IN VIVO LIPID PEROXIDATION IN NEWBORN RABBITS: EFFECT OF OXYGEN AND VITAMIN E

Abstract

Expired ethane and pentane are sensitive in vivo monitors of lipid peroxidation. The present study examined the effect of vitamin E (E) on lipid peroxidation in newborn rabbit pups exposed to normoxia (A) or hyperoxia (O₂). All pups were given parenteral fluid (electrolytes and glucose) and were treated with either E (100 mg/kg α-tocopherol IV) or placebo. O₂ exposure did not alter expired pentane levels in either the E- or placebo-treated pups (3.3 pmoles/100 g/min in O₂ vs 4.1 pmoles/100 g/min in A). Expired pentane levels were significantly reduced in E-treated A or O₂-exposed pups compared to placebo-treated A or O₂-exposed pups (1.6 pmoles/100 g/min in E vs 6.6 pmoles/100 g/min in placebo). Lung E levels were 162 ± 42 μg α-tocopherol/g in E-treated vs 4.2 ± 6 μg/g in controls (mean ± SD). Expired ethane levels were not different among the four treatment groups. Animals given only parenteral fluid had a 13% 3-day mortality in O₂ vs 0% in A. Elevated expired pentane levels (300 pmoles/kg/min) in an infant on parenteral lipid emulsion were not altered by E therapy (100 mg/kg α-tocopherol daily p.o. × 3). These data show that a single 100 mg/kg IV dose of E significantly increased lung E levels and reduced expired pentane in newborn rabbits given only parenteral fluids. O₂ did not effect expired ethane or pentane levels but did result in lung injury and mortality. Oxygen toxicity may arise from mechanisms other than those associated with lipid peroxidation. (Supported by NIH GM12675 and PMA Fellowship.)

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