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Background: Glutathione (GSH) is the major intracellular antioxidant protecting against free radical-mediated damage. Oxidative stress is implicated in the pathogenesis of necrotizing enterocolitis (NEC), and damage could be enhanced by a relative deficiency of GSH.We hypothesized that infants with NEC would have lower levels of erythrocyte GSH when compared with controls. Methods: Total erythrocyte GSH concentration (per gram of hemoglobin g Hb ) was determined in blood samples from infants with NEC (n = 16) referred for surgical intervention. Nonseptic infants referred for other conditions (eg, patent ductus arteriosus ligation) served as controls (n = 10). Results: Controls and infants with NEC were demographically similar. Mean erythrocyte GSH concentration in infants with NEC was 0.076 ±0.004 μmol/g Hb and in controls it was 0.078 ±0.005 μmol/g Hb (P =. 73). There was no significant correlation between GSH concentration and weight, gestational age, or C-reactive protein levels. In infants with NEC, there was no difference in GSH levels between infants with stage 2 and stage 3 diseases nor between those who died and survived, but a trend toward lower GSH levels in infants with more extensive diseases exists. Conclusions: Total GSH levels are similar in infants with NEC and controls. It is possible that a relative rather than absolute deficiency of antioxidant compounds exists and may contribute to the development of NEC.
Background: Glutathione (GSH) is the major intracellular antioxidant protecting against free radical-mediated damage. Oxidative stress is implicated in the pathogenesis of necrotizing enterocolitis (NEC), and damage could be enhanced by a relative deficiency of GSH. We hypothesized that infants with NEC would have lower levels of erythrocyte GSH when compared with controls. Methods: Total erythrocyte GSH concentration (per gram of hemoglobin g Hb) was determined in blood samples from infants with NEC (n = 16) referred for surgical intervention. Nonseptic infants referred for Results: Controls and infants with NEC were demographically similar. Mean erythrocyte GSH concentration in infants with NEC was 0.076 ± 0.004 μmol / g Hb and in controls it (n = 10) was 0.078 ± 0.005 μmol / g Hb (P = .73). There was no significant correlation between GSH concentration and weight, gestational age, or C-reactive protein levels . In infants with NEC, there was no difference in GSH levels between infants with stage 2 and stage 3 diseases nor among those who died and survived, but a trend towards lower GSH levels in infants with more extensive diseases exists. Conclusions: Total GSH levels are similar in infants with NEC and controls. It is possible that a relative rather than absolute deficiency of antioxidant compounds exists and may contribute to the development of NEC.