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PubMed1988

Plasmalogen content and distribution in the sarcolemma of cultured neonatal rat myocytes.

Phospholipids are believed to play an important role in pathology and physiology of the myocardium. Because of the distinct physico-chemical properties of plasmalogens we studied the plasmalogen content and distribution in the sarcolemma of cultured rat myocytes. Treatment with phospholipase A2 degraded all glycerophospholipids in the outer monolayer. The hydrolysis products were analyzed for plasmalogen content. It is shown that the inner sarcolemmal leaflet is highly enriched in phosphatidylcholine and ethanolamine plasmalogen. This distribution of the plasmalogens might affect bilayer stability and thereby be involved in the destruction of the sarcolemma upon ischemia and reperfusion.

Animals↗
PubMed1996

Plasmalogen and anionic phospholipid dependence of the cardiac sarcolemmal sodium-calcium exchanger.

Although plasmalogens are the predominant phospholipids of cardiac sarcolemma, their physiological role has not been forthcoming. Since the cardiac sarcolemmal sodium-calcium exchanger has been proposed to be regulated by anionic phospholipids, the roles of plasmalogens and anionic phospholipids as regulators of the sodium-calcium exchanger were explored. Reconstituted sodium-calcium exchange activity in plasmalogen-containing proteoliposomes was 10-fold higher than that in control proteoliposomes comprised of only diacyl phospholipids. Additionally, exchange activity in plasmalogen-containing proteoliposomes was regulated by anionic phospholipids. Thus, plasmalogens provide a critical lipid environment in which anionic phospholipids serve as boundary lipids for the regulation of the trans-sarcolemmal sodium-calcium exchanger.

Amino Acid Sequence↗
PubMed1989

A simple and sensitive determination for plasmalogen lysophosphatidylethanolamine in rabbit platelets.

Plasmalogen lysophosphatidylethanolamine (LPE) in rabbit platelets was quantitatively determined as glycero-3-phosphorylethanolamine (GPE) after treatment with 5% trichloroacetic acid at 20 degrees C for two hours. GPE was measured directly using a high performance liquid chromatography with monitoring the fluorescence of o-phthaldialdehyde/2-mercaptoethanol adducts. The assay was sensitive to 50 pmol of plasmalogen LPE and was linear over a 200-fold concentration range. While, 1-acyl LPE and phosphatidylethanolamine from bovine brain (containing about 50% plasmalogen) were hardly cleaved to GPE under the same conditions. These procedures were specific for plasmalogen LPE, and simpler and more sensitive in comparison with conventional analytical methods, e.g., two-dimensional thin layer chromatography with subsequent phosphorus assay. Employing the present method, plasmalogen LPE was found to increase rapidly and to decrease subsequently when rabbit platelets were stimulated by thrombin.

Animals↗
PubMed2002

Ethanolamine plasmalogens protect cholesterol-rich liposomal membranes from oxidation caused by free radicals.

The aim of the present study is to investigate the effect of ethanolamine plasmalogens on the oxidative stability of cholesterol-rich membranes by comparing it with that of diacyl glycerophosphoethanolamine, using bovine brain ethanolamine plasmalogen (BBEP) or egg yolk phosphatidylethanolamine (EYPE)-containing large unilamellar vesicles (LUVs) and the water-soluble radical initiator AAPH. Electron microscopic observation and particle size measurement visually demonstrated that ethanolamine plasmalogens protect cholesterol-rich phospholipid bilayers from oxidative collapse. Lipid analyses suggested that the effect of ethanolamine plasmalogens in stabilizing membranes against oxidation is partly due to the antioxidative action of plasmalogens involved in scavenging radicals at vinyl ether linkage.

Amidines↗
PubMed1980

Gas chromatographic determination of the fatty acid pattern of red cell membrane plasmalogens in healthy children.

A gas chromatographic technique for the determination of the fatty acid pattern of the phosphatidylcholine (PC) and phosphatidyl ethanolamine (PE) plasmalogen and non-plasmalogen fractions in human red cell membranes has been developed. The coefficient of variation lies between 5 and 10%. The technique has been applied to blood samples of healthy Belgian school children (8--10 year old). PE contains 47% plasmalogen and 53% non-plasmalogen form, whereas PC occurs only in its non-plasmalogen form. The fatty acid pattern of the various fractions and subfractions has been determined.

Child↗
PubMed1988

Behaviour of plasmalogens during high-performance liquid chromatography on a silica column with a mobile phase containing phosphoric acid.

Silica high-performance liquid chromatographic separation of phospho- and sphingolipids of biological origin using a mobile phase containing phosphoric acid leads to gradual hydrolysis of plasmalogens during their passage through the column. The resulting 2-acyl lyso analogues give rise to peaks that tail in the direction of the parent intact plasmalogen. Tailing can be prevented by previous complete acid hydrolysis of plasmalogens. Direct high-performance liquid chromatographic profiling of phospholipids, their plasmalogens (as 2-acyl lyso analogues) and sphingolipids is probably the method of choice for the diagnosis of patients with deficient plasmalogen biosynthesis caused by peroxisomal abnormalities.

Chromatography, High Pressure Liquid↗
PubMed2003

Gas chromatography/mass spectrometry analysis of very long chain fatty acids, docosahexaenoic acid, phytanic acid and plasmalogen for the screening of peroxisomal disorders.

Very long chain fatty acids (VLCFAs) and docosahexaenoic acid (DHA), phytanic acid, and plasmalogens are usually measured individually. A novel method for the screening of peroxisomal disorders, using gas chromatography/mass spectrometry (GC/MS), was developed. Saturated and unsaturated fatty acids, including VLCFAs and DHA, phytanic acid, and plasmalogen were detected by a selected ion monitoring-electron impact method, using 100 microl of serum or plasma. Methyl-esterification and extraction could be done in one tube, and data were obtained within 4 h. All patients with Zellweger syndrome (ZS), X-linked adrenoleukodystrophy (ALD), isolated deficiency of peroxisomal beta-oxidation enzyme, and most ALD carriers showed increased VLCFA ratios, including C24:0/C22:0, C25:0/C22:0 and C26:0/C22:0. The ratio of DHA to palmitic acid (C16:0) and plasmalogen (measured as hexadecanal dimethyl acetal) to C16:0 in ZS patients was significantly lower than for the controls (P<0.001 for healthy high school students, P<0.05 for infants with other disorders). Plasmalogen was also decreased in patients with isolated deficiency of plasmalogen biosynthesis. Two of eight patients with ZS, two of four with RCDP, and all of three classical Refsum patients showed increased levels of phytanic acid. This method will simplify the screening for peroxisomal disorders.

Adolescent↗
PubMed1999

The protective role of plasmalogens in iron-induced lipid peroxidation.

The role of plasmalogens in iron-induced lipid peroxidation was investigated in two liposomal systems. The first consisted of total brain phospholipids with and without plasmalogens, and the second of phosphatidylethanolamine/phosphatidylcholine liposomes with either diacyl- or alkenylacyl-phosphatidylethanolamine. By measuring thiobarbituric acid reactive substances, oxygen consumption, fatty acids and aldehydes, we show that plasmalogens effectively protect polyunsaturated fatty acids from oxidative damage, and that the vinyl ether function of plasmalogens is consumed simultaneously. Furthermore, the lack of lag phase, the increased antioxidant efficiency with time, and the experiments with lipid- and water-soluble azo compounds, indicate that plasmalogens probably interfere with the propagation rather than the initiation of lipid peroxidation, and that the antioxidative effect cannot be related to iron chelation.

Azo Compounds↗
PubMed1993

Identification of phosphocholine plasmalogen as a lipid component in mammalian pulmonary surfactant using high-resolution 31P NMR spectroscopy.

High-resolution 31P NMR spectroscopy was used to analyze the phospholipid composition of mammalian pulmonary surfactant from two different sources. Under conditions which considerably narrow the usually broad 31P phospholipid signals, solution-phase NMR spectra of these surfactant preparations unequivocally demonstrate that a phosphocholine plasmalogen (i.e., 1-O-(1'-alkenyl)-2-acyl-sn-glycero-3-phosphocholine) exists as a major secondary component (approximately 4 mol%) in mammalian pulmonary surfactant. Phosphocholine (PC) plasmalogen was identified in preparations obtained from both adult cow lung surfactant extract as well as in ovine (lamb) fetal pulmonary liquid. PC plasmalogens have not previously been identified any mammalian pulmonary surfactant preparation. The amount of PC plasmalogen in these preparations occurs at fractional levels that are comparable to that of phosphoglycerol (PG), which previously had been thought of as the second-most common phospholipid class in pulmonary surfactant. The presence of PC plasmalogen in pulmonary surfactant may have important physiological ramifications and immediately suggests new directions for biochemical and biophysical investigations of pulmonary surfactant.

Animals↗
PubMed1985

Identification of plasmalogen as the major phospholipid constituent of cardiac sarcoplasmic reticulum.

The phospholipid molecular species of canine myocardial sarcoplasmic reticulum were identified by fast atom bombardment mass spectrometry, reverse-phase high-performance liquid chromatography, and other conventional techniques. Cardiac sarcoplasmic reticulum contains 1.4 mumol of lipid Pi/mg of protein which is comprised of 53% plasmalogen. Cardiac sarcoplasmic reticulum ethanolamine glycerophospholipid contains 73% plasmalogen that is predominantly comprised of moieties with 18-carbon vinyl ethers at the sn-1 position and arachidonic acid at the sn-2 position. In contrast, canine skeletal muscle sarcoplasmic reticulum contains only 19% plasmalogen that is predominantly comprised of ethanolamine plasmalogen (78% of skeletal muscle sarcoplasmic reticulum ethanolamine glycerophospholipid) with arachidonic and docosatetraenoic acids at the sn-2 position. The possibility that tetraenoic ethanolamine plasmalogens in both cardiac and skeletal muscle sarcoplasmic reticulum facilitate calcium translocation by their propensity for adopting a hexagonal II conformation at physiologic temperatures is discussed.

Animals↗
PubMedDate not supplied

Severe plasmalogen deficiency in tissues of infants without peroxisomes (Zellweger syndrome).

The Zellweger syndrome is a lethal hereditary disease characterized by the absence of peroxisomes (microbodies) in liver and kidney, and variable abnormalities in mitochondria. We show here that tissues from five infants that had died of this syndrome contain less than 10% of the normal levels of phosphatidylethanolamine plasmalogen (pPE), a major phospholipid component of cellular membranes. Heart and muscle, but not other tissues, also contain a substantial fraction of phosphatidylcholine plasmalogen (pPC), and this fraction is also strongly reduced in the Zellweger patients. No other abnormalities in cellular phospholipids were detected. Key enzymes of the biosynthesis of plasmalogens have previously been shown to be exclusively located in the peroxisomes of rodent liver and the microperoxisomes of rodent brain. We infer that the corresponding enzymes are also located in peroxisomes in man and that the absence of peroxisomes in Zellweger patients leads to their inability to synthesize plasmalogens. Our results support the notion that the biosynthetic role of peroxisomes in mammals has thus far been underestimated. We suggest that the defect in plasmalogen synthesis and possibly as yet unknown peroxisomal reactions are responsible for the diverse abnormalities observed in Zellweger patients.

Abnormalities, Multiple↗
PubMed1997

Delayed oxidative degradation of polyunsaturated diacyl phospholipids in the presence of plasmalogen phospholipids in vitro.

The oxidative degradation of plasmalogen (alkenylacyl) phospholipids was analysed in the absence and the presence of polyunsaturated ester phospholipids by 1H-NMR and by chemical determination. Brain lysoplasmenylethanolamine (lyso-P-PE), brain P-PE and erythrocyte P-PE, containing an increasing number of intrachain double bonds at sn2, were oxidized with 2,2'-azobis-(2-amidinopropane hydrochloride) (AAPH; 2 or 10 mM) in Triton X-100 micelles (detergent/phospholipid 1:5, mol/mol). The formation of two peroxyl radicals was accompanied by the degradation of approx. one molecule of brain lyso-P-PE. On oxidation of brain P-PE or erythrocyte P-PE (320 nmol) with 2 mM AAPH, the (alpha-vinyl) methine 1H signal of the enol ether decreased more rapidly than the methine proton peak of intrachain double bonds. The rate of enol ether degradation increased in the order: erythrocyte P-PE>brain P-PE>brain lyso-P-PE. The disappearance of the polyunsaturated ester phospholipids 1-palmitoyl-2-arachidonoyl phosphatidylcholine (16:0/20:4-PC) and 1-palmitoyl-2-linoleoyl phosphatidylcholine (16:0/18:2-PC) (100 nmol), as induced by 10 mM AAPH, was nearly completely inhibited by the plasmalogens (25 nmol) in the first 30 and 60 min of incubation respectively, and was delayed at later time points. Plasmalogens and vitamin E (4-25 nmol) mitigated the decreases in 16:0/[3H]20:4-PC (100 nmol) induced by 2 mM AAPH in a similar manner. The initial rate of degradation of intrachain double bonds of 16:0/20:4-PC and 16:0/18:2-PC (320 nmol; 2 mM AAPH) was decreased by 59% and 81% respectively in the presence of 80 nmol of brain lyso-P-PE. In conclusion, plasmalogens markedly delay the oxidative degradation of intrachain double bonds under in vitro conditions. Interactions of enol ether double bonds with initiating peroxyl radicals as well as with products generated by prior oxidation of polyunsaturated fatty acids are proposed to be responsible for this capacity of plasmalogens. Furthermore, the products of enol ether oxidation apparently do not propagate the oxidation of polyunsaturated fatty acids.

Amidines↗
PubMed2001

Reactive chlorinating species produced by myeloperoxidase target the vinyl ether bond of plasmalogens: identification of 2-chlorohexadecanal.

Plasmalogens contain a vinyl ether bond linking the sn-1 aliphatic chain to the glycerol backbone of this predominant phospholipid molecular subclass, which is found in many mammalian tissues. The present study demonstrates that the vinyl ether bond of plasmalogens is a molecular target of the reactive chlorinating species produced by myeloperoxidase. Analysis by thin layer chromatography revealed that reactive chlorinating species produced by myeloperoxidase target the vinyl ether bond of the plasmalogen, lysoplasmenylcholine (1-O-hexadec-1'-enyl-sn-glycero-3-phosphorylcholine), resulting in the production of a neutral lipid. Capillary gas chromatographic analyses demonstrated that the neutral lipid generated from lysoplasmenylcholine was neither hexadecanal nor did it contain masked hexadecanal (i.e. the vinyl ether) because the dimethyl acetal of hexadecanal produced by acid methanolysis derivatization was no longer present. Electrospray ionization mass spectrometry of the myeloperoxidase-generated neutral lipid product was consistent with the production of a 16-carbon fatty aldehyde containing one chlorine atom. Furthermore, proton NMR analysis indicated that this neutral lipid product was a 2-chloro-fatty aldehyde. Additional structural analysis of this neutral lipid by gas chromatography-mass spectrometry of the underivatized product as well as its pentafluorobenzyl oxime-derivative product was consistent with the neutral lipid being 2-chlorohexadecanal. The reactive chlorinating species, hypochlorous acid and chlorine gas, both attacked the vinyl ether bond of lysoplasmenylcholine resulting in the production of 2-chlorohexadecanal. The production of 2-chlorohexadecanal was dependent on the presence of the plasmalogen masked aldehyde (i.e. the vinyl ether) in the substrate because the free fatty aldehyde, hexadecanal, was not converted to 2-chlorohexadecanal by the reactive chlorinating species generated by myeloperoxidase. Taken together, the present studies demonstrate for the first time the targeting of the vinyl ether bond of plasmalogens by the reactive chlorinating species produced by myeloperoxidase resulting in the production of novel chlorinated fatty aldehydes.

Aldehydes↗
PubMed1991

The rapid and reversible activation of a calcium-independent plasmalogen-selective phospholipase A2 during myocardial ischemia.

Recent studies have demonstrated the existence of two members of a novel family of calcium-independent plasmalogen-selective phospholipases A2 in mammalian myocardium (Wolf, R. A., and R. W. Gross. 1985. J. Biol. Chem. 260:7295-7303; and Hazen, S. L., D. A. Ford, and R. W. Gross. 1991. J. Biol. Chem. 266:5629-5633). To examine the potential role of these calcium-independent phospholipases A2 in mediating membrane dysfunction during early myocardial ischemia, the temporal course of alterations in phospholipase A2 activity during global ischemia in Langendorf perfused rabbit hearts was quantified and compared with traditionally accepted markers of myocytic ischemic injury and anaerobic metabolism. We now report that membrane-associated calcium-independent plasmalogen-selective phospholipase A2 activity increased over 400% during 2 min of global ischemia (P less than 0.01), was near maximally activated (greater than 10-fold) after only 5 min of ischemia, and remained activated throughout the entire ischemic interval examined (2-60 min). Activation of membrane-associated plasmalogen-selective phospholipase A2 after 5 min of myocardial ischemia was rapidly reversible during reperfusion of ischemic tissue. Both the activation of phospholipase A2 and its reversibility during reperfusion were temporally correlated to alterations in myocytic anaerobic metabolism. Furthermore, activation of membrane-associated phospholipase A2 was essentially complete before electron microscopic evidence of cellular damage. Collectively, these results identify dynamic alterations in calcium-independent plasmalogen-selective phospholipase A2 activity during myocardial ischemia which precede irreversible cellular injury and demonstrate that activation of plasmalogen-selective phospholipase A2 is amongst the earliest biochemical alterations in ischemic myocardium.

Animals↗
PubMed1999

Plasmalogen status influences docosahexaenoic acid levels in a macrophage cell line. Insights using ether lipid-deficient variants.

Previously, this laboratory reported the isolation of variants, RAW. 12 and RAW.108, from the macrophage-like cell line RAW 264.7 that are defective in plasmalogen biosynthesis [Zoeller, R.A. et al. 1992. J. Biol. Chem. 267: 8299-8306]. Fatty acid analysis showed significant changes in the mutants in the ethanolamine phospholipids (PE), the only phospholipid class in which the plasmalogen species, plasmenylethanolamine, contributes significantly. Within the PE fraction, docosapentaenoic (DPA; 22:5n-3) and docosahexaenoic (DHA; 22:6n-3) acids were reduced by approximately 50% in the variants while the levels of arachidonic acid (AA; 20:4n-6) remained unaffected. The decrease in DHA was accompanied by a 50% decrease in labeling PE with [3H]DHA over a 90-min period. Restoration of plasmenylethanolamine by supplementing the growth medium with sn -1-hexadecylglycerol (HG) completely reversed these changes in RAW. 108. Pre-existing pools of plasmenylethanolamine were not required for restoration of normal [3H]DHA labeling; addition of HG only during the labeling period was sufficient. Due to the loss of Delta1'-desaturase in RAW.12, HG supplementation resulted in the accumulation of plasmenylethanolamine's immediate biosynthetic precursor, plasmanylethanolamine. Even though this latter phospholipid contained only the ether functionality (lacking the vinyl ether double bond) it was sufficient to restore wild type-like fatty acid composition and DHA labeling of the ethanolamine phospholipids, identifying the ether bond as a structural determinant for this specificity. In summary, we have used these mutants to establish that the plasmalogen status of a cell can influence the levels of certain polyunsaturated fatty acids. These results support the notion that certain polyunsaturated fatty acids, such as DHA, can be selectively targeted to plasmalogens and that this targeting occurs during de novo biosynthesis, or shortly thereafter, through modification of nascent plasmalogen pools.

Animals↗
PubMed1977

The role of the plasmalogen in the cross-reaction between group A streptococcus and human myocardium.

Ethanol-soluble mycardial material which reacts with anti-streptococcal sera in a number of immunological tests has been isolated and identified as ethanolamine plasmalogen. The reactions of cardiac plasmalogen with antistreptococcal sera was specific and could be inhibited by streptococcus-derived materials. Guinea-pigs sensitized to streptococci gave positive skin reactions when challenged with myocardial plasmalogen. The pattern of the immunofluorescent staining given by antiplasmalogen sera was very much like that given by antistreptococcal sera. Nevertheless, the plasmalogen failed to compete for tissue-bound myocardial antigens when tried as an inhibitor of the immunofluorescent staining of myocardium either by antistreptococcal sera or by antiplasmalogen sera. A hypothesis of the role of the plasmalogen in the formation of complexes between streptococci and myocardium-derived material in the initiation of autoimmune processes is presented.

Antibodies, Bacterial↗
PubMedDate not supplied

[Ratio and composition of the plasmalogen and diacylated forms of phospholipids in subcellular fractions of the avian brain].

Studies have been made on the specific content of plasmalogen and diacylated forms of phosphatidylethanolamine and phosphatidylcholine in subcellular fractions (myelin, nuclei, microsomes, mitochondria, synaptosomes) from the brain of pigeons, as well as in the myelin fraction from the brain of the crow Corvus cornix and the hawk Accipiter gentelis. Fatty acid composition and fatty aldehyde composition of these two main phospholipids of the brain were studied in the subcellular fractions obtained. It was shown that plasmalogen forms of phospholipids are localized in birds mainly in the myelin fraction which exhibits the highest plasmalogen concentration as compared to the same fraction of all the vertebrates investigated. With respect to fatty acid and fatty aldehyde composition, as well as to the degree of their unsaturation, myelin plasmalogens from birds are similar to those from other cold-blooded and warm-blooded animals. This fact indicates that high relative content of plasmalogens together with their high unsaturation account for normal functional activity of myelin membranes in all vertebrates.

Aldehydes↗
PubMed1995

Plasmalogens, phospholipases A2 and signal transduction.

Several lines of evidence indicate that the breakdown of plasmalogens in neural membranes during neurodegenerative diseases is a receptor-mediated process catalyzed by a plasmalogen-selective phospholipase A2. This enzyme has recently been purified from bovine brain. It does not require Ca2+ and is localized in cytosol. It has a molecular mass of 39 kDa and is strongly inhibited by glycosaminoglycans, with the pattern of inhibition being heparan sulfate > hyaluronic acid > chondroitin sulfate > heparin. This plasmalogen-selective phospholipase A2 is also inhibited by gangliosides and sialoglycoproteins. Substrate specificity and the effects of metal ions, detergents and inhibitors suggest that this phospholipase A2 is different from the well-known 85 kDa Ca(2+)-dependent cytosolic phospholipase A2 that has recently been cloned and is not plasmalogen-selective. The plasmalogen-selective phospholipase A2 may be regulated by glycosaminoglycans and sialoglycoconjugates and may be involved in the regulation of K+ channels. This enzyme, which plays a major role in the release of fatty acids during ischemic injury and reperfusion, shows promise as a major target for drug therapy.

Animals↗