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PubMed1975

The biosynthesis of plasmalogens by rat brain: involvement of the microsomal electron transport system.

The biosynthesis of 1-alk-1'-enyl-2-acyl-sn-glycero-3-phosphoethanolamine (ethanolamine plasmalogens) was studied using 1-[1-14C]hexadecyl-sn-glycero-3-phosphoethanolamine as the substrate and EDTA-washed microsomes from brains of 14-day-old rats. It was found that the 1-E11-14C]hexadecyl-sn-glycero-3-phosphoethanolamine was first acylated to form 1-[1-14C]hexadecyl-2-acyl-sn-glycero-3-phosphoethanolamine, then was desaturated to form 1-[1-14C]hexadec-1'-enyl-2-acyl-sn-glycero-3-phosphoethanolamine. The desaturation required O2 and NADH or NADPH and was inhibited by KCN but not by CO. The data indicated that the desaturation is carried out by a mixed-function oxidase system similar to that involved in the desaturation of fatty acids and that the pathway for the biosynthesis of plasmalogens in brain is similar to that previously found in other tissues. The desaturase was not stimulated by ATP and Mg2plus nor inhibited by EDTA. The specific activity of microsomes from brains of rats of different ages was determined; the activity decreased with age until in adults the activity was only 15% that of the 12--14-day-old rats.

Animals↗
PubMed1990

Phospholipase A2 activities with a plasmalogen substrate in brain and in neural tumor cells: a sensitive and specific assay using pyrenesulfonyl-labeled plasmenylethanolamine.

We have developed a new assay method for phospholipase A2 (EC 3.1.1.4.), towards ethanolamine plasmalogen using pyrenesulfonyl-labeled plasmenylethanolamine as the substrate. This procedure is sensitive to about 3 pmol/ml per min and is absolutely specific for plasmalogen. In this method, the product of phospholipase A2, pyrenesulfonyl-labeled lysoplasmalogen, is hydrolyzed to aldehyde and labeled glycerophosphoethanolamine with hydrochloric acid exposure, and after TLC separation, the pyrenesulfonyl-glycerophosphoethanolamine is quantitated spectrofluorometrically. The excitation and emission wave lengths were 340 and 376 nm, respectively. The activity of bovine brain homogenate was 44.1 +/- 6.47 pmol/min per mg protein (n = 3). Among bovine brain subcellular fractions, the distribution and specific activity of the enzymes were highest in cytosol (38.7 +/- 1.58% and 102.6 +/- 16.2 pmol/min per mg protein, n = 3). The activities of neural tumor cells, PC12 pheochromocytoma, Neuro2A and SKNSH neuroblastoma and U1242MG glioblastoma, were 34.4 +/- 6.83 (n = 5), 7.05 +/- 0.97 (n = 4), 5.25 +/- 1.69 (n = 5), and 9.68 +/- 1.35 (n = 4), pmol/min per mg protein (M +/- S.E.M.), respectively.

Adrenal Gland Neoplasms↗
PubMed1993

Limited metabolic interaction of serine with ethanolamine and choline in the turnover of phosphatidylserine, phosphatidylethanolamine and plasmalogens in cultured glioma cells.

Modulation of choline phosphoglyceride turnover has been investigated extensively but less is known about regulation of serine and ethanolamine phosphoglyceride synthesis and turnover. We investigated incorporation and interactions of [3H(G)]L-serine, [1,2-14C]ethanolamine and [methyl-3H]choline in cultured glioma cells. Exogenous serine did not compete with ethanolamine or choline incorporation and did not chase labeled headgroup from ethanolamine phosphoglycerides (PE); serine displaced headgroup of prelabeled phosphatidylserine (PtdSer) resulting in less labeled PtdSer for decarboxylation. In contrast, exogenous ethanolamine markedly chased labeled headgroup of non-plasmenylethanolamine phosphoglycerides (NP-PE) with less effect on plasmalogen (1-O-alk-1'-enyl-2-acyl-sn-glycero-3-phosphoethanolamine) whether headgroup was derived from [3H]serine or [14C]ethanolamine. Label in chase medium was mainly ethanolamine to 12 h; phosphoethanolamine was present with longer chase (12-48 h). Choline did not compete with serine incorporation and had little chase effect on PtdSer and PE. Choline and ethanolamine competitively interacted with preference for choline. These data suggest that (1) PtdSer synthesis in cultured glioma cells may involve more than headgroup exchange; (2) PE turnover with metabolite release to medium may involve both phospholipase D and phospholipase C; (3) acceleration of PE turnover by exogenous ethanolamine primarily involves NP-PE with lesser involvement of plasmalogen; and (4) in contrast to lack of interaction between serine and other headgroup precursors, choline and ethanolamine compete primarily at uptake.

Animals↗
PubMed1995

Incorporation of acetyl-CoA generated from peroxisomal beta-oxidation into ethanolamine plasmalogen of rat liver.

We have reported that peroxisomal beta-oxidation has an anabolic function, supplying acetyl-CoA for biosyntheses of bile acids and phospholipids. Here we deal with its role in the biosynthesis of the subclasses of ethanolamine- and choline-containing phosphoglycerides (EPG, CPG, respectively). Rats were fed for 2 weeks on chow containing 0.25% clofibrate, which inhibits cholesterol and bile acid biosyntheses, but stimulates peroxisomal beta-oxidation. [1-14C]Lignoceric acid, which is exclusively degraded by peroxisomal beta-oxidation to acetyl-CoA, was intravenously injected, and 3 h later the rats were killed. The EPG-rich and CPG-rich fractions were prepared from the liver. When they were treated with phospholipase A2, the radioactivity was predominantly recovered in the 1-radyl group. The radioactivity in EPG was easily dissociated with HCl vapor, and the lipid containing radioactivity was found to be a fatty aldehyde mixture consisting of steary aldehyde (approx. 58%) palmityl aldehyde (approx. 40%) and oleyl aldehyde (approx. 2%). Thus, in the case of EPG, acetyl-CoA from peroxisomal beta-oxidation is incorporated mainly into the 1-alkenyl group of ethanolamine plasmalogen. The radioactivity in CPG, however, was found in fatty alcohol (formed from fatty acid), but not in alkylglycerol after reduction of the fraction with Vitride. Thus, in the case of CPG, acetyl-CoA from peroxisomal beta-oxidation is exclusively incorporated into the 1-acyl group of diacyl glycerophosphocholine, but not into the 1-alkyl group. The above results were supported by the results of phospholipase C treatment. The above data indicate that peroxisomal beta-oxidation plays a role in supplying acetyl-CoA for 1-alkenyl group of plasmalogen-type phospholipid, but this channel may open only to synthesis of EPG, and almost not to CPG.

Acetyl-CoA C-Acyltransferase↗
PubMedDate not supplied

Conversion of radiolabelled ethanolamine plasmalogen into the dimethylethanolamine and choline analogue via transphosphatidylation by phospholipase D from cabbage.

Starting from biosynthetically prepared ethanolamine plasmalogen 14C-labelled in the O-alkenyl moiety, choline and dimethylethanolamine plasmalogen were prepared by transphosphatidylation utilizing phospholipase D from cabbage. Investigation of the time course of the reaction showed that transphosphatidylation was simultaneously accompanied by hydrolysis of both the substrate and the desired product, resulting in a maximum of product yield after 1-3 h under the reaction conditions investigated. Optimal reaction conditions gave yields of 40% and 62% (of total radioactivity) respectively for the purified choline and dimethylethanolamine derivatives.

Animals↗
PubMed1993

Transmembrane distribution and translocation of spin-labeled plasmalogens in human red blood cells.

We have synthesized two new spin-labeled alkenylacyl phospholipids (plasmalogens) in order to investigate the transmembrane distribution and transport of this subclass of glycerophospholipids in human red blood cells. The plasmenylethanolamine analogue diffuses rapidly from the outer to the inner leaflet with a half time at 37 degrees C of 30 min comparable to that of the corresponding diacyl-phosphatidylethanolamine spin-label in an ATP-requiring and N-ethyl maleimide sensitive manner. The plateau corresponds to 79% of the aminophospholipids on the inner leaflet. By contrast, after 4 h incubation less than 20% of the plasmenylcholine spin-labels reach the interior. Thus plasmalogens behave as the corresponding diacyl-lipids. We infer that plasmenylethanolamine is transported from the outer to the inner leaflet of the red cell membrane by the aminophospholipid translocase.

Biological Transport↗
PubMed1987

Endothelium-dependent vasorelaxation induced by Cn-acetal plasmalogens.

In this study the effects of the synthetic acetal plasmalogens (AP) C17-AP, C13-AP, C9-AP on isolated rabbit aorta were investigated with emphasis on their putative relationship with endothelium-dependent relaxing factor (EDRF). The various AP were obtained by total synthesis from the related fatty acid chlorides. In isolated rabbit aorta precontracted with phenylephrine (PE, 10(-7) M), C17-AP (greater than 10(-6) M) and C13-AP (greater than 10(-5) M) exerted an endothelium-dependent relaxation (EDR). In contrast, C9-AP was totally devoid of effect. Given 30 or 45 min before PE, C17-AP (greater than 10(-6) M) and C13-AP (greater than 10(-5) M) abolished the carbachol-induced ERD; moreover, following preincubation with C17-AP, enhanced contraction was obtained with carbachol. Similar effects were obtained with preincubation of aortas with both AA(10(-4) M) and A 23 187 (10(-8) M). Conversely preincubation of aortas with carbachol (3X 10(-6) M) and ATP (3 X 10(-5) M) did not significantly modify the carbachol-induced EDR. Atropine (3 X 10(-7) M) did not affect the relaxation induced by C17-AP and C13-AP. The in vivo effects are correlated with the in vitro actions of acetal plasmalogens: C17-AP and C13-AP but not C9-AP, given iv (5 mg/kg) induced a pronounced but transient hypotension which lasted 2-3 min and which was followed by a persistent hypertensive state. Atropine (0.5 and 1 mg/kg; iv) given 5 min before C17-AP inhibited the secondary hypertensive phase. These results show that C17-AP and C13-AP should be added to the list of compounds capable of releasing EDRF.

Adenosine Triphosphate↗
PubMedDate not supplied

Identification and characterization of plasmalogen fatty acids in swine heart.

Reperfusion of ischemic swine myocardium is associated with the loss of sarcolemmal phospholipids resulting in the accumulation of amphiphilic metabolites, lysophosphoglycerides and free fatty acids, especially arachidonic acid, causing electro-physiological dysfunction and cell death. Recently, phospholipids containing a vinyl ether bond at the Sn-1 position, commonly known as plasmalogens, have been identified as major constituents of heart, which contain a large amount of arachidonic acid in the Sn-2 position. Because of the potential importance of plasmalogens, the fatty acid composition of the choline and ethanolamine phosphoglycerides in swine heart was determined. Lipids were extracted from the left ventricular biopsies from swine heart, phosphoglycerides were separated from the neutral lipids by thin layer chromatography, converted into methyl derivatives and analysed by GC. The peaks for fatty acid methyl ester (FAME) and dimethylacetal (DMA) derivatives of choline and ethanolamine phosphoglycerides were confirmed using GC-MS. The results showed high amounts of 18:1 (17 mol%), 18:2 (24 mol %) FAME in choline phosphoglycerides in contrast to the occurrence of a high amount of 20:4 (28 mol%) FAME in ethanolamine phosphoglycerides, suggesting that plasmenylethanolamine, and not plasmenylcholine, may serve as the depot for arachidonic acid in swine heart.

Animals↗
PubMed1995

Fatty acid profiles of plasmalogen choline and ethanolamine glycerophospholipids in pig and rat hearts.

The presence of relatively high concentrations of plasmalogen choline and ethanolamine in the heart of many animal species suggests a role of these ether-linked phospholipids in the pathophysiology of certain myocardial diseases. However, the fatty acid composition of myocardial plasmalogens in many species is not known. This study examined the fatty acid composition of the choline and ethanolamine glycerophospholipids in pig heart and compared the results with those in rat heart. Lipids were extracted from the heart biopsies obtained from pig and rat by standard techniques. Phosphoglycerides were separated by thin-layer chromatography followed by their derivatization into fatty acid methyl esters (FAMEs) and dimethyl acetals (DMAs). FAME and DMA samples were analyzed using gas chromatography-mass spectroscopy. Our results indicate striking differences in the fatty acid composition of both choline and ethanolamine glycerophosphates between rat heart and pig heart. Pig heart ethanolamine glycerophosphates are rich in linoleic acid (18:2) and arachidonic acid (20:4), but low in descosahexenoic (22:6) fatty acids while choline glycerophosphates are poor in both 20:4 and 22:6 fatty acids compared to those in rat hearts.

Animals↗
PubMed2006

Phospholipase A2-catalyzed hydrolysis of plasmalogen phospholipids in thrombin-stimulated human platelets.

In the present study, phospholipase A(2) (PLA(2))-catalyzed hydrolysis of platelet membrane phospholipids was investigated by measuring PLA(2) activity, phospholipid hydrolysis, arachidonic acid release and choline lysophospholipid production in thrombin-stimulated human platelets. Thrombin-stimulated platelets demonstrated selective hydrolysis of arachidonylated plasmenylcholine and plasmenylethanolamine, with little change in diacyl phospholipids. Accelerated plasmalogen hydrolysis was accompanied by increased arachidonic acid and thromboxane B(2) release and increased lysoplasmenylcholine production. Thrombin stimulation caused an increase in PLA(2) activity measured in the cytosolic fraction with plasmenylcholine only; no increase in activity was measured with phosphatidylcholine. No change in membrane-associated PLA(2) activity was observed with either substrate tested. Pretreatment with the Ca(2+)-independent PLA(2)-selective inhibitor, bromoenol lactone, inhibited completely any thrombin-stimulated phospholipid hydrolysis. Thus, thrombin stimulation of human platelets activates a cytosolic PLA(2) that selectively hydrolyzes arachidonylated plasmalogen phospholipids.

Arachidonic Acid↗
PubMed1988

Quantification of plasmalogen, alkylacyl and diacyl glycerophospholipids by micro-thin-layer chromatography.

A method for the determination of plasmalogen, alkylacyl and diacyl glycerophospholipids based on mild alkaline deacylation and acid hydrolysis of plasmalogens on plates with subsequent micro-thin-layer chromatography on silica gel is presented. It is effective in quantifying alkyl and alkenyl analogues of phosphatidylethanolamine and phosphatidylcholine at concentrations up to 0.1% (of the total of the forms in individual classes of phospholipids.

Animals↗
PubMed2002

Facile synthesis of plasmalogens via Barbier-type reactions of vinyl dioxanes and vinyl dioxolanes with alkyl halides in LiDBB solution.

Plasmalogens (i.e. plasmenylcholines or plasmenylethanolamines) are a biologically important class of glycerophospholipids that have been difficult to synthesize due to the presence of an acid and oxidatively labile (Z)-vinyl ether substituent at the sn-1 position and a base-labile sn-2 acyl substituent that easily migrates during silica gel purification. We report two facile synthetic methods for the preparation of racemic plasmenylcholines via a tandem reductive vinyl dioxane/dioxolane ring opening and alkyliodide coupling process that proceeds in a single pot reaction. The key step in the formation of (Z)-vinyl ether precursors for the production of plasmenylcholines is accomplished using LiDBB under Barbier-type conditions to give the corresponding TBDMS-protected 1-O-Z'-vinylglycerol intermediate in moderate yields. This pathway is the most direct synthetic route for the formation of plasmenylcholines to date, requiring a total of six transformations from acrolein and glycerol or solketal as inexpensive starting materials, to generate glycerophosphocholine-type plasmalogens in 4% overall yield.

Catalysis↗
PubMed1999

Temporal and quantitative expression of the myelin-associated lipids, ethanolamine plasmalogen, galactocerebroside, and sulfatide, in the differentiating CG-4 glial cell line.

We determined the expression of three myelin-typical lipids in the continuous CG-4 glial cell line of oligodendrocyte progenitor cells, as the cells differentiated into oligodendrocytes. On 6 different days during the first 9 days of oligodendrocyte development, cells were labeled for 24 h with [3H]ethanolamine to label ethanolamine plasmalogens or with [3H]galactose to label the galactocerebroside and sulfogalactocerebroside; and the amount of labeled lipid expressed on each day was determined. Each labeled lipid was expressed with its own specific time course and in a defined amount on each day of differentiation. Increased labeling of plasmalogens and sulfogalactocerebroside started at early developmental stages, and increased labeling of galactocerebroside started at later stages. The results indicate that the differentiating CG-4 cell line provides a valuable system to investigate factors affecting the early time course of myelin-lipid expression and the amounts expressed.

Animals↗
PubMed1997

Membrane phospholipid alterations in Alzheimer's disease: deficiency of ethanolamine plasmalogens.

The ethanolamine plasmalogens are decreased whereas serine glycerophospholipids are significantly increased in plasma membrane phospholipid in affected regions of brain in Alzheimer's disease. This may be due to stimulation of Ca(2+)-independent plasmalogen-selective phospholipase A2 which was recently discovered in brain. This phospholipase A2 differs from other Ca(2+)-independent phospholipases A2 in response to ATP and various inhibitors. It may be responsible for excess release of arachidonic acid and accumulation of prostaglandins and lipid peroxides in AD. Accumulation of the above lipid metabolites due to abnormal receptor function and signal transduction may contribute to neurodegeneration in AD.

Alzheimer Disease↗
PubMed2004

Studies of myo-inositol and plasmalogen metabolism in rat brain.

Plasmalogens are ether-linked phospholipids that are abundant in nervous tissues. Their biological role is unclear, but may involve membrane structure/function and antioxidant activities. This study further investigates a recent report that chronic administration of myo-inositol in rats increased brain phosphatidylethanolamine plasmalogen (PlsEtn). We examined the effects of myo-inositol administration on the incorporation of [2-(13)C]ethanolamine ([2-(13)C]Etn) into rat brain phospholipids using NMR spectroscopy. Rats received either acute myo-inositol (single dose) +/- [2-(13)C]Etn, or chronic myo-inositol (10-day treatment) + [2-(13)C]Etn. Controls received saline rather than myo-inositol. Acute myo-inositol produced a 68% increase in brain [myo-inositol] and an increase in the incorporation of [2-(13)C]Etn into phospholipids (P < .05). The PlsEtn/phosphatidylethanolamine ratio and the [PlsEtn] were increased by 27% and 30%, respectively. The PlsEtn content as a mole percentage of total phospholipids was elevated (P < or = .05). Acute administration of myo-inositol + ethanolamine illustrates a positive correlation between the brain [myo-inositol] and the biosynthesis of ethanolamine phospholipids, with preferential synthesis of PlsEtn.

Animals↗
PubMed1995

Plasmalogen phospholipid hydrolysis during hypoxic injury of rabbit proximal tubules.

We have identified and quantified the major species of arachidonate-containing phospholipids in proximal tubules by high performance liquid chromatographic and gas chromatographic analyses. Arachidonate was found to comprise 53% of the total mass of fatty acids esterified at the sn-2 position of ethanolamine phospholipids, and 51% of that amount resides in three plasmenylethanolamine species containing the vinyl ethers of palmitaldehyde, oleylaldehyde or stearylaldehyde at the sn-1 position. Choline phospholipids contained 21% arachidonylated species and 33% of that amount resides in a single plasmenylcholine species containing the vinyl ether of palmitaldehyde at the sn-1 position. Ten minutes of hypoxia did not cause a significant change in the total phospholipid mass of ethanolamine or choline phospholipids; however, phosphate analysis of the individual phospholipid molecular species containing esterified arachidonic acid in isolated proximal tubules demonstrated a 24% reduction in the mass of the plasmenylethanolamine molecular species with the vinyl ether of oleylaldehyde at the sn-1 position and a 35% reduction in the mass of plasmenylcholine species with palmitaldehyde at the sn-1 position. These studies underscore the pathophysiological importance of plasmalogen phospholipid hydrolysis and suggest that activation of PLA2s, which utilize endogenous proximal tubule plasmalogen substrates, may play an important role in the early generation of arachidonic acid and accompanying phospholipid catabolism during hypoxic cell injury.

Animals↗
PubMedDate not supplied

Free radical oxidation of plasmalogen glycerophosphocholine containing esterified docosahexaenoic acid: structure determination by mass spectrometry.

Plasmalogen phospholipids have a vinyl ether substituent at the sn-1 position that is susceptible to oxidative reactions that occur at cell membranes. However, the mechanism by which this oxidation occurs and the effect of the polyunsaturated fatty acid at the sn-2 position have not been established. To gain insight into these mechanisms, the oxidized phospholipid products resulting from the exposure of 1-O-hexadec-1'-enyl-2-docosahexaenoyl-sn-glycero-3-phosphocholine (16:0p/22:6-GPCho) to the free radical initiator 2, 2'-azobis (2- amidinopropane) hydrochloride were examined. Electrospray ionization tandem mass spectrometry, UV spectroscopy, and electron ionization-gas chromatography/mass spectrometry were used to structurally characterize the oxidized glycerophosphocholine (GPCho) products. The radical-induced peroxidation of 16:0p/22:6-GPCho revealed two major classes of oxidized phospholipids. The first class of products was formed by oxidation at the sn-1 position and included 1-lyso-2-docosahexaenoyl-GPCho and 1-formyl-2-docosahexaenoyl-GPCho. Additionally, the second class of oxidized products where oxidation occurred at the sn-2 position was classified into three categories that included chain-shortened omega-aldehydes, terminal gamma-hydroxy-alpha,beta-unsaturated aldehydes, and the addition of one or two oxygen atoms onto the sn-2 position of 16:0p/22:6-GPCho. These results clearly indicate that free radical-induced oxidation of plasmalogen phospholipids with esterified docosahexaenoic acid at the sn-2 position underwent oxidation at both the sn-1 and sn-2 positions.

Aldehydes↗
PubMed1983

Homogenized bovine milk xanthine oxidase: a critique of the hypothesis relating to plasmalogen depletion and cardiovascular disease.

A hypothesis has repeatedly been promoted that xanthine oxidase from homogenized bovine milk is absorbed intact, damaging cardiovascular tissue by depleting plasmalogens and initiating atherosclerotic changes that culminate in heart disease. In the light of recent experimental evidence, the present paper examines the validity of this hypothesis and associated claims. The evidence leads to the conclusion that 1) absorption of dietary xanthine oxidase has not been demonstrated; 2) a relationship between intakes of homogenized milk and levels of serum xanthine oxidase activity have not been established; 3) a direct role for xanthine oxidase in plasmalogen depletion has not been established; 4) neither liposome formation during homogenization of milk nor absorption of intact liposomes from the gastrointestinal tract has been demonstrated; and 5) data are lacking to support the claim that large doses of folic acid inhibit xanthine oxidase in vivo and/or are therapeutic in heart disease. Experimental evidence has failed to substantiate, and in many cases has refuted, the xanthine oxidase/plasmalogen depletion hypothesis.

Animals↗