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Reactive oxygen species generation via Fenton-like reaction (Fenton reaction)

Target
Fenton reaction
Molecular classification
Other (chemical reaction/process)
01

Overview

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.

Other names
Fenton reactionFenton-like reactionFenton chemistryiron-catalyzed ROS generationmetallic-ROS generation
02

Mechanism of action

Iron chelation (prevents free iron from catalyzing the Fenton reaction); Antioxidant activity (scavenging hydroxyl radicals); Inhibition of hydrogen peroxide production (downstream modulation)

03

Biological functions

Cell death (via oxidative damage)DNA damage and mutagenesisLipid peroxidationProtein oxidation and aggregationOxidative stressOther (environmental/industrial contaminant degradation)
04

Disease associations

Cancer (through DNA and cellular damage)Neurodegenerative disease (via oxidative neuronal injury)Inflammation (promotion of tissue damage)Cardiovascular disease (lipid peroxidation, atherosclerosis)Other (toxic injury, infection-related tissue damage)
05

Safety considerations

Iron supplementation in infection/inflammation may aggravate tissue damage via Fenton chemistryIron-overload states (e.g., hemochromatosis) intensify oxidative injuryOff-target effects of iron chelators or antioxidantsUncontrolled ROS generation leads to broad toxicity
06

Interacting drugs

Iron chelators (e.g., deferoxamine, deferasirox)

1 more in the full profile.

07

Biomarkers

Oxidative DNA adducts (e.g., 8-oxo-dG)Lipid peroxidation products (e.g., malondialdehyde, 4-HNE)Protein carbonyl contentCellular or tissue ferritin/iron level

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