EFFECT OF MATERNAL ETHANOL-CONSUMPTION DURING PREGNANCY ON THE PHOSPHOLIPID MOLECULAR-SPECIES COMPOSITION OF FETAL GUINEA-PIG BRAIN, LIVER AND PLASMA

被引：43

作者：

BURDGE, GC ^{[1
]}

POSTLE, AD ^{[1
]}

机构：

[1] UNIV SOUTHAMPTON, SOUTHAMPTON, HANTS, ENGLAND

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-LIPIDS AND LIPID METABOLISM | 1995年 / 1256卷 / 03期

关键词：

FETAL ALCOHOL SYNDROME; PHOSPHOLIPID; DOCOSAHEXAENOIC ACID; BRAIN; (GUINEA-PIG);

D O I：

10.1016/0005-2760(95)00044-D

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：346 / 352

页数：7