Iron ions (Fe2+/Fe3+)

Iron ions, particularly in their ferrous (Fe2+) and ferric (Fe3+) states, serve as critical mediators of cellular redox chemistry. In the context of Fenton chemistry, ferrous iron reacts with hydrogen peroxide to produce the hydroxyl radical, one of the most reactive and damaging oxygen species in biological systems (Winterbourn, 1995, PubMed: 8597169). This reaction is a key driver of oxidative stress and is the fundamental mechanism underlying ferroptosis, a form of regulated cell death characterized by iron-dependent lipid peroxidation (Dixon et al., 2012, PubMed: 22632970). While iron is essential for functions such as oxygen transport and DNA synthesis, an excess of the labile iron pool can lead to tissue damage in conditions like hemochromatosis, thalassemia, and various neurodegenerative diseases (Mobarra et al., 2016, PubMed: 27822364). Pharmacological intervention typically focuses on iron chelation therapy, using agents like deferoxamine or deferasirox to sequester redox-active iron and prevent the initiation of radical-generating cycles (Koppenol & Hider, 2019, PubMed: 30213779). Consequently, managing iron homeostasis is a vital therapeutic target for mitigating oxidative injury and controlling cell death pathways in diverse clinical settings.

Other names

Ferrous ironFerric ironLabile iron poolRedox-active ironFree ironFenton reagents

Chelation of redox-active iron to prevent the formation of hydroxyl radicals via the Fenton reaction, thereby reducing oxidative stress and lipid peroxidation.