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The ferric ion (Fe3+) within the labile iron pool (LIP) refers to a fraction of cellular or systemic iron that is loosely bound to low-molecular-weight ligands like organic acids, phosphates, or polyphosphates (Kakhlon & Cabantchik, 2002). Unlike iron sequestered in storage proteins like ferritin or transport proteins like transferrin, this pool is chemically reactive and readily available for metabolic processes or pathological redox reactions (Breuer et al., 2008). In healthy cells, the LIP is maintained at low levels to provide a source of iron for the synthesis of iron-sulfur clusters and heme groups while minimizing oxidative damage. However, in conditions of iron overload, such as thalassemia or hemochromatosis, the expansion of this pool leads to the generation of hydroxyl radicals through Fenton-like chemistry, causing lipid peroxidation and cell death (Kalinowski & Richardson, 2005). Therapeutic strategies targeting this pool primarily utilize iron chelators, such as deferoxamine and deferasirox, which bind Fe3+ with high affinity to form stable complexes for excretion (Hider & Zhou, 2005). These interventions are vital for preventing organ failure in patients with chronic iron toxicity and are being explored for their potential in treating neurodegenerative diseases and cancer (Borgna-Pignatti & Marsella, 2015).
Chelation of ferric ions to form stable, non-toxic complexes that are excreted from the body (Hider & Zhou, 2005).
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