Reactive oxygen species (ROS) and lipid peroxidation products can enhance inflammation in the lungs by activating stress kinases and redox-sensitive transcription factors, such as nuclear factor (NF)-κB and activator protein-1. This activation leads to increased expression of pro-inflammatory mediators. Oxidative stress also inhibits histone deacetylase activity, further enhancing inflammatory gene expression and potentially reducing the sensitivity to glucocorticoids. Various antioxidants, including thiol molecules, dietary polyphenols, and specific spin traps, have been shown to control NF-κB activation and affect histone modifications, thereby influencing inflammatory gene expression in lung epithelial cells. The review discusses the role of oxidative stress and redox status in lung inflammation, the mechanisms by which ROS and lipid peroxidation products modulate cell signaling and gene transcription, and the potential of antioxidant compounds in treating chronic obstructive pulmonary disease (COPD).Reactive oxygen species (ROS) and lipid peroxidation products can enhance inflammation in the lungs by activating stress kinases and redox-sensitive transcription factors, such as nuclear factor (NF)-κB and activator protein-1. This activation leads to increased expression of pro-inflammatory mediators. Oxidative stress also inhibits histone deacetylase activity, further enhancing inflammatory gene expression and potentially reducing the sensitivity to glucocorticoids. Various antioxidants, including thiol molecules, dietary polyphenols, and specific spin traps, have been shown to control NF-κB activation and affect histone modifications, thereby influencing inflammatory gene expression in lung epithelial cells. The review discusses the role of oxidative stress and redox status in lung inflammation, the mechanisms by which ROS and lipid peroxidation products modulate cell signaling and gene transcription, and the potential of antioxidant compounds in treating chronic obstructive pulmonary disease (COPD).