NEWBORN RED BLOOD CELLS (RBC's), THE NATURE OF OXIDANT INJURY

Abstract

Unlike adult cells, newborn RBC's readily undergo oxidant damage. The nature of the defect causing this is unclear. In order to determine those factors related to newborn RBC oxidant susceptability, cord blood was obtained from 88 term infants. As expected, acetylphenylhydrazine (APH) induced Heinz Body (HB) formation was greater in newborn vs adult RBC's (3.24 HB/RBC vs 0.27). Although newborn RBC superoxide dismutase (SOD) activity, at 91% of adult levels, was slightly but significantly lower than adult RBC's (paired T-4.0 p<0.001), higher levels of SOD were associated with greater APH induced HB and H2O2 formation (as determined by the aminotriazole - catalase inhibition assay). The addition of SOD to newborn RBC's produced additional significant increases in HB and H2O2. No correlation existed between %HbF, amount of HbF oxidized and HB or H2O2 formed although H2O2 production was 82% > in newborn RBC's. With equivalent H2O2 production, HB formed readily in newborn cells only. Glutathione peroxidase (GSH Px) levels were equivalent in newborn and adult RBC's. Despite the H2O2 formed, the fall in newborn RBC reduced glutathione (GSH) levels induced by menadione failed to exceed that of adult RBC's when incubated in the absence of glucose.These data demonstrate that SOD deficiency is not a cause of the vulnerability of newborn RBC's to oxidant damage; in fact > SOD is associated with > oxidant effect. It appears that > H2O2 generation and ineffective detoxification by GSH (inspite of “normal” levels of GSH Px) are the major determinants of oxidative damage.