Iron Overload and Lipid Peroxidation in Biological Systems

Fe is an essential element for the growth and well-being of almost all living organisms, except for some strains of lactobacillus, where the role of Fe may be assumed by another metal [1]. It is involved in many biological functions since by varying the ligands to which it is coordinated, Fe has access to a wide range of redox potentials and can participate in many electron transfer reactions, spanning the standard redox potential range. It is also involved in O2 transport, activation, and detoxification, in N2 fixation and in several of the reactions of photosynthesis [2]. However, there are problems in the physiological management of Fe, since in spite of its overall abundance, usable Fe is in short supply because at physiological pH under oxidizing conditions, Fe is extremely insoluble. Anytime Fe exceeds the metabolic needs of the cell it may form a low molecular weight pool, referred to as the labile iron pool (LIP), which catalyzed the conversion of normal by-products of cell respiration, like superoxide anion (O2-) and hydrogen peroxide (H2O2), into highly damaging hydroxyl radical (•OH) through the Fenton reaction (reaction 1) or by the Fe2+ catalyzed Haber-Weiss reaction (reaction 2), or into equally aggressive ferryl ions or oxygen-bridged Fe2+/Fe3+ complexes. Fe3+ can be reduced either by O2(reaction 3) or by ascorbate leading to further radical production.