Non-transferrin-bound iron and labile iron pool (NTBI/LIP)

Non-transferrin-bound iron (NTBI) and the labile iron pool (LIP) refer to the chemically reactive, low-molecular-weight iron fractions found in the plasma and within cells, respectively (Cabantchik, 2014). Under normal physiological conditions, iron is safely sequestered by proteins such as transferrin and ferritin to prevent toxicity. However, when iron levels exceed the binding capacity of these proteins, NTBI and LIP accumulate and participate in the Fenton reaction, generating highly reactive hydroxyl radicals (Hershko, 2014). This oxidative stress leads to significant cellular damage, including lipid peroxidation and DNA fragmentation, which contributes to the pathogenesis of iron overload disorders like thalassemia and hemochromatosis (Porter, 2001). Furthermore, these iron pools play a role in neurodegeneration and the induction of ferroptosis, a form of regulated cell death. Therapeutic strategies focus on iron chelation therapy using agents like deferoxamine and deferasirox, which bind these free ions to facilitate their excretion (Breuer et al., 2000). Effective management of these pools is essential to prevent end-organ damage, particularly in the heart, liver, and endocrine glands.

Other names

Free ferric ironLabile plasma ironLPIChelatable iron poolRedox-active ironCatalytic ironNon-ferritin-bound iron

Iron chelation; the drugs bind to free or loosely bound ferric (Fe3+) and ferrous (Fe2+) ions to form stable, non-toxic, and water-soluble complexes that are subsequently excreted from the body, thereby preventing the iron from participating in the Fenton reaction and generating reactive oxygen species.