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Reactive oxygen species are highly reactive molecules containing oxygen, including superoxide (O₂⁻), hydrogen peroxide (H₂O₂), hydroxyl radical (·OH), and singlet oxygen, among others. These molecules are produced endogenously as byproducts of aerobic metabolism, predominantly in mitochondria, and can also arise from enzymatic sources such as NADPH oxidase and xanthine oxidase[1][3][4]. While low to moderate levels of ROS act as signaling molecules in processes such as cell proliferation, differentiation, immune response, and autophagy, excessive ROS leads to oxidative stress, damaging cellular lipids, proteins, and DNA[1][3][5]. Antioxidant pathways refer to the ensemble of enzymatic and nonenzymatic mechanisms that maintain redox homeostasis by neutralizing ROS. Key enzymes include superoxide dismutase, catalase, and glutathione peroxidase, while non-enzymatic antioxidants include glutathione, vitamins E and C, and others[1][3][4]. The complex interplay between ROS and antioxidant defenses influences the development and progression of numerous diseases, including cancer, neurodegenerative and cardiovascular diseases, and is the target of various therapeutic approaches designed to modulate oxidative stress[5][3]. This entry refers to a broad system, not a single valid therapeutic target, and should be replaced with the specific molecule, enzyme, or pathway of interest (e.g., "NADPH oxidase", "superoxide dismutase", "Nrf2").
ROS scavenging (neutralization of free radicals); Enhancement of antioxidant enzyme activity; Inhibition of ROS-producing enzymes (e.g., NADPH oxidase inhibitors); Activation of transcription factors for antioxidant response (e.g., Nrf2-Keap1 pathway)
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