Iron(II) complexes (Labile Iron Pool) (LIP)

Iron complexes involved in Fenton chemistry, primarily represented by the labile iron pool (LIP), consist of redox-active ferrous iron (Fe2+) that catalyzes the decomposition of hydrogen peroxide into highly reactive hydroxyl radicals [1]. This process, known as the Fenton reaction, is a central driver of oxidative stress and lipid peroxidation, particularly in the context of ferroptosis, a form of regulated cell death [2]. In healthy cells, iron is strictly sequestered by proteins like ferritin and transferrin; however, pathological accumulation of labile iron occurs in conditions such as hereditary hemochromatosis, thalassemia, and various neurodegenerative disorders [3]. Therapeutic intervention typically involves the use of iron chelators, such as deferoxamine, deferiprone, or deferasirox, which bind to these iron complexes to prevent their participation in radical-generating reactions [4]. Targeting these complexes is also a burgeoning strategy in oncology, where modulating iron levels can sensitize cancer cells to ferroptotic stimuli or inhibit tumor growth [2]. Beyond chelation, research into small-molecule inhibitors of the Fenton reaction aims to mitigate ischemia-reperfusion injury and chronic inflammation [1]. Monitoring these complexes often involves measuring labile plasma iron (LPI) to assess the risk of oxidative damage in patients with iron overload [4].

Other names

Ferrous ironFe2+Labile ironNon-heme ironRedox-active ironLabile plasma iron (LPI)

Iron chelation to prevent the catalytic formation of hydroxyl radicals via the Fenton reaction