Iron and oxygen radicals in brain.

Abstract

The brain has been shown to contain regions with high concentrations of non-heme iron, and some of this iron can be chelated, which suggests that it is in a low molecular mass form. The chelatable iron appears to be responsible for the in vitro peroxidation of homogenized brain tissue lipids. It has been suggested that low molecular mass iron is essential for normal brain functions, and that iron is present in the reduced ferrous state. Recent studies have shown that chelatable iron is often present in micromolar concentrations in apparently normal cerebrospinal fluids (CSF), and that this iron is often increased in certain neurological diseases. Using a molecular recognition assay, based on the in vitro degradation of DNA by bleomycin and chelated ferrous ions, it has been possible to conclude that the low molecular mass iron present in CSF is also in the reduced ferrous state. Ferrous ions are able to transfer electrons to molecular oxygen to form reactive and damaging intermediates of oxygen, some of which are free radicals. Increased levels of iron in brain tissue or CSF, however, are not necessarily synonymous with increased activation of oxygen. Detailed studies of brain iron deposits in neurological diseases are long overdue, and require new and pioneering methodologies to approach the problem.