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PubMed1991

Activation of a membrane-associated phospholipase A2 during rabbit myocardial ischemia which is highly selective for plasmalogen substrate.

Recently, the prototype of a novel class of calcium-independent plasmalogen-selective phospholipase A2 activities was identified in the cytosolic fraction of canine myocardium (Wolf, R.A., and Gross, R.W. (1985) J. Biol. Chem. 260, 7295-7303) and subsequently purified and characterized (Hazen, S.L., Stuppy, R.J., and Gross, R.W. (1990) J. Biol. Chem. 265, 10622-10630). We now demonstrate that 15 min of myocardial ischemia utilizing a rabbit Langendorf perfused heart model results in a 10-fold increase in membrane-associated calcium-independent phospholipase A2 activity whose detection is entirely dependent upon utilization of plasmalogen substrate. Ischemia-induced phospholipase activity was identified as a membrane bound member of this class of phospholipases A2 by demonstration of: 1) concomitant production of lysoplasmenylcholine and sn-2 fatty acid from plasmenylcholine substrate; 2) maximal enzymatic activity in the absence of calcium ion; and 3) a 16-fold higher maximum reaction velocity utilizing plasmenylcholine compared to phosphatidylcholine substrate at multiple surface concentrations. Ischemia-induced phospholipase A2 activity was specifically localized to the microsomal fraction and could not be solubilized by sonication, salt treatment, exposure to chelators, or utilization of submicellar concentrations of detergent. The appearance of microsomal phospholipase A2 activity did not require ischemia-induced transcription or translation since identical increases in enzymic activity were obtained in hearts previously treated with actinomycin D and cycloheximide. Collectively, these results demonstrate that a membrane-associated calcium-independent phospholipase A2 that selectively hydrolyzes plasmalogen molecular species is the likely enzymic mediator of accelerated phospholipid catabolism during early myocardial ischemia.

Animals↗
PubMedDate not supplied

Membrane phospholipids and plasmalogens in the ischemic myocardium.

This review begins with discussion concerning the effects of changes in phospholipid compositions on membrane functions. Next, pathogenetic mechanisms of ischemic cell damage are reviewed; a) membrane phospholipid breakdown, caused by the activation of phospholipases, as well as the intracellular Ca2+ overload, and b) univalent oxygen reduction and lipid peroxidation, probably all play important roles. Consequently, hydrophilic metabolites of lipid peroxidation may accumulate in the hydrophobic membrane bilayer during ischemia, causing membrane dysfunction. Free radicals may involve the cross-linking of membrane proteins as well. Previous results in support of the free radical hypothesis of myocardial ischemic injury are described; they were obtained from ESR studies, measurements of tissue antioxidants, determinations of lipid breakdown products, and studies using scavengers. The distribution, biosynthesis and physical-chemistry of plasmalogens are then discussed. Excepting the platelet activating factor recently discovered, only fragmentary information is available concerning the function of plasmalogens. It is possible that membrane plasmalogens, which contain large amounts of polyunsaturated fatty acids, are vulnerable to free radical/ischemic injury.

Animals↗
PubMed1989

Plasmalogen biosynthesis in the diagnosis of peroxisomal disorders.

Fibroblasts of patients suffering from peroxisomal disorders such as chondrodysplasia punctata (rhizomelic type), neonatal adrenoleukodystrophy, Zellweger syndrome and control fibroblasts were used for the evaluation of a procedure suitable for pre- and postnatal diagnosis. This technique is based on the detection of impaired peroxisomal plasmalogen synthesis by means of a double substrate, double labelling technique using 14C-labelled hexadecanol and 3H-labelled hexadecylglycerol as precursors for peroxisomal and microsomal plasmalogen synthesis. Pathological cells are characterized by a decreased utilization of hexadecanol, thus resulting in an increased 3H/14C ratio within plasmalogens. Sensitivity and reproducibility of this method were improved by changing both the chromatographic conditions and the calculation of the diagnostic parameters.

Adrenoleukodystrophy↗
PubMed1988

[Time-course changes in the alkenyl and acyl chain composition of plasmalogens from the heart and kidneys of rats ingesting trielaidin].

Weaned rats were fed for 7 or 32 days a semi-purified diet containing 10% of fat supplement in which elaidic acid accounted for 64.5% of total fatty acids. Alkenyl groups from plasmalogens of kidney and heart mitochondria were analysed as their alkyl-substituted dioxane derivatives by gas liquid chromatography (GLC). Acyl chains of total and individual phospholipids (phosphatidylcholine: PC; phosphatidylethanolamine: PE, diacyl and alkenyl-acyl forms; phosphatidylinositol: PI; cardiolipin: CL) were also analysed by GLC. Maximum level of elaidic acid incorporation was attained after only one week on the experimental diet in either total or individual phospholipids. Heart mitochondria phospholipids contained about 40% more trans-monounsaturated acids (20.9%) than kidney mitochondria phospholipids (12.5%) after one month. trans-Monounsaturated acids (t-18: 1 plus t-16: 1 acids) were incorporated in individual phospholipids from both organs in decreasing order: PI greater than PE (total) greater than PC much greater than CL. The order of incorporation of elaidic acid seemed to be related to the content of stearic acid in these phospholipids when the diet was devoid of elaidic acid (PI greater than PE greater than PC much greater than CL). The content of elaidic acid in alkenyl-acyl-glycerophosphoethanolamine (alkenyl-acyl-GPE) was the same (6% of total fatty acids) in both organs. The time-course incorporation of trans-monounsaturated alkenyl chains was different. After one week on the elaidic acid-enriched diet, they represented only 65% (kidney) or 43% (heart) of the values reached after one month. At the end of the feeding period, the trans-monounsaturated alkenyl chains were also about 40% less in total plasmalogens from kidney mitochondria (27.8%) than from heart mitochondria (46%). trans-Monounsaturated acyl chains were incorporated at a higher rate in the 2-position of alkenyl-acyl-GPE than trans-monounsaturated alkenyl chains in their 1-position. Our results confirm the unique observation of Kramer et al. (1985) who noticed that the fatty acid composition of phospholipids was much more rapidly equilibrated than the alkenyl chain composition of plasmalogens (1 week vs 2-3 weeks) from heart of rats fed diets supplemented with different oils.

Animals↗
PubMedDate not supplied

[Correlation and composition of the plasmalogen and diacyl forms of phosphatidylethanolamine in subcellular brain fractions of the trout Salmo irideus and the frog Rana temporaria].

In myelin, nuclear, microsomal, mitochondrial and synaptosomal fractions from the brain of the trout and frog, studies have been made on the composition of fatty acids and fatty aldehydes of the plasmalogen form and fatty acids of the diacylic form of phosphatidylethanolamin. It was shown that alongside with the increase of the relative content of the plasmalogen form of phosphatidylethanolamin in subcellular fractions of the brain in the frog, especially in the myelin, changes also take place in the composition of fatty acids (the increase in the content of polyenic acids, especially of arachidonic one) and fatty aldehydes (the increase in the degree of unsaturation). Brain myelin of coldblooded vertebrates exhibits similarity with myelin from higher vertebrates in its high content of plasmalogens with a high degree of unsaturation of fatty acids and fatty aldehydes.

Aldehydes↗
PubMed1982

[Plasmalogen content of phospholipid classes of various organs and tissues of pigs].

A comparison of the plasmalogen contents of phospholipid classes of 12 organs and tissues of pig (brain, heart, lung, liver, spinal cord, kidney, spleen, pancreas adrenula, muscles, blood plasma, aorta) was carried out, using reaction microthin-layer chromatography. Only phosphatidylethanolamine, phosphatidylcholine and phosphatidylserine were found to contain plasmalogen form. The minor components were represented by phosphatidic acid and phosphatidylglycerol. Phosphatidylethanolamine was shown to contain the plasmalogen form making up from 9% (in liver) to 80% (in spinal cord).

Animals↗
PubMed1977

Plasmalogens in arterial wall.

Plasmalogens have been determined in blood plasma, arterial and myocardial tissue of rats intubated with an atherogenic diet (vitamin D2 + cholesterol). These lipids are significantly decreased in arterial tissue after the administration of these substances for 5 consecutive days. Folic acid involved in the synthesis of plasmalogens and a powerful inhibitor of xanthine oxidase, on the contrary, increases enormously the concentration of plasmalogens in arterial tissue even with an atherogenic diet.

Animals↗
PubMedDate not supplied

Plasmalogen phospholipids - facts and theses to their antioxidative qualities.

Fatty aldehyde dimethyl acetals (DMA) derived from plasma and erythrocyte membrane plasmalogen phospholipids of 109 donors, aged 25-91 years, were measured as weight percent of total phospholipid fatty acids and DMA. The age range from 70 to 90 years (n = 82) was divided into age groups of five years each. Cumulative distributions of the DMA values of these age groups, when compared with those of 17 younger persons (aged 25-41 years), revealed a tendency to higher DMA values in the youngest age group, and to lower values in the oldest one. Linear regressions were computed between age and hexadecanaldimethylacetal (16:0 DMA) or octadecanaldimethylactal (18:0 DMA) of erythrocyte membrane and plasma phospholipids. Statistically significant negative correlations with age were obtained. Because of their sensitivity to oxidation reactions, a role of plasmalogens as a natural antioxidant in oxidative defense mechanisms appears to be convincing. However, it will possibly be difficult to separate the effects of normal aging on the decline of plasmalogen phospholipid levels in some tissues from those of certain pathological conditions - including hyperlipidemia and atherosclerosis.

Journal Article↗
PubMed1998

Plasmalogen-derived lysolipid induces a depolarizing cation current in rabbit ventricular myocytes.

Plasmalogen rather than diacyl phospholipids are the preferred substrate for the cardiac phospholipase A2 (PLA2) isoform activated during ischemia. The diacyl metabolite, lysophosphatidylcholine, is arrhythmogenic, but the effects of the plasmalogen metabolite, lysoplasmenylcholine (LPLC), are essentially unknown. We found that 2.5 and 5 micromol/L LPLC induced spontaneous contractions of intact isolated rabbit ventricular myocytes (median times, 27.4 and 16.4 minutes, respectively) significantly faster than lysophosphatidylcholine (>60 and 37.8 minutes, respectively). Whole-cell recordings revealed that LPLC depolarized the resting membrane potential from -83.5+/-0.2 to -21.5+/-1.0 mV. Depolarization was due to a guanidinium toxin-insensitive Na+ influx. The LPLC-induced current reversed at -18.5+/-0.9 mV and was shifted 26.7+/-4.2 mV negative by a 10-fold reduction of bath Na+ (Na+/K+ permeability ratio, approximately 0.12+/-0.06). In contrast, block of Ca2+ channels with Cd2+ and reducing bath Cl failed to affect the current. The actions of LPLC were opposed by lanthanides. Gd3+ and La3+ were equally effective inhibitors of the LPLC-induced current and equally delayed the onset of spontaneous contractions. However, the characteristics of lanthanide block imply that Gd3+-sensitive, poorly selective, stretch-activated channels were not involved. Instead, the data are consistent with the view that lanthanides increase phospholipid ordering and may thereby oppose membrane perturbations caused by LPLC. Plasmalogens constitute a significant fraction of cardiac sarcolemmal choline phospholipids. In light of their subclass-specific catabolism by phospholipase A2 and the present results, it is suggested that LPLC accumulation may contribute to ventricular dysrhythmias during ischemia.

Action Potentials↗
PubMed1998

Dual parallel mass spectrometers for analysis of sphingolipid, glycerophospholipid and plasmalogen molecular species.

Analysis of phospholipids was performed using a liquid chromatographic separation with two mass spectrometers in parallel providing electrospray ionization (ESI) and atmospheric pressure chemical ionization (APCI) data simultaneously from a triple quadrupole instrument and a single quadrupole instrument, respectively. The output from UV-Vis and evaporative light scattering detectors were also acquired by the two mass spectrometers, respectively, for four detectors overall. This arrangement was used to identify and calculate area percents for molecular species of dihydrosphingomyelin (DHS) and sphingomyelin (SPM) in commercially available bovine brain SPM, in human plasma extract and in porcine lens extract. Molecular species of phosphatidylethanolamine and its plasmalogen, and phosphatidylcholine and its plasmalogen were identified and semi-quantitative analysis performed. Commercially available bovine brain SPM was found to contain 11.5% DHS and 88.5% SPM. The only DHS molecular species identified in human plasma was 16:0-DHS, at or below 1% of the sphingolipid content. Porcine lens membranes were found to contain 14.4% DHS and 85.6% SPM. Other findings reported here include: (1) phospholipids were found to undergo dimerization in the electrospray source, giving masses representing combinations of species present. (2) Triacylglycerols gave usable mass spectra under electrospray ionization conditions, as well as under APCI-MS conditions. (3) Triacylglycerols gave ammonium adducts as base peaks in their APCI mass spectra, which reduced fragmentation and increased the proportions of molecular ions. (4) Mass spectra were obtained for phospholipids which underwent both protonation and sodium adduct formation in different chromatographic runs.

Animals↗
PubMed1988

Lipids of the developing human retina: I. Total fatty acids, plasmalogens, and fatty acid composition of ethanolamine and choline phosphoglycerides.

The total fatty acid composition of the human retina was studied during early normal development and compared to that found in infancy and in adulthood. The retina of an infant undernourished prenatally and of two malnourished postnatally were also studied and compared to the normal values for the age. The fatty acid patterns of ethanolamine phosphoglycerides (EPG) and choline phosphoglycerides (CPG) were also studied. Total and ethanolamine plasmalogens (EP) were estimated by the aldehyde dimethyl acetal (DMA) content of total lipids and of EPG, respectively. After acid methanolysis, analyses of fatty acid methyl esters (FAME) and of DMA were effected by capillary GLC on a single 30 m long, SP-2330, capillary column. The main developmental fatty acid changes were an increase in 22:6 omega 3, 22:5 omega 3 and 20:3 omega 6 and a decrease in 20:4 omega 6. The 22:6 omega 3/20:4 omega 6 ratio increased in a very significant, parabolical way throughout development. In contrast to the brain, the proportion of ethanolamine plasmalogens decreased with maturation, whereas the ratio 18DMA/16DMA increased. The two postnatally malnourished infants had a very significant increase in retinal 22:5 omega 6, but only the child that had been fed on a very unbalanced omega 3/omega 6 diet since 25 weeks of gestation showed an important decrease in retinal 22:6 omega 3.

Aging↗
PubMed1987

Decreased plasmalogen ratios in cultured skin fibroblasts from myotonic dystrophy.

It has become known that hypolipidemic agents, which can induce experimental myotonia in humans and animals, may alter the lipid metabolisms of intracellular organelles, peroxisomes. However, there has been no reported study on peroxisomal lipid metabolisms in myotonic dystrophy showing myotonia as well as experimental myotonia. We investigated one of the peroxisomal lipid metabolisms, i.e., plasmalogen metabolism in cultured skin fibroblasts from myotonic dystrophy, and found plasmalogen ratios to be significantly reduced.

Cells, Cultured↗
PubMed1995

Assay of plasmalogens and polyunsaturated fatty acids (PUFA) in erythrocytes and fibroblasts.

The direct transesterification method of Lepage and Roy is described as used in our laboratory for the analysis of plasmalogens and polyunsaturated fatty acids in erythrocytes and cultured fibroblasts by gas chromatography. An overview is given of the plasmalogen ratios and docosahexaenoic acid concentrations from controls and patients with different peroxisomal disorders investigated in our laboratory.

Adolescent↗
PubMed2005

Administration of myo-inositol plus ethanolamine elevates phosphatidylethanolamine plasmalogen in the rat cerebellum.

Plasmalogens are ether-linked phospholipids highly abundant in nervous tissue. Previously we demonstrated that acute administration of myo-inositol (myo-Ins) + [2-(13)C] ethanolamine ([2-(13)C]Etn) significantly elevated phosphatidylethanolamine plasmalogen (PlsEtn) in rat whole brain. Current experiments investigated the effects of acute myo-Ins+[2-(13)C]Etn administration on [PlsEtn] and the biosynthesis of new Etn lipids using NMR spectroscopy in rat cerebral cortex, hippocampus, brainstem, midbrain and cerebellum. Treated rats received a single dose of myo-Ins + [2-(13)C]Etn and controls received saline rather than myoIns. Data reveal that the cerebellum is the brain region most affected by treatment, which resulted in a 22% increase in [PlsEtn] and 89% increase in newly synthesized Etn lipids relative to controls (P < 0.05). Furthermore, the cerebellar PlsEtn/phosphatidylethanolamine ratio and molar percentage of PlsEtn were significantly elevated by 12% and 8%, respectively (P < 0.05). These data suggest that myo-Ins influences Etn lipid metabolism in brain, particularly in the cerebellum where there is a stimulation in the biosynthesis of new Etn lipids with a preference towards PlsEtn.

Animals↗
PubMed2002

Platelet phospholipids are differentially protected against oxidative degradation by plasmalogens.

The oxidative degradation of phospholipids in the presence and absence of plasmalogens (plasmenyl phosphatidylethanolamine: PPE) was followed by chemical analysis. Human platelet phospholipids, either intact or after removal of PPE by acid treatment, were oxidized with 28 mM 2,2'-azobis(2-amidinopropane di-HCl in Triton X-100 micelles (detergent/phospholipid 5:1, mol/mol). PPE (12% of all phospholipids, mol/mol) disappeared about three times more rapidly than glycerophospholipids, whereas sphingomyelin remained unaltered and the lysophosphatidylethanolamine (lysoPE) generated became progressively more unsaturated. After 60 min oxidation, the FA compositions of PS, PC, and PI were similar in extracts with or without plasmalogens. In contrast, diacyl phosphatidylethanolamine (DPE) became more saturated in the absence of PPE. The rate of phospholipid destruction was always unique to each class, but for all phospholipids slowed down in the presence of PPE. This protective effect increased in the order DPE < PS < PC < PI and did not seem to be simply related to the class unsaturation. Alpha-tocopherol had no influence on the time courses of the quantities and compositions of the phospholipids, even at a molar ratio of alpha-tocopherol to phospholipids four times higher than in platelet membranes. Thus, PPE protected phospholipids efficiently but differentially against peroxidative attack, whereas the contribution of alpha-tocopherol appeared to be negligible even at a concentration four times greater than in platelet membranes.

Blood Platelets↗
PubMed1984

Phospholipid composition of dystrophic chicken erythrocyte plasmalemmae. II. Characterization of a unique lipid from dystrophic erythrocyte membranes as ethanolamine plasmalogen.

The phospholipid content of normal (line 412) and dystrophic (line 413) chicken erythrocyte plasmalemmae has been quantified on a developmental basis using sex matched controls. A specific minor phospholipid component, ethanolamine plasmalogen, is identified from dystrophic erythrocyte membrane preparations. To arrive at this identification, data from studies utilizing gas-liquid chromatography, thin-layer chromatography, [14C]ethanolamine incorporation, and biochemical assay for specific organic moieties were correlated. This phospholipid has the potential to alter and regulate membrane fluidity and thus membrane function. The possible presence of significant concentrations of plasmalogen in human dystrophic tissues may serve as a marker for dystrophy and thus be of clinical importance.

Animals↗
PubMed1988

Calcium diphosphatidate membrane traversal is inhibited by common phospholipids and cholesterol but not by plasmalogen.

Phosphatidate-mediated Ca2+ membrane traversal is inhibited by phospholipids (PL) such a phosphatidylcholine (PC), phosphatidylinositol (PI), phosphatidylserine (PS), sphingomyelin and lysoPC, but not by PC-plasmalogen. Kinetics of Ca2+ traversal through a 'passive' bilayer consisting of OH-blocked cholesterol show competition between PC and phosphatidic acid (PA); it appears likely that a Ca(PA.PC) complex is formed which is not a transmembrane ionophore but will reduce the amount of phosphatidic acid available for the formation of the ionophore, Ca(PA)2. PS and PI may inhibit Ca2+-traversal in the same manner by forming Ca(PA.PL) complexes. We suggest that PC-plasmalogen, with one of the Ca2+-chelating ester CO groups missing, cannot engage in calcium cages, i.e., Ca(PA.PL) complexes, and thus does not interfere with Ca(PA)2 formation. Double-reciprocal plotting of Ca2+ traversal rates in cholesterol-containing liposomes vs. calcium concentration suggests that cholesterol inhibits Ca2+ traversal by competing with Ca2+ for PA. The inhibition does not seem to be caused by a restructuring or dehydration of the membrane 'hydrogen belts' affected by cholesterol; most probably, it is due to hydrogen bonding of the cholesterol-OH group to a CO group of PA; this reduces the amount of PA available for the calcium ferry. The inhibition by sphingomyelin and lysoPC may also be explained by their OH group interacting with PA via hydrogen bonding. The pH dependence of Ca2+ traversal suggests that H[Ca(PA)2]- can serve as Ca2+ cross-membrane ferry but that at physiological pH, [Ca(PA)2]2- is the predominant ionophore. In conclusion, the results indicate that Ca2+ traversal is strongly dependent on the structure of the hydrogen belts, i.e., the membrane strata occupied by hydrogen bond acceptors (CO of phospholipids) and donors (OH of cholesterol, sphingosine), and that lipid hydrogen belt structures may regulate storage and passage of Ca2+.

Binding, Competitive↗
PubMed1996

Triggerable plasmalogen liposomes: improvement of system efficiency.

A photoactivated liposome release system that is generally applicable for triggered release of encapsulated hydrophilic materials is described. This approach to phototriggered release, derived from the known effects of plasmalogen photooxidation on membrane permeability in whole cells and model membrane systems, relies on producing a lamellar phase change or increase in permeability upon cleaving its constitutive lipids to single-chain surfactants using 630-820 nm light to sensitize the photooxidation of the plasmalogen vinyl ether linkage. Semi-synthetic plasmenylcholine liposomes containing encapsulated calcein and a membrane-bound sensitizer, such as zinc phthalocyanine, tin octabutoxyphthalocyanine, or bacteriochlorophyll a, were prepared by extrusion. Irradiation of air-saturated liposome solutions enhanced membrane permeability toward calcein and Mn2+, and promoted membrane fusion processes compared to non-irradiated or anaerobic controls. Bacteriochlorophyll a sensitization produced the fastest observed photoinitiated release rate from these liposomes (100% calcein release in less than 20 min; 800 nm irradiation at 300 mW); the observed release rate was two orders of magnitude slower for egg lecithin liposomes prepared and irradiated under identical experimental conditions. Liposome aggregation, interlipidic particle formation, and membrane fusion between adjoining liposomes was observed by 31P-NMR, freeze-fracture/freeze-etch TEM, and cryo-TEM as a function of irradiation time. The use of near-infrared sensitizers and the capacity of photolyzed plasmenylcholine liposomes to undergo membrane fusion processes make photodynamic therapy with these liposome-borne sensitizers an attractive adjunct to biochemical targeting methods.

Drug Delivery Systems↗