Summaryof an unidentified factor in plasma for induction to be dcmonRed cell superoxide dismutase (SOD) enzyme activity was determined in 5 8 cord blood specinlens obtained from infants over a range of gestational ages. An inverse relationship between red cell S O D activity and gestational age was demonstrated. Red cell S O D activity showed a progressive fall from 263.1 k 30.5 units/mg non-hemoglobin protein (NIIP) in infants of less than 29 weeks of gestation to 168.9 +. 21.3 unitslmg N H P in infants of more than 36 weeks of gestation (P < 0.05).Infants treated for RDS showecl an increase in red cell S O D activity which reached significance at 72 hr when colnpared to cord blood levels from the same population ( P < 0.05). No similar significant difference could be demonstrated in gestational age-matched control subjects over the same time period. IIowever, initial cord blood S O D enzylne levels were lower in premature infants with RDS (229.5 k 30.6 unitslmg NI1P) than in premature infants without RDS (264.0 k 38.0 unitslmg ~1 1~) .When infants with RDS were exan~ined for oxygen toxicity and survival, red cell S O D levels were noted to decrease over 24 hr in four of five infants who died, three of whom developed bronchopul~nonary dysplasia. In the surviving infants, red cell S O D levels showed a significant increase by 4 8 hr ( P < 0.05).None developed bronchopulmonary dyplasia and all survived. SpeculationIncreases in red cell superoxide dis~liutase activity in response to hyperoxic stress may prevent toxic effects of 0,-radicals and oxygen toxicity to the lung.Oxygen is fundamental to survival of aerobic systems. However, in excess, molecular oxygcn has bccn associated with toxic tissue effects as noted in bronchopulmonary dysplasia (4,8,33,38) and retrolental fibroplasia (22). The complete reduction of 1 molecule of oxygen yields intern~ediates which include 0,-(superoxide radical), OH.(hydroxyl radical), and H,O, (24). Fridovich (12,13,17,18,25,40) and others (32) have recently proposed that a major part of oxygen toxicity at the cellular level may be mediated by the superoxide radical. All oxygen-metabolizing cells so far examined have been found to contain enzymes that catalyze the reaction: 0 , -+ 0 , -+ 2H+ + H,O, + 0,.These enzymes, which have been characterized as metalloproteins, are designated superoxide dismutases (1 2).Mammalian studies have only recently been attempted in an effort to delineate the relationship of SOD enzyme levels and the occurence of pulmonary oxygen toxicity (3,8,14). Decreased levels of lung SOD have been demonstrated in those infants dying from RDS (4, 38). Induction of enzyme activity has been observed in rat lungs after exposure to increased oxygen concentrations ( 3 , 8 , 14) and seems to be dependent upon the presence strated (3).The red cell provides an accessible source of human SOD. Although the relationship of SOD to bronchopulmonary dysplasia is not clearly understood, measurement of red cell S O D activity in red cells may reflect a response to intrapulmonary...