Non-transferrin-bound iron (NTBI) (NTBI)

Non-transferrin-bound iron (NTBI) refers to a heterogeneous collection of iron species in the plasma that are not associated with the primary transport protein, transferrin. Under normal physiological conditions, transferrin is approximately 30% saturated, but when iron levels exceed the binding capacity of transferrin (typically >70-80% saturation), NTBI begins to accumulate in the circulation (Brissot et al., 2012). This form of iron is highly reactive and can be rapidly taken up by parenchymal cells in the liver, heart, and endocrine organs through non-regulated pathways, leading to systemic iron overload. Within these tissues, NTBI contributes to the labile iron pool and catalyzes the formation of reactive oxygen species (ROS) via the Fenton reaction, resulting in oxidative damage to cellular membranes and DNA (Hershko, 2014). Therapeutic management of NTBI involves the use of iron chelators such as deferoxamine, deferiprone, and deferasirox, which bind the ferric iron to form stable complexes for excretion. Monitoring NTBI and its redox-active component, Labile Plasma Iron (LPI), is essential for assessing the risk of organ damage and the efficacy of chelation therapy in patients with conditions like thalassemia and hereditary hemochromatosis (Breuer et al., 2000).

Other names

NTBILabile plasma ironLPIRedox-active ironNon-transferrin bound ironFerric iron (non-transferrin bound)

Chelation of ferric iron (Fe3+) to form stable, non-toxic complexes that are subsequently excreted through the kidneys or bile, thereby reducing the circulating pool of reactive iron and preventing tissue deposition (Hershko, 2014; Brissot et al., 2012).