Red blood cell involvement in fetal/neonatal hypoxia

Free radical release plays an important role in the development of brain in jury following hypoxic-ischemic encephalopathy. It causes endothelial cell damage and anomalies in NMDA receptors, synaptosome structure and astrocyte function. Mitochondrial dysfunctions caused by asphyxia, reperfusion after ischemia, arachidonic acid cascade, catecholamine metabolism and phagocyte activation are known sources of reactive oxygen species, particularly the superoxide anion (O-2(-)). O-2(-) mainly induces peroxidation by the Fenton /Haber Weiss reaction or via iron-oxygen complexes. Since both reactions re quire reactive heavy metals, non-protein-bound iron (NPBI) is essential for the induction of lipid peroxidation. Experimental studies have demonstrate d the neurotoxicity of iron in ischemia-reperfusion. Normal axonal transpor t of brain iron is also reported to be disrupted in hypoxia-ischemia, leadi ng to a buildup of iron in the white matter. The free iron content of eryth rocytes (ICRBC) is considered a marker of oxidative stress. Free iron relea se is accompanied by the oxidation of membrane proteins and the appearance of senescent antigen, as measured by autologous IgG binding. Our preliminar y results suggest a significant positive correlation between plasma free ir on and the number of nucleated red cells in cord blood, currently considere d a reliable index of lasting intrauterine asphyxia but also possessing a h igh predictive value for poor neurodevelopmental outcome. The rate of eryth ropoiesis and the entity of ICRBC are related to the degree of asphyxia and the probability of neurological impairment. Since even an increase in NPBI during asphyxia is related to a poor outcome, iron released by red cells c ould possibly also contribute to NPBI levels. Copyright (C) 2001 S. Karger AG. Basel.