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DNA strand breakage via free radical formation is a molecular process wherein reactive oxygen species, especially the hydroxyl radical (•OH), attack DNA, abstracting hydrogen atoms from the deoxyribose backbone and generating carbon-centered radicals. These radicals can interact with molecular oxygen and transition metals (iron, copper) to create DNA single-strand and double-strand breaks. Such damage is implicated in aging, cancer, neurodegeneration, and other pathologies. Drugs that intentionally produce or scavenge these radicals are used experimentally or therapeutically, but free radical-initiated DNA strand breakage itself is not a canonical drug target—it's a pathway affected by various biological and pharmacological agents[2][4][5][6][1].
Radical generators: produce hydroxyl radicals (•OH) that attack the sugar backbone, causing breaks\nRadiomimetic drugs: generate carbon-centered radicals leading to double-strand breaks\nMetal ion catalysis: iron and copper catalyze Fenton reaction, producing hydroxyl radicals\nRadical scavengers: block free radical formation and DNA breakage
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