Fetal brain and liver phospholipid fatty acid composition in a guinea pig model of fetal alcohol syndrome: Effect of maternal supplementation with tuna oil

Abstract

Chronic prenatal ethanol exposure may impair neurological development and function severely. We have shown previously that feeding ethanol to guinea pigs throughout pregnancy leads to decreased docosahexaenoic acid 22:6ω3) content in brain phospholipids, accompanied by impaired motor function comparable to some features of human fetal alcohol syndrome. We have tested the hypothesis that dietary supplementation of pregnant guinea pigs with 22:6ω3-enriched tuna oil may reduce the ethanol-induced deficit in 22:6ω3 accumulation into fetal brain. Guinea pigs (n = 5/ group) were maintained on chow diet either alone or supplemented with 6 gm ethanol/kg/day, ethanol, and tuna oil (0.5 gm/day; 130 mg 22:6ω3/day), or tuna oil alone both before and throughout pregnancy. Fetuses were assessed at term for brain and liver phospholipid fatty acid composition. Prenatal ethanol exposure significantly decreased fetal brain phosphatidylcholine (PC) and phosphatidylethanolamine (PE) 22:6ω3 contents and increased the PC PE ratio in fetal brain. Feeding both tuna oil and ethanol increased brain PC and PE 22:6ω3 content above control values, whereas the PC PE ratio was similar to control fetuses. Feeding tuna oil alone did not alter significantly the polyunsaturated content of fetal brain phospholipids. These feeding regimens induced markedly different changes to fetal liver phospholipid compositions compared with brain, which suggests that the effects of ethanol and/or tuna oil were tissue-specific. These results show that increased 22:6ω3 availability modified the effect of ethanol on developing fetal brain phospholipid composition. Such alterations to brain fatty acid content may potentially reduce some aspects of the harmful effects of maternal ethanol consumption on prenatal neurological development.