This review discusses the role of oxidative stress and redox regulation in lung inflammation, particularly in chronic obstructive pulmonary disease (COPD). Reactive oxygen species (ROS), such as superoxide anion and hydroxyl radical, contribute to inflammation by activating stress kinases and redox-sensitive transcription factors like NF-κB and AP-1. These factors increase the expression of pro-inflammatory mediators. Oxidative stress activates NF-κB through the activation of its inhibitor IκB-α kinase or by enhancing the recruitment of transcriptional co-activators. This leads to targeted increases in histone modifications, such as acetylation, which enhance inflammatory gene expression. The glutathione redox couple plays a dynamic role in regulating protein function through reversible disulphide bond formation on kinases, phosphatases, and transcription factors. Oxidative stress also inhibits histone deacetylase activity, further enhancing inflammatory gene expression and reducing glucocorticoid sensitivity. Antioxidants such as glutathione, N-acetyl-L-cysteine, and dietary polyphenols have been shown to control NF-κB activation or affect histone modifications, influencing inflammatory gene expression in lung epithelial cells. Oxidative stress in the alveolar space is enhanced in smokers due to the release of ROS from macrophages and neutrophils. Smokers have increased levels of neutrophils and myeloperoxidase, which correlate with pulmonary dysfunction. Alveolar macrophages from smokers are more activated and release more ROS. Neutrophils from smokers and COPD patients release more superoxide anion, and their MPO content is increased, contributing to oxidative stress in the lungs. Oxidative stress in the blood is associated with increased neutrophil numbers and ROS release, which may contribute to bronchial hyperresponsiveness in COPD. Studies show increased ROS production in peripheral blood neutrophils during COPD exacerbations, which returns to normal when patients are clinically stable. Neutrophils from COPD patients show upregulated surface adhesion molecules, possibly due to oxidant-mediated effects. ROS-mediated lipid peroxidation products, such as 4-hydroxy-2-nonenal and acrolein, play a role in lung inflammation by acting as chemoattractants for neutrophils and modulating various cellular functions. These products can activate glutathione synthesis and pro-inflammatory genes, contributing to oxidative stress and inflammation. Glutathione metabolism is crucial for maintaining the cellular redox state. GSH is the most important nonprotein sulphydryl in cells and plays a key role in maintaining the cellular redox status. The ratio of GSH to GSSG is a good indicator of the cellular redox state. Antioxidant enzymes such as glutathione peroxidase and glutathione reductase are involved in maintaining the cellular reductive potentialThis review discusses the role of oxidative stress and redox regulation in lung inflammation, particularly in chronic obstructive pulmonary disease (COPD). Reactive oxygen species (ROS), such as superoxide anion and hydroxyl radical, contribute to inflammation by activating stress kinases and redox-sensitive transcription factors like NF-κB and AP-1. These factors increase the expression of pro-inflammatory mediators. Oxidative stress activates NF-κB through the activation of its inhibitor IκB-α kinase or by enhancing the recruitment of transcriptional co-activators. This leads to targeted increases in histone modifications, such as acetylation, which enhance inflammatory gene expression. The glutathione redox couple plays a dynamic role in regulating protein function through reversible disulphide bond formation on kinases, phosphatases, and transcription factors. Oxidative stress also inhibits histone deacetylase activity, further enhancing inflammatory gene expression and reducing glucocorticoid sensitivity. Antioxidants such as glutathione, N-acetyl-L-cysteine, and dietary polyphenols have been shown to control NF-κB activation or affect histone modifications, influencing inflammatory gene expression in lung epithelial cells. Oxidative stress in the alveolar space is enhanced in smokers due to the release of ROS from macrophages and neutrophils. Smokers have increased levels of neutrophils and myeloperoxidase, which correlate with pulmonary dysfunction. Alveolar macrophages from smokers are more activated and release more ROS. Neutrophils from smokers and COPD patients release more superoxide anion, and their MPO content is increased, contributing to oxidative stress in the lungs. Oxidative stress in the blood is associated with increased neutrophil numbers and ROS release, which may contribute to bronchial hyperresponsiveness in COPD. Studies show increased ROS production in peripheral blood neutrophils during COPD exacerbations, which returns to normal when patients are clinically stable. Neutrophils from COPD patients show upregulated surface adhesion molecules, possibly due to oxidant-mediated effects. ROS-mediated lipid peroxidation products, such as 4-hydroxy-2-nonenal and acrolein, play a role in lung inflammation by acting as chemoattractants for neutrophils and modulating various cellular functions. These products can activate glutathione synthesis and pro-inflammatory genes, contributing to oxidative stress and inflammation. Glutathione metabolism is crucial for maintaining the cellular redox state. GSH is the most important nonprotein sulphydryl in cells and plays a key role in maintaining the cellular redox status. The ratio of GSH to GSSG is a good indicator of the cellular redox state. Antioxidant enzymes such as glutathione peroxidase and glutathione reductase are involved in maintaining the cellular reductive potential