recent observations. Finally, we explained the findings of recent clinical and experimental studies evaluating the efficacy of antioxidative interventions for COPD. Future breakthroughs in antioxidative therapy may provide a promising therapeutic strategy for the prevention and treatment of COPD.
Highlights
Enhancement of oxidative stress is thought to be caused by the coordination of exogenous oxidants, such as cigarette smoke, biomass smoke, and air pollution; endogenous reactive oxygen species (ROS), such as O2 − and H2 O2 ; and reduction of antioxidants, such as superoxide dismutase (SOD), glutathione (GSH), and nuclear factor erythroid 2-related factor 2 (Nrf2) [20]
In another previous study, advanced oxidation protein products were increased in the plasma of patients with Chronic obstructive pulmonary disease (COPD)
Oxidative stress in the lungs is enhanced by ROS released from activated inflammatory cells, such as neutrophils, macrophages, and resident cells, in addition to environmental exposure, such as cigarette smoke, air pollutants, and genetic factors
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. In patients with COPD, oxidative stress occurs after long-term exposure to environmental cigarette smoke and combustion products of biomass fuels, as well as due to a variety of immune and inflammatory stimuli in the airways [20]. Pulmonary inflammation gains strength by increased oxidative stress that subsequently recruits and activates immune cells into the lungs and produce inflammatory mediators [8]. In this context, a crucial factor that dictates the severity and progression of COPD might be the ability of the host to provide protection against oxidative stress by upregulating lung antioxidant defenses [20,21]
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