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 intracerebra
l 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 sufferin
g 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 suppor
t the theory that iron-catalyzed lipid peroxidation of the brain durin
g reoxygenation after perinatal asphyxia may be involved in the pathog
enesis of pIVH.