Abstract
Chronic obstructive pulmonary disease (COPD) includes chronic bronchitis and emphysema. Environmental exposure, primarily cigarette smoking, can cause high oxidative stress and is the main factor of COPD development. Cigarette smoke also contributes to the imbalance of oxidant/antioxidant due to exogenous reactive oxygen species (ROS). Moreover, endogenously released ROS during the inflammatory process and mitochondrial dysfunction may contribute to this disease progression. ROS and reactive nitrogen species (RNS) can oxidize different biomolecules such as DNA, proteins, and lipids leading to epithelial cell injury and death. Various detoxifying enzymes and antioxidant defense systems can be involved in ROS removal. In this review, we summarize the main findings regarding the biological role of ROS, which may contribute to COPD development, and cytoprotective mechanisms against this disease progression.
Highlights
Chronic obstructive pulmonary disease (COPD) is a major health problem that is becoming the leading cause of morbidity and mortality throughout the world [1]
It is believed that oxidative stress is increased in patients with COPD due to chronic exposure to cigarette smoke, a main risk factor, which contains a high concentration of oxidants and reactive oxygen species (ROS) (Figure 1) [3]
We focus on the mechanism of action of endogenous and exogenous ROS that can contribute to this disease development and the cytoprotective role of antioxidant molecules [15]
Summary
Chronic obstructive pulmonary disease (COPD) is a major health problem that is becoming the leading cause of morbidity and mortality throughout the world [1]. Preclinical studies and clinical trials have shown that antioxidant molecules such as small thiol molecules (N-acetyl-L-cysteine and carbocysteine) [6,7,8], antioxidant enzymes (glutathione peroxidases) [9], activators of Nrf2-regulted antioxidant defense system (sulforaphane) [10, 11], and vitamins, for example, C, E, and D [12,13,14], can boost the endogenous antioxidant system and reduce oxidative stress. They may slow the progression of COPD. We focus on the mechanism of action of endogenous and exogenous ROS that can contribute to this disease development and the cytoprotective role of antioxidant molecules [15]
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