ABSTRACT
Chronic obstructive pulmonary disease (COPD) and asthma are the most prevalent lung diseases characterized by progressive/persistent lung inammation. The inammatory pattern is distinct in each disease; however, oxidants play a potential role in increasing the pro-inammatory gene expression and development of the disease. Oxidants generated from inhaled noxious agents, such as cigarette smoke, allergens, or environmental pollutants, disrupt the oxidant-antioxidant balance, which results in oxidative stress. Increased level of oxidative stress/damage and decreased antioxidant defense are found in the lungs of asthmatics and patients with COPD. Oxidizing environments induce activation of transcription factors, which regulate inammatory molecules, such as nuclear factor-kappaB (NF-κB) and activator protein-1 (AP-1) via several redox sensitive kinases. Activated transcription factors are translocated to the nucleus and bind to speciœc promoter regions of DNA to induce transcription of pro-inammatory genes (Rajendrasozhan et al. 2008a).
