Alcohol-related birth defects--the past, present, and future.

In 1994 Alcohol Health & Research World (now titled Alcohol Research & Health) last devoted a full issue to the topic of fetal alcohol syndrome (FAS) and other alcohol-related birth defects (ARBD). This introductory article provides readers with information on how the field has advanced since then. In addition to tracing the development of the terminology used in the field, it describes the difficulties involved in determining the true prevalence of FAS and ARBD; the mechanisms that may play a role in alcohol-derived fetal injuries; approaches to preventing drinking during pregnancy; and strategies for assisting people who have been born with FAS and ARBD.

Changes in lipid composition of rat heart mitochondria after chronic ethanol administration.

Triacylglycerols and phospholipids of mitochondria from heart ventricular muscle were analyzed following chronic ethanol administration (2 and 10 g/kg of body weight/day) to adult rats for 21 days via intragastric intubation. Triacylglycerols were elevated 57% in the high ethanol group as compared to controls, but cholesterol level was not altered. Most of the phospholipids, including lysophospholipids, showed a small increase in level after ethanol administration. However the greatest increase (50%) occurred in ethanolamine plasmalogens. Although small changes in the acyl group composition of phosphatidylethanolamines and phosphatidylcholines were observed, the acyl group profile of cardiolipin remained unaltered. It is concluded that myocardial membranes respond to the disordering effects of ethanol by altering the synthesis of selected lipids more than through altering the phospholipid acyl group composition. Some of these changes may be responsible for altered mitochondrial functions in the myocardium.

On the status of lysolecithin in rat cerebral cortex during ischemia.

Lysolecithin (lysoglycerophosphocholine, LPC) was isolated from rat cerebral cortex and quantitatively analyzed at various times after postdecapitative ischemic treatment. In addition, different procedures for extraction and analysis of the LPC in brain were evaluated. Results indicated that LPC can be quantitatively extracted into the organic phase using the conventional extraction procedure with chloroform-methanol (2:1, vol/vol). However, care should be taken to avoid using strong acids, which can hydrolyze the alkenylether side chain of the plasmalogens, resulting in the release of 2-acylphospholipids. Quantitative GLC analysis using myristoyl-LPC as internal standard revealed a level of 1.8 nmol LPC/mg protein in brain with acyl groups comprised mainly of 16:0, 18:0, and 18:1. The acyl group profile reflects that the LPC are derived mainly from phospholipase A2 action. An increase of 46% in the LPC level was observed at 1 min after ischemic treatment, but this was followed by a steady decline. Ischemia induced an increase in the LPC species that are enriched in 18:0 and 18:1 fatty acids. The transient appearance of LPC during ischemia further suggests that this phospholipid is undergoing active turnover, possibly hydrolysis by the lysophospholipase. This mechanism of action may account, at least in part, for the increase in both saturated and unsaturated fatty acids during the early phase of the ischemic treatment.

Ethanol consumption and serum lipid profiles in Sinclair(S-1) miniature swine.

Ethanol consumption was correlated with changes in acyl group profiles of phosphatidylcholine and triacylglycerols in serum of Sinclair(S-1) miniature boars. Serum triacylglycerols in the control pigs were high in linoleate (18:2) (48%) and low in stearate (18:0 (3%). Upon feeding with 10% (w/v) ethanol ad lib for two weeks, the proportion of 18:2 in serum triacylglycerols decreased to 12-15% with a concomitant increase in 16:0, 18:0 and 18:1. Similar, but less extensive, acyl group changes were observed in the serum phosphatidylcholine. In addition, there was a decrease in the proportion of 20:3(n-6), but a biphasic change was shown in 20:4(n-6) with respect to ethanol consumption. In general, the high ethanol consumers (7.0 g/kg/day) indicated a more rapid rate of acyl group change than the low consumers (3.8 g/kg/day). Upon withdrawal of ethanol, acyl groups of triacylglycerols rapidly returned towards the control values, whereas only small changes were observed for the recovery in phospholipids. In this situation, the low-consumer group indicated a more rapid recovery than the high-consumer group. Results indicate that with the swine model, serum lipid changes can be a useful parameter for correlating biological changes upon ethanol consumption.

Serum albumin washing specifically enhances arachidonate incorporation into synaptosomal phosphatidylinositols.

Arachidonate incorporation into synaptosomal phospholipids was shown to be affected by factors including the procedure for preparation of the membrane fractions and preincubation of synaptosomes prior to assay of incorporation of arachidonate into both phosphatidylcholine (PC) and phosphatidylinositol (PI). However, the inhibition toward incorporation into PIs, but not PCs, was fully reversed when the membranes were washed with bovine serum albumin. A twofold increase in arachidonate incorporation into PIs was also observed when freshly prepared synaptosomes were washed with serum albumin immediately before assay of incorporation activity. The inhibitory action is thought to be due to an increase in polyunsaturated fatty acids and/or their oxidation products which may then elicit a special effect on the acyltransferase responsible for transferring arachidonate into phosphatidylinositols. The differences in fatty acid uptake and response to serum albumin also suggest the presence of different acyltransferase for acyl transfer to PIs and PCs.