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Free radical-mediated DNA damage refers to the chemical modifications inflicted on DNA by highly reactive species such as reactive oxygen species (ROS) and reactive nitrogen species (RNS), which arise both endogenously (e.g., mitochondrial respiration, enzyme activity, immune response) and exogenously (e.g., ionizing radiation, tobacco smoke, pollution)[1][2][3]. The hydroxyl radical is especially notorious, causing DNA base modifications (like 8-OHdG), sugar backbone damage, strand breaks, and cross-linking[3][5][8]. This damage is implicated in mutagenesis, carcinogenesis, aging, and a variety of diseases[1][2][4][5]. Biomarkers like 8-hydroxy-2’-deoxyguanosine are often used to gauge oxidative DNA damage[2][4][9]. Organisms rely on antioxidant defenses (enzymatic and non-enzymatic) and DNA repair mechanisms to counteract this damage, but overwhelming free radical production can exceed these capacities, leading to pathological consequences[3][5].
Free radical scavenging, Enhancement of DNA repair pathways[3], Metal ion chelation (reducing Fenton reaction-mediated ROS production)
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