Abstract
The effect of maternal ethanol consumption during pregnancy upon accumulation of docosahexaenoic acid (22:6( n − 3)) into developing brain phospholipids was determined in a guinea-pig model of fetal alcohol syndrome. Feeding adult guinea-pigs 6 g/kg per day ethanol both before and throughout pregnancy was associated with decreased 22:6( n − 3) concentration in both fetal brain phosphatidylcholine (PC) and phosphatidylethanolamine (PE) at 40/68 days gestation and at term. Since adequate assimilation of 22:6( n − 3) into fetal brain is critical for optimal neuronal development, reduced accumulation of 22:6( n − 3) into phospholipids may be one important mechanism for ethanol-induced brain damage. Liver from ethanol-exposed fetuses contained significantly lower concentrations of both PC and PE 22:6( n − 3)-containing molecular species. However, there was no difference in plasma PC polyunsaturated fatty acid content in ethanol-exposed fetuses compared with controls. One possible explanation for impaired 22:6( n − 3) accumulation into ethanol-exposed fetal brain phospholipids may be the result of the action of inappropriate mechanisms which counteract ethanol-induced increased membrane fluidity by reducing the polyunsaturated fatty acid content of brain phospholipids.
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