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Phospholipid base-exchange enzymes catalyze the incorporation of nitrogenous bases into phosphoglycerides by a calcium-dependent mechanism. In this study, we describe the effect of ethanol on the incorporation of radioactive serine, choline and ethanolamine into their respective phospholipids in a neuroblastoma x glioma hybrid cell line (NG 108-15). Long term ethanol exposure induced a potentiation of the incorporation of [14C]serine into phosphatidylserine. Moreover, the phosphorus content of PS was found to be increased after long-term ethanol exposure. No concomitant changes in the phosphorus content of other phospholipids were observed. The results indicate that in NG 108-15 cells, the incorporation of radiolabelled serine into PS is potentiated during chronic ethanol exposure.

The effects of repeated episodes of ethanol intoxication and the hyperexcitable state of withdrawal on the synaptosomal concentration of acidic phospholipids were studied in rats. There was no indication that cumulative changes in the synaptosomal acidic phospholipid composition in general occurred during multiple episodes of ethanol intoxication and withdrawal. There was, however, a statistically significant decrease in acidic phospholipid concentration (phosphatidylinositol; PI) in synaptosomal membranes from animals revealing spontaneous convulsive behaviour during ethanol withdrawal. Hypothetically this may reflect an inability to increase acidic phospholipid membrane content and thus to adaptively increase the seizure threshold during withdrawal.

The effect of continuous and intermittent ethanol exposure on the phospholipid composition of Neuroblastoma x Glioma (NG 108-15) cell membranes was investigated. The cells were treated with ethanol for three weeks. Continuous ethanol exposure (150 mM) produced an increase (27%) in the amount of phosphatidylcholine, whereas intermittent ethanol treatment (150 mM) induced a 22% reduction of this lipid. Decreases of phosphatidylethanolamine plasmalogen (8.5%), phosphatidylinositol (16%) and phosphatidylserine (24%) were also seen after intermittent exposure. After binge administration, the concentration of total phospholipids was reduced by 17%, whereas continuous exposure produced a 19% increase. Both intermittent and continuous exposure induced a reduction in the total protein content. No changes in phosphatidic acid, sphingomyelin, phosphatidylcholine plasmalogen or phosphatidylethanolamine (diacyl form) were detected with either treatment. The importance of this study is that ethanol, irrespective of amount, can elicit different effects depending on the pattern of administration.

A densitometric method for simultaneous quantification of individual phospholipids based on visualization with molybdenum blue reagent is presented. Previously reported problems concerning colour instability have been solved. The method is specific for phosphorus-containing compounds and independent of the degree of fatty acid unsaturation. The molar absorptivities of most analysed phospholipids do not differ more than 10% from that for phosphatidylcholine from egg yolk. For cases of greater deviation (sphingomyelin, lysophosphatidylcholine and phosphatidylserine), analysis is accomplished by use of appropriate standard mixtures. The between-series coefficient of variation is ca. 9%. The method is compared to a preparative thin-layer chromatographic assay and another commonly used densitometric method.

An abnormal acidic phospholipid was found in high concentration in kidney and brain, and also in other organs of rats exposed to ethanol by i.p. injection or by a liquid diet. The compound could be identified as phosphatidylethanol. Phosphatidylethanol is probably formed in cell membranes by a phospholipase D-catalyzed transphosphatidylation reaction.

Studies on ethanol-exposed animals have revealed changes in anionic phospholipids in brain membranes. The intention of this study was to investigate whether there was a similar effect on man. Assuming platelets to be an adequate model for CNS synaptosomes, concentration and fatty acid composition of anionic phospholipids, phosphatidylserine (PS) and phosphatidylositol (PI) in the platelet membrane from alcoholics after a debauche period were examined and compared to controls. Ethanol effects on neutral lipids were also analysed in order to obtain a comprehensive view. No quantitative difference was found in anionic phospholipids between alcoholics and controls. Fatty acid composition of individual phospholipids revealed significant changes which were more obvious in neutral phospholipids than in anionic. Oleic acid was increased and linoleic and arachidonic acids were decreased. After 1 week of detoxification, the abnormalities did not decrease, on the contrary they increased and total phospholipid concentration per platelet was significantly higher than in controls. It is concluded that the ethanol toxicity on bone marrow hampers the use of platelets as a model for synaptosomes but that the observed lipid abnormalities might play a major role in the impairment of platelet function in alcoholics.