Fenton reaction

Iron carries oxygen in your blood and fuels the respiration of every one of your cells. The same atom, left free a fraction of a second too long, triggers one of the most destructive reactions in biology. This duality bears the name of a 19th-century English chemist: Henry Fenton, who described the reaction in 1894 while observing the abrupt colouring of a tartaric acid solution.

The Fenton reaction is straightforward to write: Fe²⁺ + H₂O₂ → Fe³⁺ + OH⁻ + ·OH. One ferrous iron ion meets a hydrogen peroxide molecule and produces a hydroxyl radical. This ·OH is the most reactive of all free radicals known in biology. Its half-life is measured in nanoseconds, and it attacks indiscriminately the first lipid, protein or DNA strand it crosses.

Why the body obsessively sequesters its iron

The body spends considerable energy never letting iron circulate freely. Transferrin transports it in blood, ferritin cages it inside cells, hepcidin regulates intestinal entry. As long as these locks hold, Fenton does not occur. Once transferrin saturation exceeds 70 to 80%, non-transferrin-bound iron (NTBI) starts circulating and enters passively into liver, pancreas, heart and the brain's basal ganglia. There, in the presence of hydrogen peroxide produced by mitochondria, Fenton fires. The cascade that follows, peroxidation of membrane fatty acids, is now described as a distinct mode of cell death, ferroptosis, identified in 2012 and implicated in hepatic NASH, certain forms of Parkinson's, ischaemia-reperfusion injury and several cancers.

Reading iron beyond ferritin alone

This mechanism changes how an iron panel is read. A high ferritin without an inflammatory context, especially with transferrin saturation above 45%, should raise the question of overload rather than mere storage. In men after 40 and in women after menopause, it is a genuine point of attention because physiological losses disappear. The levers are not at the pharmacy: phlebotomies if overload is confirmed, moderation of red meat, coffee or tea with meals to reduce non-haem absorption, caution with iron supplementation taken without prior testing. Membrane vitamin E and selenium (a GPX4 cofactor) help contain peroxidation, without replacing it.

Related terms

• NTBI
• Ferritin
• Hepcidin
• Ferroptosis
• GPX4