1262 PULMONARY OXYGEN TOXICITY, LIPID PEROXIDATION, AND VITAMIN E IN THE NEONATAL RAT

Abstract

We have demonstrated inhibition of lung growth and development as well as microscopic injury to result from exposure of newborn rats to 6 days of normobaric hyperoxia as low as FiO₂ 0.4 (Peds. Res. in press). The role of lipid peroxidation in the origins of these effects was investigated by measuring lung vitamin E concentrations and expired pentane during hyperoxic exposure of newborn rats. Lung vitamin E increased from 3.9 μg/g at birth to 25.3 μg/g by day 3 of age in control animals. Denying pups access to dams prevented this increase. Hyperoxia (FiO₂ >0.95, for 3 days) did not lower lung vitamin E concentrations in fed animals (30.6 μg/g). Expired pentane averaged slightly more in fed animals analyzed every 24 hours during a 3 day exposure to FiO₂ >0.95 than in air exposed controls (2.8 pmoles/min/100 g vs. 2.5, or 0.7 vs. 0.5 pmoles/ml O₂ consumed). Exposure of starved newborns to 20 hours of hyperoxia resulted in a dose-related lethality (FiO₂ 0.21, 0/14; 0.4, 6/14; >0.95, 11/15) but lung vitamin E concentrations did not decrease (FiO₂ 0.21, 3.1; 0.4, 3.9; >0.95, 3.4 μg/g). Pentane production in starved newborns fell during a 12 hour exposure to FiO₂ >0.95 (2.4 to 1.5 pmoles/min/100 g). The failure of hyperoxia to reduce lung vitamin E levels coupled with the lack of substantial increases in expired pentane suggests that lipid peroxidation may not play a major role in pulmonary oxygen toxicity in the neonate. However, until the significance of small changes in expired pentane is determined, lipid peroxidation cannot be totally excluded from the mechanism(s) of oxygen-induced lung injury. Supported by NIGMS 12675 and GM 07069.

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