Ferrous iron in the labile iron pool (LIP)

The ferrous iron in the labile iron pool (LIP) represents a transient, chelatable, and redox-active fraction of intracellular iron that is not tightly bound to storage proteins like ferritin (Kakalij et al., 2015). This pool is primarily composed of Fe2+ ions associated with low-molecular-weight ligands such as citrate, ATP, or glutathione, making it readily available for metabolic processes but also potentially hazardous (Espósito et al., 2002). Biologically, the LIP acts as a central junction for iron trafficking, providing the necessary metal for the biogenesis of heme and iron-sulfur clusters (Dixon et al., 2012). However, an expanded LIP can trigger the Fenton reaction, generating highly reactive hydroxyl radicals that cause lipid peroxidation and initiate ferroptosis, a regulated form of cell death (Stockwell et al., 2017). Therapeutic intervention typically involves iron chelators like Deferoxamine or Deferiprone, which sequester the ferrous iron to prevent oxidative damage in diseases such as thalassemia, hereditary hemochromatosis, and various neurodegenerative disorders (Mobarra et al., 2016).

Other names

Labile iron poolChelatable iron poolRedox-active ironIntracellular labile ironFree iron pool

Sequestration of redox-active ferrous iron through chelation, which prevents the iron from participating in the Fenton reaction and the subsequent generation of reactive oxygen species (ROS) and lipid peroxides (Mobarra et al., 2016).