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Reactive oxygen species (ROS) production is a fundamental biological process involving the generation of highly reactive oxygen-containing molecules, including superoxide, hydrogen peroxide, and hydroxyl radicals [1]. These molecules are primarily produced as metabolic byproducts of the mitochondrial electron transport chain or by specialized enzymes such as NADPH oxidases (NOX) and xanthine oxidase [2, 3]. At physiological levels, ROS act as vital secondary messengers in signal transduction pathways regulating cell growth, differentiation, and immune responses [1]. However, excessive ROS production leads to oxidative stress, resulting in oxidative damage to cellular macromolecules like DNA, lipids, and proteins, which contributes to the pathogenesis of cancer, neurodegeneration, and cardiovascular diseases [4]. Therapeutic strategies targeting ROS production include the use of direct antioxidants to scavenge radicals or specific inhibitors to block enzymatic sources, though clinical success has been limited by the complexity of redox biology and the potential for disrupting beneficial signaling [5].
Pharmacological intervention involves the direct scavenging of reactive intermediates, the inhibition of enzymatic sources such as NADPH oxidase or xanthine oxidase, or the induction of endogenous antioxidant defense systems.
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