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December 1988

Iron, Plasma Antioxidants, and the 'Oxygen Radical Disease of Prematurity'

Author Affiliations

From the Laboratory Service, Veterans Administration Medical Center, and the Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston.

Am J Dis Child. 1988;142(12):1341-1344. doi:10.1001/archpedi.1988.02150120095048

Oxygen radical injury may be a common pathogenic mechanism in several neonatal diseases. The list includes but is not limited to retinopathy of prematurity, bronchopulmonary dysplasia, subependymal and intraventricular hemorrhage, and necrotizing enterocolitis. The greater incidence of these disorders in preterm infants suggests that some aspect of prematurity increases susceptibility to the effects of toxic oxygen species. Saugstad1 has proposed the term "oxygen radical disease in neonatology" to describe the apparent propensity of neonates to oxygen radical injury. Because of the greater incidence in preterm infants, perhaps a better name for this disorder would be "oxygen radical disease of prematurity." Saugstad's work emphasizes increased oxygen radical production associated with increased levels of hypoxanthine, especially following hypoxia. Although elevated hypoxanthine concentrations after hypoxia increase Superoxide production in the presence of xanthine oxidase, this effect may not completely explain the selectivity of the proposed oxygen radical disease for premature infants. Premature infants

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