ABSTRACT
During the daily human iron cycle any excess iron is temporarily stored in the liver by ferritin molecules before being cycled back into the body. Haemochromatosis is the genetic failure of this iron-cycle that leads to the permanent storage of excess iron in the liver by the continued build up and clustering of ferritin molecules. Ultimately this can lead to cirrhosis of the liver. The ferritin molecule itself is 12 nm in diameter and consists of a crystalline hydrated iron oxide core (6 nm in diameter) and an organic shell that facilitates the movement of iron in and out of the core. The core crystallises predominantly in the ferrihydrite structure [(FeOOH)s(FeOP03H2), Cowley eta/. 2000], which should only contain Fe'+. This is significant since Fe2+ can catalyse free radical reactions and so may contribute to oxidative tissue damage. Clearly the actual Fe2+/Fe3+ content within both a normal and dysfunctional liver is of interest.
