Transition metal ions involved in Fenton chemistry

Transition metal ions, primarily iron (Fe2+) and copper (Cu+), are the central catalysts in Fenton and Fenton-like chemistry, where they react with hydrogen peroxide to generate the highly reactive hydroxyl radical (.OH) (Winterbourn, 1995, Toxicology Letters). This process is a major source of oxidative stress within cells, as hydroxyl radicals cause non-specific damage to DNA, proteins, and membrane lipids through lipid peroxidation (Wardman & Candeias, 1996, Radiation Research). Under physiological conditions, these metals are sequestered by storage and transport proteins like ferritin and transferrin to prevent unwanted redox activity. However, in various disease states, the labile metal pool increases, leading to pathological oxidative damage and the induction of ferroptosis, a form of regulated cell death (Dixon & Stockwell, 2014, Nature Chemical Biology). Therapeutic targeting of these ions typically involves chelation therapy, using drugs like deferoxamine or deferiprone to sequester the metals and prevent their participation in radical-generating reactions (Kontoghiorghes et al., 2004, Current Medicinal Chemistry). This approach is vital in treating iron overload disorders, Wilson's disease, and is being investigated for neurodegenerative and cardiovascular conditions (Jomova & Valko, 2011, Toxicology).

Other names

Fenton-active metalsRedox-active metal ionsLabile iron poolLabile copper poolFenton reagentsChelatable metal ions

Chelation and sequestration of redox-active metal ions to prevent the formation of reactive oxygen species (ROS) via Fenton and Fenton-like reactions.