Decreased oxidative metabolism in neonatal rat lung exposed to hyperoxia

The effect of exposure to high O2 concentration on neonatal rat lung oxidative function was determined. The water content of lungs from neonatal rats exposed to 100% O2 for the first 6 days of life was 3% greater than room-air control, indicating minimal pulmonary edema. Since neonatal rat lungs exposed to O2 have minimal pulmonary edema, they provide a model to determine the direct effect of O2 on mitochondrial oxidative function. After 6 days of exposure to 100% O2, lactate production by lung slices of neonatal rats was twofold greater than room-air controls. Lactate production by lung slices of neonatal rats exposed to six days of O2 and then 3 days of room air was equal to controls. Total pyruvate dehydrogenase activity was 45% lower in O2-exposed lung compared with control, and active pyruvate dehydrogenase activity was 20% lower. The oxidation of lauric acid, acetate, and beta-hydroxybutyrate was 40% lower in the O2-exposed lung compared with controls. These data suggest that there is a toxic effect of O2 on mitochondrial oxidative function in the absence of severe pulmonary edema and that these toxic effects are reversible within 72 h.