Intracellular iron (Fe) (Fe)

Intracellular iron, specifically the labile iron pool (LIP), represents a critical yet tightly regulated reservoir of redox-active iron ions (Fe2+ and Fe3+) within the cell. This pool serves as a source of iron for the synthesis of heme and iron-sulfur clusters, which are essential for mitochondrial respiration, DNA repair, and various enzymatic activities (Kakhlon & Cabantchik, 2002; Hentze et al., 2004). Despite its necessity, excess intracellular iron is highly toxic; it catalyzes the formation of reactive oxygen species (ROS) via the Fenton reaction, leading to oxidative stress and the induction of ferroptosis, a regulated cell death pathway (Dixon et al., 2012). In clinical settings, intracellular iron is the primary target for iron-chelating therapies used to treat systemic iron overload resulting from chronic blood transfusions or genetic disorders like hemochromatosis (Mobarra et al., 2016). Emerging research also focuses on modulating intracellular iron levels to selectively induce cell death in cancer cells or to mitigate neurodegeneration associated with iron accumulation in the brain (Dixon et al., 2012; Mobarra et al., 2016). These therapeutic strategies leverage the unique redox chemistry of iron to either protect tissues from oxidative damage or to exploit iron dependency in pathological cells.

Other names

Labile iron poolLIPCellular ironIntracellular Fe2+/Fe3+Cytosolic ironIntracellular Fe/Fe

Chelation of redox-active iron ions to form stable, non-toxic complexes that are excreted from the body, thereby preventing oxidative damage and reducing iron-dependent cellular processes.