Excessive production of reactive oxygen species associated with deficient antioxidant defenses in preterm infants have been implicated in neonatal diseases such as periventricular leukomalacia, intraventricular hemorrhage, bronchopulmonary dysplasia, retinopathy of prematurity, and necrotizing enterocolitis. Free radicals may be generated by exposure of preterm infants to high oxygen concentrations in resuscitation and mechanical ventilation and by hyperoxia during the reperfusion phase of a hypoxic-ischemic brain insult, primarily in the presence of high concentrations of nonprotein-bonded iron. In addition, free radicals are released by macrophage and neutrophil activation associated with infection and inflammation. The free radical aggression mechanisms in the pathogenesis of preterm neonatal diseases are discussed in this review. Although free radical injury is well recognized in neonatal disease pathogenesis, the effects of antioxidant therapy remain controversial. Careful and individualized control of oxygenation and blood flow perfusion, adequate intake of nutrients that have antioxidant functions, and steps to prevent infection seem to be the best recommendations for infant care in an attempt to prevent neonatal free radical aggression.
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