Home » Health » Oxidative stress plays a crucial role in the development and progression of chronic obstructive pulmonary disease (COPD), which is associated with inflammation and alveolar destruction. Free radical scavenging capacity may be a useful diagnostic tool for patients with COPD. This study aimed to determine if characteristic changes in free radical scavenging capacities are observed in patients with stable COPD and investigate the association between scavenging capacities and pathophysiology and mortality.

Oxidative stress plays a crucial role in the development and progression of chronic obstructive pulmonary disease (COPD), which is associated with inflammation and alveolar destruction. Free radical scavenging capacity may be a useful diagnostic tool for patients with COPD. This study aimed to determine if characteristic changes in free radical scavenging capacities are observed in patients with stable COPD and investigate the association between scavenging capacities and pathophysiology and mortality.

Chronic obstructive pulmonary disease (COPD) is a progressive lung disease that affects millions of people worldwide. The condition is characterized by inflammation and oxidative stress, which can cause significant damage to the lungs and lead to respiratory and other related health issues. To combat this, researchers are exploring potential treatments that target the body’s free radical scavenging capacity, which is critical in reducing oxidative stress. In this article, we will discuss the link between serum free radical scavenging capacity profiles and COPD and explore how this research can help in developing more effective treatments for the disease.


Chronic obstructive pulmonary disease (COPD) is a common, preventable, and treatable disease that affects millions of people worldwide. It is characterized by persistent airflow limitation, usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases.1 The most common risk factor of COPD is cigarette smoking, but the mechanisms of the amplified inflammation in these patients are not fully understood. Oxidative stress has been shown to play a crucial role in the development and progression of COPD.2,3 Oxidative stress may be an important amplifying mechanism in the inflammatory response in the lungs of COPD patients.4,5 The enhanced inflammation through transcription factors such as nuclear factor κB (NF-κB) impairs the function of antiproteases including α-1 antitrypsin and secretory leukoprotease inhibitor and induces the secretion of matrix metaloproteinases (MMPs), serine proteinases including neutrophil elastase, cathepsin G, and proteinase-3 which contribute to alveolar destruction and development of emphysema.6,7

While systemic inflammation is also found in patients with COPD, the oxidative stress and damage to lipids, proteins, and nucleic acids originally occur when oxidants overwhelm the capacity of antioxidants. Numerous biomarkers of oxidant and antioxidant have been investigated in different biological samples such as blood, urine, exhaled breath condensate (EBC), and induced sputum. The majority of these studies reported that patients with COPD have higher levels of oxidants, especially lipid and protein oxidation products and diminished antioxidant defenses, particularly protein SH groups, glutathione (GSH), and antioxidant enzymes such as superoxide dismutase (SOD) and catalase compared to healthy controls. However, suitable biomarkers to accurately diagnose COPD and to monitor its progression have not yet been identified.8 Oxidative stress induced by free radicals such as reactive oxygen species (ROS) and reactive nitrogen species (RNS) in cigarette smoke and air pollutants is considered a defensive capacity against oxidative stress.9,10

The aim of the present study is to identify free radical scavenging capacities in patients with stable COPD and investigate the association between the scavenging capacities and pathophysiology and mortality among these patients. Patients were recruited from the Nara Medical University Hospital in this prospective study. Control blood samples were taken from healthy controls who performed regular exercise at the gym in Doshisha University. The serum scavenging capacities of different free radical species were measured using an X-band Microwave Unit ESR instrument under different conditions, as shown in Table 1. High-resolution computed tomography (HRCT) was performed for all the patients to detect low attenuation areas characterized as pulmonary emphysema in COPD.

The results of the study may lead to a better understanding of the oxidative stress and free radical scavenging mechanisms in COPD. It may also help in the development of new biomarkers for the accurate diagnosis and monitoring of COPD progression. Furthermore, it may provide insights into the possible approaches for the prevention and treatment of COPD through the management of oxidative stress and scavenging capacities.


In conclusion, the assessment of serum free radical scavenging capacity profiles in COPD patients is a valuable tool in understanding the underlying mechanism of oxidative stress-related diseases. It provides insights into the antioxidant capacity of the body and helps in the development of novel therapeutic targets for COPD. As we continue to learn more about the role of oxidative stress in COPD, we can hope for more effective treatment options and better quality of life for those suffering from this debilitating disease.

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