Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PLASMALOGEN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,243 records · Page 69Linked to original sources
PubMed1982

Involvement of triacylglycerol in the metabolism of fatty acids by cultured neuroblastoma and glioma cells.

The metabolism (chain elongation, desaturation, and incorporation into complex lipids) of thirteen different radiolabeled fatty acids and acetate was examined in N1E-115 neuroblastoma and C-6 glioma cell lines in culture. During 6-hr incubations, all fatty acids were extensively (14-80%) esterified to complex lipids, mainly choline phosphoglycerides and triacylglycerol. With trienoic and tetraenoic substrates, inositol and ethanolamine phosphoglycerides also contained up to 30% of the labeled fatty acids; plasmalogen contained up to half of the label in the ethanolamine phosphoglyceride fraction of neuroblastoma cells. Chain elongation and delta 9, delta 6, and delta 5 desaturation occurred in both cell lines; delta 4 desaturation was not observed. Seemingly anomalous utilization of arachidic acid and some selectivity based on the geometric configuration of double bonds was observed. These studies indicate that these cell lines are capable of modulating cellular membrane composition by a combination of selective exclusion and removal of inappropriate acyl chains and of modification of other acyl chains by desaturation and chain elongation. The time courses and patterns of modification and incorporation of exogenous substrates into phospholipids and triacylglycerol suggest that exogenous unsaturated fatty acid may be incorporated into triacylglycerol and later released for further metabolism and incorporation into phospholipids. This supports a role for triacylglycerol in the synthesis of membrane complex lipids in cell lines derived from neural tissue.

Animals↗
PubMed1980

Enzymatic synthesis of 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine, a hypotensive and platelet-aggregating lipid.

1-Alkyl-2-acetyl-sn-glycero-3-phosphocholine, derived chemically from choline plasmalogens of beef heart, has been shown to possess powerful antihypertensive activity (Blank, M. L., Synder, F., Byers, L. W., Brooks, B., and Muirhead, E. E. (1979) Biochem. Biophys. Res. Commun. 90, 1194-1200) and to be an extremely potent platelet-activating factor (Demopoulos, C. C., Pinckard, R. N., and Hanahan, D. J. (1979) J. Biol. Chem. 254, 9355-9358). In the present study, microsomal preparations of rat spleen were shown to synthesize 1-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine by an acetyl-CoA:1-alkyl-2-lyso-sn-glycero-3-phosphocholine acetyltransferase reaction; the acetyltransferase appears to be different from the acyltransferase responsible for the transfer of palmitate to glycerolipids. The apparent Km for acetyl-CoA was 67 microM; the optimal concentration of 1-alkyl-2-lyso-sn-glycero-3-phosphocholine was 30 microM. Higher concentrations of the lyso substrate were inhibitory. When acetyl-CoA (100 microM) and 1-hexadecyl-sn-glycero-3-phosphocholine (30 microM) were incubated wih spleen microsomes under optimal conditions, the specific activity was approximately 10 nmol of 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine/min/mg of protein. Although the reaction was inhibited by the addition of EDTA or EGTA to the incubation mixture, the acetyltransferase did not appear to require a divalent cation. An acyl analog, 1-palmitoyl-2-lyso-sn-glycero-3-phosphocholine, also served as a substrate for the acetyltransferase; however, the unnatural isomer, 3-alkyl-2-lyso-sn-glycero-1-phosphocholine, did not. The acetyltransferase activity was found in a variety of tissues, but the spleen had the highest activity of the tissues examined; lung, lymph nodes, and thymus also had high activities. Identification of the product and the possible physiological importance of the pathway are discussed.

Acetyltransferases↗
PubMed1995

Peroxisome mosaicism in the livers of peroxisomal deficiency patients.

Peroxisomal deficiency disorders, which are genetically transmitted, are assumed to be expressed in all cells, and the use of cultured skin fibroblasts for diagnosis and research is based on this assumption. We describe three patients with clinical, biochemical, and microscopic evidence of a peroxisomal disorder. However, their liver displays mosaicism, i.e., parenchymal cells with peroxisomes are adjacent to cells without peroxisomes. Ten percent (volume), 8%, and less than 1% of the parenchyma possessed peroxisomes that can be identified in immunocytochemical tests for six matrix and membrane proteins performed by light and electron microscopy. In the bulk of the parenchyma, catalase is localized in the cytoplasm, and in such cells no peroxisomes are evident by electron microscopy and immunolabeling for the 43-kd peroxisomal membrane protein (PMP) in two patients; in the third case, peroxisomal membrane ghosts are present. Immunoblots of peroxisomal beta-oxidation enzymes show a pattern similar to that from patients with a generalized peroxisomal deficiency. In contrast to the clinical and biochemical signs of peroxisomal dysfunction and hepatic histopathology, cultured fibroblasts from two patients demonstrate normal peroxisomal functions, including very-long-chain fatty acid oxidation and plasmalogen synthesis.

Bile Acids and Salts↗
PubMed1993

Peroxisome-deficient Chinese hamster ovary cells with point mutations in peroxisome assembly factor-1.

Chinese hamster ovary (CHO) mutant cells deficient in peroxisome biogenesis regain peroxisomes after transfection with a cDNA coding for peroxisome assembly factor (PAF)-1 from rat liver. Reconstitution of the transfected mutant cells with wild-type cytoplasm was not required, demonstrating that expression of the PAF-1 gene alone was sufficient for the restoration of peroxisome biogenesis. Plasmalogen biosynthesis in the transfected mutants was also restored to approximately wild-type levels. The nucleotide sequence of the cDNA encoding the open reading frame for PAF-1 from CHO-K1 cells was determined. This allowed us to identify point mutations of PAF-1 in two peroxisomal mutant cell lines. The mutation in ZR-78 cells changed a cysteine to a tyrosine codon in a region located at the carboxyl terminus of the protein, which resembles the zinc finger motif of DNA-binding proteins. A point mutation in the PAF-1 gene of ZR-82 leads to premature termination.

Amino Acid Sequence↗
PubMed1995

Mode of transport of fatty acid to endothelial cells influences intracellular fatty acid metabolism.

Fatty acids are transported to cells from a variety of different moieties in the plasma. In this study, using oleate and human umbilical vein endothelial cells, we asked whether the vehicle that delivers fatty acid to cells has an influence on its metabolism upon its incorporation into the cell. For oleate vehicles, we compared free oleate bound to albumin with oleate in low density lipoprotein (LDL) which was delipidated and reconstituted with either radiolabeled triolein or cholesteryl oleate. Using approximately physiologic concentrations of LDL and free oleate, we demonstrated by three lines of evidence unique patterns of cellular oleate metabolism for oleate delivered as triolein within LDL, for oleate delivered as cholesteryl oleate within LDL, and for oleate delivered as free oleate bound to albumin. In fact, the difference was most marked between cholesteryl oleate and triolein, even though the oleate in cholesteryl oleate and triolein was delivered in identically reconstituted LDL particles, which were presumably incorporated into the cells and degraded in lysosomes in a similar fashion. First, we demonstrated that oleate delivered as free oleate or as triolein in reconstituted LDL was desaturated and elongated to fatty acid metabolites, but cholesteryl oleate in reconstituted LDL was not similarly metabolized. The elongated and desaturated metabolites of oleate were preferentially esterified in cellular triglyceride when oleate was delivered as free oleate, but they were preferentially esterified in phospholipids when oleate was delivered as triolein in LDL. Second, we observed that there was a difference in the distribution of oleate among phospholipids when oleate was delivered as cholesteryl oleate in reconstituted LDL versus triolein in reconstituted LDL. When the oleate was delivered as triolein in reconstituted LDL, there was greater esterification in diacyl phosphatidylethanolamine, in phosphatidylserine, and in phosphatidylinositol. When oleate was delivered as cholesteryl oleate in reconstituted LDL, there was greater esterification in diacyl phosphatidylcholine. Third, there was a marked preference for oleate delivered from triolein in LDL over cholesteryl oleate in LDL for esterification into the sn-1 position of plasmalogens as a vinyl ether-linked fatty acid. These data indicate that mode of transport of fatty acid to cells influences fatty acid metabolism upon its incorporation into the cell, even when the fatty acid is delivered from the core of the same lipoprotein.

Binding Sites↗
PubMed1994

Brain mapping activity and mental performance after chronic treatment with CDP-choline in Alzheimer's disease.

CDP-choline participates in brain phospholipid metabolism and acts as an endogenous intermediate in a biosynthetic pathway incorporating free choline into phosphatidylcholine and choline plasmalogens in several tissues, including the central nervous system (CNS). In patients with chronic cerebrovascular disorders, CDP-choline reduces the slow delta frequencies and increases alpha activity in spectral electroencephalogram analysis. We have studied the effect of CDP-choline (cytidine-S-diphosphate-choline; 1000 mg/day x 30 days, p.o.) on brain electrical activity mapping and mental performance in 19 Alzheimer's disease (AD) patients (10 males/9 females; age: 66.21 +/- 1.48 years; Mini-Mental State Examination (MMSE): 26.55 +/- 1.22, Spanish version max. score 35). EEG was registered from 19 electrodes placed according to the 10-20 system and digitalized online. Artefact-free 2-s periods were visually selected, submitted to a frequency analysis and averaged across periods. CDP-choline significantly decreased spectral amplitude in the theta band in F4, F8, and T4 electrodes, and did not modify relative power parameters in any of the frequency bands (delta, theta, alpha, beta) as compared to basal recordings. In patients with late-onset AD (LOAD; N = 6; age: 73.5 +/- 1.34 years; MMSE: 28.75 +/- 2.33), CDP-choline tended to increase relative alpha power in O1 and O2 electrodes. No changes were found in early-onset AD patients (EOAD; N = 13; age: 62.85 +/- 1.21 years; MMSE: 25.54 +/- 1.4). We detected a significant improvement in mental performance after 1 month of treatment with CDP-choline in patients with early-onset AD in whom brain electrical activity data correlated with cognitive parameters. It is likely that the bioelectrical changes induced by CDP-choline in AD are the result of its immunogenic and/or neurotrophic activity in the vicinity of the vascular microenvironment.

Aged↗
PubMed1994

In vivo effects of isatin on certain enzymes, lipids & serotonergic system of rat brain.

Isatin (10 microM) strongly inhibited the activity of rat brain monoamine oxidase-B (MAO-B) in vitro. At millimolar concentrations (1-10 mM) it inhibited brain acetylcholinesterase (AChE) and sodium, potassium-adenosine triphosphatase (Na+, K(+)-ATPase) activity also. However, isatin did not affect these enzymes after both acute and chronic treatments in vivo. Administration of isatin to rats at 300 mg/kg body weight for 2 and 6 h significantly raised brain serotonin levels. Chronic treatment for 20 days resulted in enhanced brain glycolipids and plasmalogen levels. There was no change in the levels of 5-hydroxy indole acetic acid (5 HIAA), phospholipids, cholesterol and gangliosides under these conditions.

Animals↗
PubMed1994

The effect of zinc deficiency on erythrocyte membrane lipids of force-fed rats receiving a diet containing coconut oil or fish oil.

In the present study, the effect of zinc deficiency on erythrocyte membrane lipids of force-fed rats that received either a diet with coconut oil and safflower oil (86:14, w/w) or a diet with fish oil and safflower oil (91:9, w/w) was investigated. Zinc deficiency caused in the rats fed both types of dietary fat an increase in the amounts of total phospholipids and individual phospholipid classes in erythrocyte membranes. In the rats fed the coconut oil diet, zinc deficiency caused an increase in the proportion of docosahexaenoic acid (22:6) in phosphatidylcholine (PC), diacyl phosphatidylethanolamine (PE), phosphatidylserine (PS), and in total erythrocyte membrane fatty acids. In contrast, in the rats fed the fish oil diet, zinc deficiency caused an increase in the proportion of docosahexaenoic acid only in PC, but not in the other phospholipids. However, in these rats, changes in the ratio between eicosapentaenoic acid (20:5) and the n-3 fatty acids with 20 and 22 carbon atoms were observed in PC, diacyl PE and plasmalogen PE. The most pronounced changes in fatty acid composition due to zinc deficiency in the rats fed both types of fat occurred in PC. There was a relationship between the changes in the composition of plasma total fatty acids and the changes in fatty acid composition of erythrocyte membrane PC caused by zinc deficiency in the rats fed both types of dietary fat. The amount of cholesterol was similar in all treatment groups. However, zinc-deficient rats fed the coconut oil diet-but not those fed the fish oil diet-had an increased ratio between total phospholipids and cholesterol. Thus, the study shows that the effect of zinc deficiency on erythrocyte membrane lipids is to some degree similar for rats fed a coconut oil diet and rats fed a fish oil diet, and to some degree different.

Animals↗
PubMed1993

Elongation, desaturation, and esterification of essential fatty acids by fetal rat brain in vivo.

Tracer amounts of either [1-14C]linolenic (18:3n-3, LNA), or [1-14C]linoleic (18:2n-6, LA) acids were intracranially injected into 19- to 20-day-old rat fetuses, and the time course of the in vivo formation and esterification of their long chain polyenoic metabolites was determined for up to 20 h. A rapid disappearance of free LNA and LA, with apparent half-lives of 60 and 40 min, respectively, was noticed. One hour after LNA injection, 32.3% and 14.3% of the total brain radioactivity was found in the neutral glyceride (NG) and phospholipid (PL) fractions, respectively. After 20 h, PL radioactivity attained a level of 75%. Phosphatidylcholine (PC), diacylglycerol (DG), and triacylglycerol (TG) constituted 40%, 23%, and 9% of the total brain label at 1 h, and 35%, 10% and 14% at 20 h, respectively. Ethanolamine-containing PL (including plasmalogen) radioactivity accounted for about 10% up to 6 h and increased nearly 3-fold at 20 h, primarily due to an increase in the amount of labeled docosapentaenoic and docosahexaenoic acids (DHA), the elongation-desaturation products of LNA. A similar pattern of incorporation into NG and PL fraction was observed after the administration of [1-14C]LA. After 1 h, PC, DG, and TG species constituted 23%, 10%, and 23% of the total brain radioactivity, whereas after 20 h it accounted for 44%, 6%, and 10%, respectively. Although radioactivity in the ethanolamine PL also increased substantially from 4% at 1 h to 29% at 20 h, the main labeled fatty acid in this fraction was LA. Labeled arachidonic acid (AA) constituted 42.7% of the total radioactivity in phosphatidylinositol (PI) at 20 h. At this time, it comprised 12.5% and 14% of the total radioactivity in PC and ethanolamine PL, respectively, suggesting a high degree of esterification selectivity. Comparison of the total amounts of LA and LNA and their corresponding labeled AA and DHA metabolites in brain and liver after 3 and 6 h indicated that the contribution of liver metabolism to the elongation-desaturation under these conditions was negligible. One hour after intracerebral injection of [3H]DHA (22:6n-3) or [3H]AA (20:4n-6), 29.2% and 12% of total radioactivity, respectively, was found in the ethanolamine PL while 20% and 40% was incorporated in PC, respectively. PI labeling by [3H]AA was 6- to 8-fold higher than that seen in the presence of DHA. A high percent of radioactivity (26.9% and 18.2%) was found in DG and TG species.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetyltransferases↗
PubMed1994

CDP-choline-induced blood histamine changes in Alzheimer's disease.

Histamine (HA) is a known neurotransmitter with a wide spectrum of biological actions at the central and peripheral levels. Recently, it has been found that HA is involved in the regulation of immune cell function, acting as an immunomodulator. A hyperactivation in the histaminergic system has been demonstrated in Alzheimer's disease (AD), including increased levels of HA in brain, serum, and cerebrospinal fluid of AD patients. In addition, changes in phospholipid metabolism and neuroimmune function have been reported in AD. CDP-choline (cytidine-5-diphosphate-choline) participates in the phospholipid metabolism pathway incorporating free choline into phosphatidyl-choline and choline plasmalogens in several tissues, including the central nervous system. In this study we have measured the concentration of HA in blood from patients with early-onset AD (EOAD) and late-onset AD (LOAD) under treatment with CDP-choline (1000 mg p.o. x30 days). HA was measured by high performance liquid chromatography (HPLC) with fluorometric detection. CDP-choline reduced the basal levels of blood HA in both EOAD and LOAD by 2-fold. The reduction in blood HA content was observed 2 h after CDP-choline administration and gradually progressed for 30 days of treatment. These results confirm the potential immunogenic effects of CDP-choline and also that an excess of HA might influence some etiopathogenic events in AD.

Administration, Oral↗
PubMed1993

Exclusive localization in peroxisomes of dihydroxyacetone phosphate acyltransferase and alkyl-dihydroxyacetone phosphate synthase in rat liver.

Dihydroxyacetone phosphate acyl transferase (DHAP-AT), alkyl dihydroxyacetone phosphate synthase (alkyl-DHAP-synthase), and glycerol-3-phosphate acyltransferase (GPAT) activities were investigated under optimal assay conditions using highly purified organelle preparations. The data presented clearly indicate that GPAT activity was mainly localized in mitochondria and microsomes, whereas DHAP-AT and alkyl-DHAP-synthase activities were exclusively localized in peroxisomes. A small fraction of the total DHAP-AT and alkyl-DHAP-synthase activities observed in purified mitochondrial preparations was due to the presence of intact peroxisomes. DHAP-AT and alkyl-DHAP-synthase activities were very low in purified microsomes (< 1% compared to peroxisomes) and these activities are thought to be due to sedimentation of peroxisomal fragments (generated during homogenization of liver and processing of liver homogenate) with microsomes. The results indicate that the dihydroxyacetone phosphate pathway does not contribute to the synthesis of glycerolipids other than ether lipids in rat liver. The ether bond formation occurs exclusively in peroxisomes, and all the biosynthetic reactions for plasmalogen synthesis may also be operating within peroxisomes in rat liver.

Acyltransferases↗
PubMed1993

Effect of fish oil supplementation on the composition of molecular species of choline and ethanolamine glycerophospholipids in ruminant muscle.

Choline glycerophospholipids and ethanolamine glycerophospholipids of ruminant skeletal muscle contain approximately 40% and 65% plasmalogen, respectively. In the 1,2-diacyl-sn-glycero-3-phosphocholine (diacyl CPG), 16:0-18:2(n-6) and 16:0-18:1(n-9) accounted for about 50% of the total molecular species; in the 2-acyl-1(1-alkenyl)-sn-glycero-3-phosphocholine (alkenyl CPG), 16:0-18:2(n-6) was the predominant species. Fish oil supplementation resulted in a sixfold increase in the proportion of 16:0-20:5(n-3) and a two- to threefold increase in the proportion of 18:1-20:5(n-3) and 16:0-22:6(n-3) in the diacyl CPG, and there was a 40% decrease in the proportion of 16:0-18:1(n-9). In the alkenyl CPG, fish oil supplementation increased the proportion of molecular species containing C20 and C22 polyenoic fatty acids from 34% to 64%; in both sheep and cattle, the proportion of 16:0-20:5(n-3) was greater than any other molecular species. In contrast to the diacyl CPG, there was also an increase in the proportion of 18:0-20:5(n-3) in the alkenyl CPG. In the 1,2-diacyl-sn-glycero-3-phosphoethanolamine (diacyl EPG), 18:0-20:4(n-6) represented about 30% of the molecular species and this was reduced to less than 20% by fish oil supplementation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

The role of peroxisomes in intermediary metabolism.

The dominant position among oxidoreduction processes in peroxisomes is ascribed to catalase, a number of aerobic oxidases, and Cu,Zn-superoxide dismutase. The peroxidase reaction of catalase requires substrates for hydrogen donation, other than H2O2, e.g. alcohols, aldehydes, formic acid. The peroxisomes contain an alternative system of beta-oxidation of higher carboxylic acids which in some types of plant cells is functionally very closely associated with the glyoxylate cycle. Regarding the role of peroxisomes in the metabolism of carboxylic acids, a very important finding has taken place, namely that besides acyl-CoA synthetase which is specific for long chains, the peroxisomes contain still another enzyme which allows the synthesis of CoA esters of fatty acids with very long chains. It is assumed that the entry of acyl-CoA esters or fatty acids into the perxisomes is performed by means of pores in membranes or acyl-carnitine transferases. Peroxisomes oxidize a very wide scale of substrates and contain several types of acyl-CoA oxidases: palmitoyl-CoA oxidase, pristanoyl-CoA oxidase, trihydroxy-coprostanoyl-CoA oxidase. The second and third reactions of peroxisomal beta-oxidation are catalyzed by the so-called three-functional enzyme, the activities of which are identical to those of 2-enoyl-CoA hydratase, beta-hydroxyacyl-CoA dihydrogenase and enoyl-CoA isomerase. The peroxisomes sufficiently oxidize dicarboxylic acids with a higher number of carbons beginning with the adipic acid. The peroxisomal system of beta-oxidation is utilized in metabolism of prostaglandins, pristanic acid-being the product of phytanic acid alpha-oxidation, and cholesterol. Several enzymatic activities needed for the synthesis of cholesterol partially take place in peroxisomes. The peroxisomes represent a decisive compartment for the initial phases of synthesis of plasmalogens. They contain the following enzymes: NAD(+)-glycerol-P-dehydrogenase, dihydroxyacetone-3-P-acyl-transferase, alkyl-dihydroxyacetone-P synthetase and acyl/alkyl-dihydroxyacetone-P reductase. The metabolism of amino acids takes place under the effect of peroxisomal enzymes--oxidase of diamino acids, D-aspartate oxidase, oxidase of L-pipecolic acid and alanine-glyoxylate aminotransferase. Only a few published sources consider it obvious that liver peroxisomes participate in degradation of spermine and spermidine. Polyamine oxidase oxidizes spermine resulting in the origin of spermidine and 3-aminopropionaldehyde, and spermidine is oxidized to putrescine and 3-aminopropionaldehyde. Peroxisomes in many phylogenetically lower animal species enable the break down of purine bases to urea and glyoxylic acid. In phylogenetically higher primates and in man, the activities of urate oxidase in peroxisomes are absent. (Fig. 14, Ref. 166).

Amino Acids↗
PubMed1995

Magnesium and cardiovascular biology: an important link between cardiovascular risk factors and atherogenesis.

In this review, a rationale is presented for how hypercholesterolemia, hypertension, diabetes mellitus, end-stage renal disease, renal dialysis, and prolonged stress can all lead to atherosclerosis, ischemic heart disease, and stroke. The data indicate that Mg deficiency caused either by poor diet and/or errors in Mg metabolism may be a missing link between diverse cardiovascular risk factors and atherosclerosis. Data from our laboratories and others indicate that reduction in extracellular and intracellular free Mg ions (Mg2+) can induce an entire array of pathophysiological phenomena known to be important in atherogenesis, that is, vasospasm, increased vascular reactivity, elevation in [Ca2+]i, formation of proinflammatory agents, oxygen radicals, platelet aggegation, reduction in cardiac bioenergetics, cardiac failure, oxidation of lipoproteins, gender-related modulation of endothelial-derived relaxing factor/NO, changes in membrane fatty acid saturation, changes in membrane plasmalogens and N-phospholipids (suggesting changes in intracellular phospholipid signals), and probably transcription factors.

Animals↗
PubMed1996

Phospholipid composition in the rat heart exposed to pressure overload from birth.

A pressure overload was induced in 2-day-old male rats by abdominal aortic constriction, and the phospholipid composition of the left ventricle (LV) and the right ventricle (RV) were determined. Sixty days after the surgery, body weights was lower and LV weight were higher in aorta-constricted (AC) rats in comparison with shamoperated animals. Increased ventricular/body weight ratios indicated a significant degree of hypertrophy of LV and smaller hypertrophy of RV. The concentrations of total phospholipids (PL), choline phosphoglycerides (PC), ethanolamine phosphoglycerides (PE), diphosphatidylglycerol (DPG) and phosphatidylinositol (PI) were decreased in both ventricles of AC rats. The concentrations of sphingomyelin (SM) and plasmalogen PE (PLPE) increased in LV only. The changes in phospholipid composition in the developing pressure-overloaded myocardium may contribute to altered membrane functions connected with heart hypertrophy.

Animals↗
PubMed1996

Isolation and characterization of the basal cell membranes of the human term placenta.

A relatively simple and rapid method is described for the isolation of basal cell membranes (BCM) from the human placenta at term which showed considerable improvement in the yield, purity and membrane characteristics as compared to the earlier described methods. The method is based on thorough washings of the syncytium in balanced salt solution, selective grinding, hypotonic lysis, sonication, incubation with EDTA and then more conventional differential centrifugation and ultracentrifugation. The isolated material showed smooth surfaced vesicular structure of various sizes as revealed by both positive and negative staining and transmission electron microscopic analysis. The membrane was highly enriched in Na+/K+, Ca2+ and Mg2+ dependent ATPase activities while the cross contamination with brush border surfaces was low as revealed by the marker enzyme assays specific for the brush border membrane (BBM) such as the disaccharide hydrolases, aminopeptidase and alkaline phosphatase. The membrane showed a relatively low lipid/protein ratio and the lipid composition represented by a variety of phospholipids (phosphatidyl choline, phosphatidyl ethanolamine, sphingomyelin, phosphatidyl inositol and phosphatidyl serine), neutral lipids (cholesterol, triacyl glycerol, free fatty acids) and glycosphingolipids (ganglioside, cerebroside and sulfatide). It also contained plasmalogens. On SDS-PAGE analysis and Coomassie blue staining reaction, the isolated membrane showed 14 major bands with as many minor ones with a molecular weight ranging between 30-110 kDa.

Adenosine Triphosphatases↗
PubMedDate not supplied

[The phospholipid composition of the heart in rats with acute vasopressin-modelled myocardial ischemia].

The phospholipid composition of the heart of intact and experimental animals has been studied under conditions of simulated acute myocardium ischemia. It is shown that already at the 10th min the phospholipid composition of the heart ventricles changes expressively. The absolute amount of phosphatidylcholine, phosphatidylserine, diphosphatidylglycerol and phosphatidylglycerol decreases reliably. In this case lysophosphatidylethanolamine which is absent in control rats is identified. The amount of other phospholipids does not vary. Simultaneously the percentage of individual phospholipids varies: the phosphatidylethanolamine level significantly increases against the decrease of phosphatidylcholine and phosphatidylserine. As a result of the study of the amount of acylic and plasmalogenic forms of phospholipids it has been found that the level of the diacylic form of phosphatidylcholine in experimental animals falls. The data obtained testify to a definite participation of phospholipids in the pathogenesis of the acute myocardium ischemia.

Acute Disease↗
PubMed1976

Preparative isolation of cerebrosides (galactosyl and glucosyl ceramide).

An improved method for isolating cerebrosides from natural sources is described. The method is particularly suited to large scale work and can be adapted to the isolation of sphingolipids that are less polar than the gangliosides. It is based on the use of sodium sulfate to absorb the water from chloroform-methanol tissue extracts, the use of triiodide to cleave the ether linkage of plasmalogens, and the use of alkaline methanolysis to cleave the ester linkages of the glycerolipids. The final separation of the lipids is done with a silica gel column.

Animals↗