FETAL BRAIN AND LIVER PHOSPHOLIPID FATTY-ACID COMPOSITION IN A GUINEA-PIG MODEL OF FETAL ALCOHOL SYNDROME - EFFECT OF MATERNAL SUPPLEMENTATION WITH TUNA OIL

Chronic prenatal ethanol exposure may impair neurological development and function severely. We have shown previously that feeding ethanol t o guinea pigs throughout pregnancy leads to decreased docosahexaenoic acid 22:6 omega 3) content in brain phospholipids, accompanied by impa ired motor function comparable to some features of human fetal alcohol syndrome. We have tested the hypothesis that dietary supplementation of pregnant guinea pigs with 22:6 omega 3-enriched tuna oil may reduce the ethanol-induced deficit in 22:6 omega 3 accumulation into fetal b rain. Guinea pigs (n = 5/group) were maintained on chow diet either al one or supplemented with 6 gm ethanol/kg/day, ethanol, and tuna oil (0 .5 gm/day; 130 mg 22:6 omega 3/day), or tuna oil alone both before and throughout pregnancy. Fetuses were assessed at term for brain and liv er phospholipid fatty acid composition. Prenatal ethanol exposure sign ificantly decreased fetal brain phosphatidylcholine (PC) and phosphati dylethanolamine (PE) 22:6 omega 3 contents and increased the PC/PE rat io in fetal brain. Feeding both tuna oil and ethanol increased brain P C and PE 22:6 omega 3 content above control values, whereas the PC/PE ratio was similar to control fetuses. Feeding tuna oil alone did not a lter significantly the polyunsaturated content of fetal brain phosphol ipids. These feeding regimens induced markedly different changes to fe tal liver phospholipid compositions compared with brain, which suggest s that the effects of ethanol and/or tuna oil were tissue-specific. Th ese results show that increased 22:6 omega 3 availability modified the effect of ethanol on developing fetal brain phospholipid composition. Such alterations to brain fatty acid content may potentially reduce s ome aspects of the harmful effects of maternal ethanol consumption on prenatal neurological development. (C) Elsevier Science Inc. 1997.