Reduced iron-associated antioxidants in premature newborns suffering intracerebral hemorrhage

Oxygen radical injury may be a common pathogenic mechanism in several neonatal diseases. The term “oxygen radical disease of prematurity” has been proposed in the face of the greater incidence of intracerebral hemorrhage, bronchopulmonary dysplasia, and retinopathy in premature neonates. To test the hypothesis that overload with ionic iron due to decreased concentrations of iron-oxidizing and iron-binding proteins induces free radical damage in premature asphyxiated newborns suffering periventricular-intraventricular hemorrhage (PIVH), blood plasma of newborns with PIVH (n = 7) was compared with that of controls (n = 10) within the first 12 h of life. We found reduced transferrin (2.05 vs. 2.24 g/l; p < 0.05) and ceruloplasmin (89.9 vs. 126.3 mg/l; p < 0.01) levels and an increased transferrin saturation (54.2 vs. 38.4%; p < 0.05) in those newborns who later developed PIVH. These findings support the theory that iron-catalyzed lipid peroxidation of the brain during reoxygenation after perinatal asphyxia may be involved in the pathogenesis of PIVH.