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PubMed1996

Mammalian phospholipase D: phosphatidylethanolamine as an essential component.

Bovine kidney phospholipase D (PLD) was assayed by measuring the formation of phosphatidylethanol from added radioactive phosphatidylcholine (PtdCho) in the presence of ethanol, guanosine 5'-[gamma-thio]triphosphate, ammonium sulfate, and cytosol factor that contained small GTP-binding regulatory proteins. The PLD enzyme associated with particulate fractions was solubilized by deoxycholate and partially purified by chromatography on a heparin-Sepharose column. This PLD preferentially used PtdCho as substrate. After purification, the enzyme per se showed little or practically no activity but required an additional factor for the enzymatic reaction. This factor was extracted with chloroform/methanol directly from particulate fractions of various tissues, including kidney, liver, and brain, and identified as phosphatidylethanolamine (PtdEtn), although this phospholipid did not serve as a good substrate. Plasmalogen-rich PtdEtn, dioleoyl-PtdEtn, and L-alpha-palmitoyl-beta-linoleoyl-PtdEtn were effective, but dipalmitoyl-PtdEtn was inert. Sphingomyelin was 30% as active as PtdEtn. The results suggest that mammalian PLD reacts nearly selectively with PtdCho in the form of mixed micelles or membranes with other phospholipids, especially PtdEtn.

Animals↗
PubMed1997

Peroxisomal impairment in Niemann-Pick type C disease.

Niemann-Pick type C disease (NPC) belongs to the group of lysosomal storage diseases characterized by an accumulation of cholesterol and sphingomyelin. Using a mutant mouse strain, enzymatic markers for lysosomes, mitochondria, microsomes, and peroxisomes were investigated in the liver and brain. Aside from lysosomal changes, we found a sizable decrease of peroxisomal beta-oxidation of fatty acids and catalase activity in the brain and liver. Isolated peroxisomes displayed a significant decrease of these enzyme activities. Furthermore, the only phospholipid change in brain was a decreased content of the plasmalogen form of phosphatidylethanolamine, and the dimethylacetal pattern was also modified. The electron microscopical appearance of peroxisomes did not display any large changes. The defect of peroxisomal enzymes was already present 18 days before the onset of the disease. In contrast, the lysosomal marker enzyme increased in activity only 6 days after appearance of the symptoms. The events of the studied process have previously been considered to be elicited by a lysosomal deficiency, but this study demonstrates disturbances similar to those in a number of peroxisomal diseases. It appears that the peroxisomal impairment is an early event in the process and could be a factor in the development of Niemann-Pick type C disease.

Acid Phosphatase↗
PubMed1999

Phospholipid-assisted refolding of an integral membrane protein. Minimum structural features for phosphatidylethanolamine to act as a molecular chaperone.

Escherichia coli-derived phosphatidylethanolamine (PE) or PE with fully saturated fatty acids was able to correct in vitro a defect in folding in the lipid-dependent epitope 4B1 of lactose permease (LacY) resulting from in vivo assembly in the absence of PE. PE plasmalogen, PE with two unsaturated fatty acids, and lyso-PE, which all do not favor bilayer organization, did not support proper refolding. Proper refolding occurred when these latter lipids were mixed with a bilayer-forming lipid (phosphatidylglycerol), which alone could not support refolding. L-Phosphatidylserine (PS; natural diastereomer) did support proper refolding. PE derivatives of increasing degrees of methylation were progressively less effective in supporting refolding, with phosphatidylcholine being completely ineffective. Therefore, the properties of nonmethylated aminophospholipids capable of organization into a bilayer configuration are essential for the recovery of the native state of epitope 4B1 after misassembly in vivo in the absence of PE. Neither D-PS (sn-glycero-1-phosphate backbone) nor P-D-S (D-serine in the head group) is competent in supporting proper refolding unless used in binary mixtures with phosphatidylglycerol. The detailed characterization of phospholipid-assisted refolding reported here further supports a specific rather than nonspecific role for PE in structural maturation of lactose permease in vivo (Bogdanov, M., and Dowhan, W. (1998) EMBO J. 17, 5255-5264).

Amines↗
PubMed2003

Ether phospholipids and glycosylinositolphospholipids are not required for amastigote virulence or for inhibition of macrophage activation by Leishmania major.

Ether phospholipids are major components of the membranes of humans and Leishmania. In protozoan parasites they occur separately or as part of the glycosylphosphatidylinositol (GPI) anchor of molecules implicated in virulence, such as lipophosphoglycan (LPG), smaller glycosylinositolphospholipids (GIPLs), and GPI-anchored proteins. We generated null mutants of the Leishmania major alkyldihydroxyacetonephosphate synthase (ADS), the first committed step of ether lipid synthesis. Enzymatic analysis and comprehensive mass spectrometric analysis showed that ads1- knock-outs lacked all ether phospholipids, including plasmalogens, LPG, and GIPLs. Leishmania ads1- thus represents the first ether lipid-synthesizing eukaryote for which a completely null mutant could be obtained. Remarkably ads1- grew well and maintained lipid rafts (detergent-resistant membranes). In virulence tests it closely resembled LPG-deficient L. major, including sensitivity to complement and an inability to survive the initial phase of macrophage infection. Likewise it retained the ability to inhibit host cell signaling and to form infectious amastigotes from the few parasites surviving the establishment defect. These findings counter current proposals that GIPLs are required for amastigote survival in the mammalian host or that parasite lyso-alkyl or alkylacyl-GPI anchors are solely responsible for inhibition of macrophage activation.

Alkyl and Aryl Transferases↗
PubMed1978

Effect of undernutrition on the metabolism of phospholipids and gangliosides in developing rat brain.

1. Phospholipid content of brains of 3- or 8-week-old undernourished rats was 7--9% less than that for the corresponding control animals and this deficit could not be made up by rehabilitation. Phosphatidyl ethanolamine and plasmalogen were the components most affected in brains of undernourished rats. 2. Incorporation of 32P into phospholipids by brain homogenates was 28% higher in 3-week-old undernourished rats. It is suggested that enhanced phospholipid metabolism in undernourished animals may be related to behavioural alterations noted previously (Sobotka, Cook & Brodie, 1974). 3. Ganglioside concentrations in 3- and 8-week-old undernourished animals were 14% and 11.5% less respectively than those of the control animals and this difference could be made up by rehabilitation. [14C]Glucosamine incorporation in vivo into brain gangliosides was not affected by undernutrition.

Animals↗
PubMed2002

Docosahexaenoic acid abundance in the brain: a biodevice to combat oxidative stress.

Docosahexaenoic acid (DHA) (22:6) is a polyunsaturated fatty acid of the n - 3 series which is believed to be a molecular target for lipid peroxides (LPO) formation. Its ubiquitous nature in the nervous tissue renders it particularly vulnerable to oxidative stress, which is high in brain during normal activity because of high oxygen consumption and generation of reactive oxygen species (ROS). Under steady state conditions potentially harmful ROS and LPO are maintained at low levels due to a strong antioxidant defense mechanism, which involves several enzymes and low molecular weight reducing compounds. The present review emphasizes a paradox: a discrepancy between the expected high oxidability of the DHA molecule due to its high degree of unsaturation and certain experimental results which would indicate no change or even decreased lipid peroxidation when brain tissue is supplied or enriched with DHA. The following is a critical review of the experimental data relating DHA levels in the brain to lipid peroxidation and oxidative damage there. A neuroprotective role for DHA, possibly in association with the vinyl ether (VE) linkage of plasmalogens (pPLs) in combating free radicals is proposed.

Aldehydes↗
PubMed1990

Isolation and characterization of Chinese hamster ovary cell mutants defective in assembly of peroxisomes.

We made use of autoradiographic screening to isolate two Chinese hamster ovary (CHO) cell mutants deficient in peroxisomal dihydroxyacetonephosphate acyltransferase, a key enzyme for the biosynthesis of ether glycerolipids such as plasmalogens. Morphological analysis revealed no evidence of peroxisome in these mutants. Catalase was as active as in the normal cells but was not sedimentable. Pulse-chase radiolabeling experiments and cell-free translation of RNA demonstrated that acyl-CoA oxidase, the first enzyme of the peroxisomal beta-oxidation system, was synthesized as the 75-kD form but was not converted to 53- and 22-kD mature components that were present in the wild-type CHO cells; rather, degradation was apparent. Peroxisomal thiolase was synthesized as in normal cells but remained as a larger, 44-kD precursor, whereas maturation to the 41-kD enzyme was detected in the wild-type cells. The peroxisomal 70-kD integral membrane protein was also equally synthesized, as in the wild-type cells, and was not degraded. These results suggest that assembly of the peroxisomes is defective in the mutants, whereas the synthesis of peroxisomal proteins appears to be normal. Cell-fusion studies revealed that the two mutants are recessive to the wild-type CHO cells and belong to different complementation groups. Thus, these mutants presumably contain different lesions in gene(s) encoding factor(s) required for peroxisome assembly.

Acetyl-CoA C-Acetyltransferase↗
PubMedDate not supplied

Mitochondrial H2O2 production is reduced with acute and chronic eccentric exercise in rat skeletal muscle.

Oxidative stress with acute/chronic exercise has been so far examined using exercise involving a combination of concentric and eccentric contractions, but skeletal muscles are likely to be injured to a greater extent by pliometric contractions. In the present study, the effects of acute and chronic bouts of downhill running exercise on mitochondrial hydrogen peroxide (H2O2) generation (fluorimetric detection of a dimer with homovanillic acid in presence of horseradish peroxidase) and oxygen consumption in conjunction with antioxidant enzymes activity were examined. The results show that acute eccentric exercise was accompanied by a significantly reduced mitochondrial H2O2 production that is likely due to a decrease in complex I of the electron transport chain (ETC). On the other hand, eccentric training leads to positive adaptations, reflected by a higher citrate synthase activity and decreased mitochondrial H2O2 production. The decrease in mitochondrial H2O2 cannot be attributed to alterations in antioxidant capacities but rather to changes in mitochondrial membrane composition characterized by an increased polyunsaturated to saturated fatty acids ratio, and decreased contents in arachidonic acid and plasmalogens. These results suggest that changes in mitochondrial membrane properties with eccentric training can affect H2O2 production by muscle mitochondria. It is hypothesized that these changes resulted in a mild uncoupling sufficient to reduce electron back flow through complex I of the ETC, the major generator of reactive oxygen species by skeletal muscle mitochondria.

Animals↗
PubMed1985

The degradation of phospholipids, formation of metabolites of arachidonic acid, and demyelination following experimental spinal cord injury.

Spinal cord injury has been studied using a cat compression model. Very early changes in lipid metabolism were found that compromise the integrity of the plasma membrane and decrease the activities of ATPases. Up to 18% of the ethanolamine plasmalogens are lost, with very marked elevations of the free fatty acids, arachidonic acid, diacylglycerols, prostaglandins, thromboxanes, and leukotrienes. These changes result in edema, inflammation, necrosis of oligodendroglia, demyelination, and paralysis.

Animals↗
PubMed1986

Choline, phosphatidylcholine and sphingomyelin in human and bovine milk and infant formulas.

Choline is a precursor for the biosynthesis of phosphatidylcholine (lecithin), sphingomyelin, and choline plasmalogens--all essential constituents of membranes. Choline is also needed to make acetylcholine, a major neurotransmitter. The major choline-containing compounds of human milk (unesterified choline, phosphatidylcholine, sphingomyelin) were measured in samples obtained from mothers of full-term infants. Unesterified choline concentrations were highest (greater than 600 nmol/ml) during the first week of lactation, but thereafter remained relatively constant at 70-200 nmol/ml. There was no difference among foremilk, middle milk and hind milk, nor was there a diurnal pattern of variation in unesterified choline concentrations. Milk phosphatidylcholine and sphingomyelin concentrations remained relatively constant throughout lactation (100-200 nmol/ml). Hind milk always contained more of these phospholipids than did foremilk or middle milk. There was no consistent diurnal pattern of variation in milk concentrations of phosphatidylcholine or sphingomyelin. Milk contained no phospholipase activity capable of forming free choline from phosphatidylcholine or sphingomyelin. Bovine milk contained approximately the same concentrations of choline, phosphatidylcholine and sphingomyelin as did human milk from mothers more than 15 d postpartum. The same was true of "humanized" infant formulas made from cow's milk. Soy protein-based formulas had much more unesterified choline (up to 650 nmol/ml) and much less sphingomyelin than did mature human milk.

Adult↗
PubMed1980

Lipid analysis of isolated plasma membranes of lymphoid cells in benign thymomas of Buffalo/Mna rats.

Plasma membranes were isolated from lymphoid cells of benign thymomas obtained from inbred BUF/Mna rats (21 mo old) and from normal thymocytes obtained from young rats (7 wk old) of the same strain. The isolated plasma membranes were electron microscopically pure, and the specific activities of Na+, K+-ATPase, and 5'-nucleotidase were enhanced. The lipid compositions of the plasma membranes from these two sources were analyzed and compared. The cholesterol and plasmalogen contents of membranes from both sources were similar, but the phospholipid content of the benign thymoma lymphoid cell membranes was slightly lower than that of the normal thymocytes, resulting in a somewhat higher molar ratio of cholesterol to phospholipid. The plasma membranes of the thymoma lymphoid cells also exhibited a slightly higher microviscosity as measured with fluorescence polarization. No significant differences were observed in the phospholipid compositions of the two membrane preparations.

Animals↗
PubMed1994

Structural analysis of underivatized and derivatized aminophospholipids and phosphatidic acid by positive ion liquid secondary ion and collisionally induced dissociation tandem mass spectrometry.

This paper describes an approach for structurally analyzing aminophospholipids, including glycerophosphatidylethanolamine, glycerophosphatidylserine and their lyso analogues, and glycerophosphatidic acid by positive-ion liquid secondary-ion and four-sector tandem mass spectrometry. Polar head groups and the composition and position of the fatty acid chains in aminophospholipid species as well as diacyl and monoacyl phosphatidylethanolamine and their plasmalogen species can be characterized by collisionally induced dissociation of [M+H]+ ions of underivatized molecular species. Tandem mass spectrometry of [M+Na]+ and [M + 2Na-H]+ ions of 9-fluorenylmethyloxycarbonyl-derivatized glycerophosphatidylethanolamine and glycerophosphatidylserine induces fragmentation processes, but product ions are generally less structurally informative. Collisionally induced dissociation of [M + 2Na-H]+ ions of the molecular species of glycerophosphatidic acid not only yields information on the composition and position of fatty acid chains, but also allows the double bond location to be identified. This common positive-ion method is particularly effective in characterizing the molecular species of natural ethanolamine glycerophospholipids because of the advantage of a low detection limit. This approach also represents a useful alternative for the analysis of the molecular species from natural aminophospholipids by tandem mass spectrometry.

Amines↗
PubMed1995

Peroxisome structure, function, and biogenesis--human patients and yeast mutants show strikingly similar defects in peroxisome biogenesis.

Peroxisomes are found in almost all eukaryotic cells. Two major functions of the organelle are in lipid metabolism: peroxisomes catalyze the initial steps in the biosynthesis of plasmalogens, which are phospholipids that are present in large amounts in myelin. Peroxisomes also catalyze the beta-oxidation of fatty acids; this pathway is essential for the catabolism of a variety of substrates that are not oxidized by mitochondria. A third important function is in cellular respiration, involving the metabolism of H2O2, for which the peroxisome is named. Peroxisomes increase in size by the post-translational import of newly synthesized proteins from the cytosol; these pre-existing peroxisomes divide to form new peroxisomes. Proteins are targeted to peroxisomes by three different types of topogenic sequences, and it is hypothesized that a receptor exists for each type. The newly made proteins are translocated through the peroxisomal membrane into the interior by a machinery that is energized by ATP hydrolysis. Human patients and yeast mutants have remarkably similar defects in peroxisome biogenesis. Some such mutants are defective in the import of a subset of peroxisomal proteins that share a topogenic sequence type; other mutants fail to import all newly made proteins into peroxisomes, regardless of the type of targeting sequence they possess. These mutants might be defective in receptors and in translocation machinery components, respectively. Cloned genes that are essential for peroxisome biogenesis encode diverse proteins: some likely receptors, some transmembrane proteins possibly involved in translocation, and others hydrophilic proteins that may play other roles in peroxisome assembly.

Amino Acid Sequence↗
PubMed1994

Clentiazem, diltiazem, and cold cardioplegia in isolated ischemic rabbit hearts: relation between additive cardioprotection, physicochemical properties, and preservation of myocardial lipid components.

Diltiazem is known to exert significant cardioprotection, but its efficacy under hypothermic conditions has not been documented. Because of its lipophilicity and its better tissue penetration, clentiazem, a chlorobenzothiazepine derivative of diltiazem, may offer cytoprotection additive to cold cardioplegia. We investigated the cardioprotective actions of clentiazem and diltiazem (10(-8) and 10(-6) M) when added to cold cardioplegia (myocardial temperature of 10 degrees-12 degrees C), in isolated rabbit heart subjected to 90-min global ischemia. Functional recovery was assessed by measuring left ventricular developed pressure (LVDP), coronary flow (CF) and heart rate (HR). To explore the potential beneficial mechanisms of these agents, we measured myocardial lipids and total calcium at the end of a 30-min period of reperfusion as well as their myocardial accumulation. Addition of 10(-8) M clentiazem to cold cardioplegia resulted in significant improvement in mechanical recovery (postischemic LVDP of 88.5 mm Hg with cardioplegia alone vs. 105.5 mm Hg with added clentiazem at 25 mm Hg diastolic pressure, DP). The additive cardioprotection afforded by clentiazem appeared to be concentration dependent since significant cardiodepression (postischemic LVDP of 79.8 mm Hg and 18% reduction in HR) was observed at a higher concentration (10(-6) M) and these effects were correlated with myocardial accumulation of the drug. The additive cardioprotective effect of clentiazem appeared to be structure related because diltiazem at both 10(-8) and 10(-6) M concentrations offered no benefits in addition to cold cardioplegia. These results indicate that the additive cardioprotection observed with 10(-8) M clentiazem could be related to its coronary vasodilator action since it reversed the cold cardioplegia-induced attenuation of hyperemic CF at reperfusion. Other factors must be involved, however, because addition of 10(-6) M diltiazem resulted in increased postischemic CF but without improving myocardial recovery. The functional protection offered by 10(-8) M clentiazem was associated with preservation of myocardial lipid components. Myocardial cholesterol content, which is essential for maintenance of membrane integrity, was preserved in that group, whereas a loss was observed in groups treated with cardioplegia alone and in the other treated groups. Total myocardial phospholipids were preserved in groups receiving 10(-8) M clentiazem plus cold cardioplegia or cold cardioplegia alone. A reduction in plasmalogen content, the predominant myocardial phospholipid species, and an increase in total myocardial calcium were noted only in ischemic hearts that received neither cardioplegia nor benzothiazepines, suggesting that cold cardioplegia is sufficient to prevent irreversible damage. Clentiazem affords cardioprotective benefits additive to cold cardioplegia.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1979

Characteristics of a lipolytic and fatty acid-requiring Butyrivibrio sp. isolated from the ovine rumen.

A naturally occurring fatty acid-requiring Butyrivibrio sp. (strain S2), isolated from the ovine rumen, deacylates plant galactolipids, phospholipids and sulpholipids to obtain sufficient fatty acid for growth. Growth in vitro was promoted by adding to the growth medium a single straight-chain saturated fatty acid (C13 to C18) or vaccenic acid. Palmitoleic and oleic acids also supported growth but gave lengthy lag phases probably due to their toxicity. Linolenic and linoleic acids supported good growth but they were completely hydrogenated to trans-11-octadecenoic acid which was incorporated into the bacterial complex lipids. No chain elongation, chain shortening or desaturation of the added fatty acids occurred and all were substantially incorporated into bacterial lipids of the plasmalogen type, partially as a new type of hydrophobic grouping derived from two molecules of fatty acid. The absence of fatty acid unsaturation poses the question of the maintenance of membrane fluidity within this bacterium.

Animals↗
PubMed1983

Lipid composition in the classification of the butyric acid-producing clostridia.

An examination of 20 strains of butyric acid-producing Clostridium species for phospholipid class compositions, plasmalogen content, and acyl and alk-l-enyl chains showed that the deoxyribonucleic acid homology groups I (Clostridium butyricum) and II (Clostridium beijerinckii) could be distinguished by their lipid compositions. The phospholipids of C. butyricum strains had ethanolamine as the major nitrogenous lipid polar head-group moiety, more octadecenoate plus C19-cyclopropane than hexadecenoate plus C17-cyclopropane acyl chains, and the predominant alk-l-enyl chain was C18-monounsaturated. Clostridium beijerinckii strains had N-methylethanolamine plus ethanolamine in phospholipid head-groups, more hexadecenoate plus C17-cyclopropane than octadecenoate plus C19-cyclopropane acyl chains, and the major alk-l-enyl chain was C16-saturated. Three species falling outside the two homology groups Clostridium fallax, Clostridium pseudofallax and Clostridium acetobutylicum had ethanolamine as the major phospholipid base, but these species could be distinguished from C. butyricum by their acyl and alk-l-enyl chain compositions. The lipid composition of Clostridium pasteurianum is even more distinct.

Butyrates↗
PubMed1984

The lipids of the rumen fungus Piromonas communis.

The major phospholipids of the anaerobic rumen phycomycete Piromonas communis were phosphatidylethanolamine (38%), phosphatidylcholine (26%) and phosphatidylinositol (13%); no sphingolipids, glycolipids, plasmalogens or phosphonyl lipids were detected. Free fatty acids, triacylglycerols, 1:2 diacylglycerols and a variable amount of 1:3 diacylglycerol were identified, as were minor amounts of squalene and a triterpenol which is probably tetrahymanol. Approximately half the fatty acids were straight chain, even 12 to 24 carbon, saturated acids, the remainder being even 16 to 24 carbon, mono-unsaturated fatty acids. The double bonds in all except the 16 carbon acid were in the omega 9 position. The unsaturation is introduced by a delta 9 desaturase which uses stearic acid as substrate and which does not use oxygen as a terminal electron acceptor. 14C from acetate and glucose was incorporated into the fatty acids of all complex lipids, as were lauric, myristic, palmitic, stearic and oleic acids. [14C]Choline was incorporated into phosphatidylcholine and [14C]ethanolamine into phosphatidylethanolamine and phosphatidylcholine. Label from [14C]serine was recovered in phosphatidylserine and phosphatidylethanolamine, but was not detected in phosphatidylcholine.

Animals↗
PubMed1994

A haemorrhagic platelet disorder associated with altered stimulus-response coupling and abnormal membrane phospholipid composition.

Haemorrhagic diatheses due to platelet function defects are a heterogenous and poorly understood group of conditions. We report the investigation of a female with a lifelong history of epistaxes, haemarthroses, menorrhagia and persistent iron-deficiency anaemia. Although platelet numbers and morphology were normal, platelet function was abnormal both in vivo and in vitro. Skin bleeding time was prolonged and aggregation thresholds in platelet-rich plasma to a variety of weak and strong agonists were increased. Platelet granule contents were normal and membrane glycoproteins GpIb and GpIIIa were present in normal amounts. Polyphosphoinositide metabolism and phosphatidic acid generation were diminished in thrombin-stimulated platelets, as was phosphorylation of the 47 kD substrate for protein kinase C and the 20 kD protein myosin light chain kinase, indicating impaired generation of the intracellular second messengers diacylglycerol and inositol trisphosphate due to diminished stimulated phospholipase C activity. Although intracellular free calcium, calmodulin activity and basal cAMP concentrations were normal, washed platelets showed increased cAMP accumulation following stimulation with prostaglandin E1 and forskolin. Platelet membrane lipid analysis revealed a reduction in plasmalogen phosphatidylethanolamine content. It is suggested that the membrane phospholipid abnormalities cause the abnormal platelet reactivity by interfering with signal transduction from platelet receptor, via intermediary G proteins, to phospholipase C and adenylate cylase. The bleeding tendency is likely to be a consequence of the altered stimulus-response coupling.

Blood Platelet Disorders↗