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The Fenton reaction is a chemical process in which hydrogen peroxide is catalytically decomposed by iron ions or iron hydroxides to produce highly reactive oxygen species such as hydroxyl radicals. These species are extremely reactive, non-selective oxidants implicated in damage to DNA, proteins, and lipids, leading to cell dysfunction or death. While this reaction is exploited in industrial and environmental applications to degrade organic pollutants, in biological systems, inappropriate or excessive activation of this chemistry underlies tissue damage in diseases such as cancer, neurodegeneration, atherosclerosis, and infections. Modulation of Fenton chemistry—via iron chelation or antioxidant use—is an area of therapeutic interest but presents challenges due to the ubiquity of iron and the centrality of ROS in physiological and pathological processes. Key caveat: This entry describes a biochemical process and not a single, druggable protein/receptor; it should not be catalogued as a canonical molecular target for drugs in the conventional sense.
Iron chelation (prevents free iron from catalyzing the Fenton reaction); Antioxidant activity (scavenging hydroxyl radicals); Inhibition of hydrogen peroxide production (downstream modulation)
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