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PubMed1986

Human plasma lecithin-cholesterol acyltransferase. An elucidation of the catalytic mechanism.

Human plasma lecithin-cholesterol acyltransferase (LCAT) transacylates the sn-2 fatty acid of lecithin to cholesterol forming cholesteryl ester and lysolecithin. Measurement of the phospholipase A2 and transacylase activities of the enzyme using proteoliposome substrates and following selective chemical modification of serine, histidine, and cysteine residues of pure homogeneous LCAT indicated the following catalytic mechanism: HS-Cys-E-Ser-OH + lecithin in equilibrium HS-Cys-E-Ser-O-FA + lysolecithin, HS-Cys-E-Ser-O-FA in equilibrium FA-S-Cys-E-Ser-OH, FA-S-Cys-E-Ser-OH + cholesterol-OH in equilibrium HS-Cys-E-Ser-OH + cholesterol-O-FA, where FA denotes fatty acid. Modification of 2 LCAT cysteine residues with 5,5'-dithiobis-(2-nitrobenzoic acid) or treatment with ferricyanide inactivated the transacylase but not the phospholipase A2 activity. Modification of 1 serine residue with phenylmethanesulfonyl fluoride or 1 histidine residue with diethyl pyrocarbonate inhibited cholesteryl ester formation and phospholipase A2 activity. Proteoliposome substrates protected both activities against chemical inactivation. Lecithin alone protected the phospholipase A2 activity against phenylmethanesulfonyl fluoride inactivation but not the transacylase against 5,5'-dithiobis-(2-nitrobenzoic acid) inactivation. Incubation of native LCAT with arachidonyl-CoA or the lecithin-apo-A-I proteoliposome resulted in acylation of three enzyme sites, only one of which was stable to neutral hydroxylamine after denaturation. Fatty acylenzyme oxy- and thioesters were demonstrable in both cases. No transfer of arachidonic acid from iodoacetamide-modified LCAT to cholesterol occurred, indicating that the fatty-acylated serine residue cannot directly esterify cholesterol. Cholesterol arachidonate was formed upon incubation of phenylmethanesulfonyl fluoride-modified LCAT with arachidonyl-CoA.

Acyltransferases↗
PubMedDate not supplied

[Interaction of the fluorescent probe diS-C3-(5) with lecithin-cholesterol membranes].

Behaviour of fluorescent carbocyanine probe disS-C3(5) in the egg lecithin-cholesterol membrane suspension was studied in relation to the lecithin/cholesterol ratio. The partition coefficient of the probe between aqueous and lipid phases decreases unlinearly with increase of cholesterol molar part in a bilayer. This parameter over molar part units was estimated to be (2.4 +/- 0.1) X 10(6) for egg lecithin membranes and (1.8 +/- 0.2) X 10(6) for 10 mol% cholesterol, (1.2 +/- 0.1) X 10(6) for 20, (0.8 +/- 0.1) X 10(6) for 30, and (0.48 +/- 0.02) X 10(6) for 50 mol% cholesterol. It is suggested that the probe partition coefficient value consists of two components: one caused by pure lecithin bilayer regions and another by local lecithin concentration fluctuations in the mixed lecithin-cholesterol regions.

Cholesterol↗
PubMed1985

Interaction of human plasma lecithin:cholesterol acyltransferase and venom phospholipase A2 with apolipoprotein A-I recombinants containing nonhydrolyzable diether phosphatidylcholines.

Partially reassembled high density lipoproteins (R-HDL) composed of apolipoprotein A-I and nonhydrolyzable analogues of phosphatidylcholine have been prepared, and their physical properties and reactivities as substrates for lecithin: cholesterol acyltransferase and three phospholipases were tested. The stereo-chemical pairs L-DMPC-ether (1,2-O-ditetradecyl-sn-glycero-3-phosphorylcholine) and D-DMPC-ether (2,3-O-ditetradecyl-sn-glycero-1-phosphoryline) or L-DMPC (1,2-dimyristoyl-sn-glycero-3-phosphoryl-choline) and D-DMPC (2,3-dimyristoyl-sn-glycero-1-phosphorylcholine) have similar thermal properties. R-HDL composed of these four lipids also have similar thermal properties as well as lipid/protein ratios, molecular weights, and protein conformations. Vmax and apparent Km values for lecithin: cholesterol acyltransferase on R-HDL consisting of linear combinations of L-DMPC and D-DMPC, L-DMPC-ether, or D-DMPC-ether plus 6 mol % cholesterol were measured. For the ether lecithins, there was a linear increase in Vmax with percentage of the acyl donor, L-DMPC, in R-HDL; over the same range, there was no change in Km. A comparison with bee venom and Naja melanoleuca phospholipase A2 demonstrated that the venom enzymes have turnover numbers almost 3 orders of magnitude greater than has lecithin:cholesterol acyltransferase; the activity of the phospholipases was profoundly affected by the physical state of the lipid, whereas lecithin: cholesterol acyltransferase activity was not. The differences between these two types of enzymes, which cleave the same bonds of a phosphatidylcholine, are assigned to different catalytic mechanisms. These studies show that R-HDL containing sn-glycero-3-phosphorylcholines and sn-glycero-3-phosphorylcholine ethers have similar structure, properties, and affinities for phospholipolytic enzymes.

Apolipoprotein A-I↗
PubMed1985

[Liposomes from hydrogenated egg yolk lecithin].

Egg yolk lecithin is a lipid, frequently been used for the liposome preparation. Such liposomes, however, are sensitive to oxidation and relatively permeable to encapsulated substances. The catalytic hydrogenation of egg yolk lecithin is one possibility to modify the properties mentioned. The authors deal with preparation and characterization of hydrogenated egg yolk lecithin. Liposomes from native and hydrogenated egg yolk lecithin--also in combination with cholesterol--are compared. Liposomes with hydrogenated egg yolk lecithin as phospholipid component exhibit a significantly increased encapsulation capacity and an essentially improved stability. The permeation of electrolytes, carboxyfluorescein and of the cytostatic drug daunorubicin is studied.

Animals↗
PubMed1977

Role of biliary lecithin in lymphatic transport of fat.

This study was undertaken to asses the role of luminal lecithin in the lymphatic transportation of fat as chylomicrons. Two doses of fat, the low and high dose, were fed to two different groups of rats, control and bile fistula. At low dose, infusing at 35 mumoles of total fatty acid per hr of a mixture of oleic acid and monoolein, molar ratio 2:1, solubilized in 55 mumoles of sodium taurocholate, there was no difference in the lymphatic output of absorbed fat during steady state (7th and 8th hour) absorption. Infusing at a high dose, 173 mumoles of total fatty acid per hr of a mixture of oleic acid and monoolein, molar ratio 2:1, solubilized in 55 mumoles of sodium taurocholate, the bile fistula rats had lower triglyceride and phospholipid output, with a higher proportion of oleic acid in lymph lecithin than did control rats. These alterations in bile fistula rats returned to normal by addding 10 mumoles per hr of biliary lecithin to the infusate. We conclude that intraluminal biliary lecithin plays a significant role in the translocation of high doses of absorbed fat into lymph and in the amount and type of lecithin synthesized.

Animals↗
PubMed1979

[Biliary lipids and the cholesterol saturation rate in relation to lecithin administration by oral route].

Lecithin is, at present, a contradictory drug to increase the solubility degree of bile cholesterol. Our main purpose in this work was to study the lipidic bile composition of gallstone patients under lecithin treatment, in order to value its action on biliary lipids and cholesterol saturation rate. Men and women with gallstones and radiologically functioning gallbladder were included. They were divided into 2 groups: "A", including 12 patients and "B", 13. In both groups, percentage values of cholesterol, phospholipids, total bile acids and cholesterol saturation rate were determined, before and after the administration of lecithin, everyday during a period of 30 years, 8 grams on group "A" and 2 grams placebo, on group "B". No significant differences were found in the studied samples. Before and after the administration of 8 grams of lecithin orally. Total bile acids: 67--78 +/- 4,42, 72,07 +/- 4,61 p greater than 0,05; cholesterol; 15,88 +/- 2,29, 1689 +/- 2,87 p greater than 0,05; phospholipids 16,25 +/- 3,10, 12,04 +/- 2,29 p greater than 0,05; cholesterol saturation rate; 1,70 +/- 0,24, 2,10 +/- 0,36 p greater than 0,05. It is concluded that lecithin orally administered on patients with the established characteristics and diet and the used methodology results in a useless treatment to increase the solubility of bile cholesterol.

Administration, Oral↗
PubMed1967

Incorporation of acetate into fatty acids and lecithin by lung slices from fetal and newborn lambs.

Incorporation of acetate-1-(14)C into phospholipids and fatty acids by lung slices from fetal and newborn lambs and from ewes was studied in vitro. The distribution of radioactivity in the fatty acids of neutral lipids, phospholipids, and lecithin was determined. Acetate-1-(14)C was incorporated into myristic, palmitic, and C(18) fatty acids. Of the lecithin fatty acids, myristic and palmitic were the major radioactive fatty acids. The results indicate that the lung of fetal lambs is able to synthesize lecithin containing saturated fatty acids, a major constituent of pulmonary surfactant. A marked increase in the rate of acetate incorporation into lecithin was observed during maturation, and these rates were higher than those obtained in the ewes. A possible relationship between developmental changes in lecithin biosynthesis and pulmonary surfactant is discussed.

Acetates↗
PubMed1984

Correlation of ultrasonic epiphyseal centers and the lecithin: sphingomyelin ratio.

Ossification centers about the fetal knee were identified and measured by ultrasound in 133 nondiabetic patients who underwent amniocentesis for determination of the amniotic fluid lecithin:sphingomyelin ratio (L:S ratio) between 28 and 42 weeks' gestation. A distal femoral epiphysis measuring greater than or equal to 5 mm and a proximal tibial epiphysis measuring 3 mm or greater was seen at 34 to 35 weeks' gestation. A mature lecithin: sphingomyelin ratio (lecithin: sphingomyelin greater than or equal to 2.0) was present with 66, 94, and 100% of proximal tibial epiphysis measuring 0 to 2, 3 to 4, and 5 to 7 mm, respectively. A mature lecithin: sphingomyelin ratio was present with 39, 76, and 95% of distal femoral epiphysis measuring 0 to 2, 3 to 4, and 5 to 7 mm, respectively. These results suggest that in nondiabetic patients, the ossification centers about the fetal knee as measured by ultrasound correlate well with amniotic fluid lecithin: sphingomyelin ratio.

Amniocentesis↗
PubMed1982

Effects of consumption of choline and lecithin on neurological and cardiovascular systems.

This report concerns possible adverse health effects and benefits that might result from consumption of large amounts of choline, lecithin, or phosphatidylcholine. Indications from preliminary investigations that administration of choline or lecithin might alleviate some neurological disturbances, prevent hypercholesteremia and atherosclerosis, and restore memory and cognition have resulted in much research and public interest. Symptoms of tardive dyskinesia and Alzheimer's disease have been ameliorated in some patients and varied responses have been observed in the treatment of Gilles de la Tourette's disease, Friedreich's ataxia, levodopa-induced dyskinesia, mania, Huntington's disease, and myasthenic syndrome. Further clinical trials, especially in conjunction with cholinergic drugs, are considered worthwhile but will require sufficient amounts of pure phosphatidylcholine. The public has access to large amounts of commercial lecithin. Because high intakes of lecithin or choline produce acute gastrointestinal distress, sweating, salivation, and anorexia, it is improbable that individuals will incur lasting health hazards from self-administration of either compound. Development of depression or supersensitivity of dopamine receptors and disturbance of the cholinergic-dopaminergic-serotinergic balance is a concern with prolonged, repeated intakes of large amounts of lecithin.

Acetylcholine↗
PubMed1983

Formation of methylamines from ingested choline and lecithin.

Humans ingest substantial amounts of choline and lecithin as part of common foods. Physicians have recently begun administering large doses of these compounds to individuals with neurological diseases. A significant fraction of ingested choline is destroyed by enzymes within gut bacteria, forming trimethylamine (TMA), dimethylamine (DMA) and monomethylamine (MMA). Some of these methylamines are eventually excreted into the urine, presumably after being absorbed and carried to the kidneys via the bloodstream. The methylamines formed after choline is eaten could be substrates for the formation of nitrosamines, which have marked carcinogenic activity. Twenty-seven millimoles of choline chloride, choline stearate or lecithin were administered to healthy human subjects. It was found that these treatments markedly increased the urinary excretion of TMA, DMA and MMA, with choline chloride having the greatest effect. Rats were treated with 2 mmol/kg b.wt. of choline chloride or lecithin, and it was found that these treatments significantly increased urinary TMA excretion and did not alter DMA or MMA excretion. Our choline chloride preparation contained no MMA, DMA or TMA; however, it was found that our choline stearate and all the commercially available lecithins tested were contaminated with methylamines. Prior removal of methylamines from our lecithin preparation minimized the effect of oral administration of this compound on methylamine excretion in urine of rats and humans.

Administration, Oral↗
PubMed1977

[Effect of glutaryl-lecithins on human erythrocytes (author's transl)].

Effect of glutaryl-lecithins on red blood cells is studied and compared to effect to egg lysolecithins. 1. Glutaryl-lecithins exhibit a hemolytic activity which appears in the first minutes. The rate of hemolysis increases proportionally with glutaryllecithin concentration up to concentrations of 1 X 10(-7) mole. 2. Glutaryl-lecithins methylation causes a decrease of lytic activity; this might indicate that the carboxylic group plays a role in the process of hemolysis. 3. Glutaryl-lecithins can produce echinocytes, in a similar fashion to lysolecithins. These findings suggest that glutaryl-lecithin hemolytic activity plays an important role in the process of post irradiation hemolysis.

Erythrocytes↗
PubMed1984

Self-adaptive modification of red-cell membrane lipids in lecithin: cholesterol acyltransferase deficiency. Lipid analysis and spin labeling.

In a patient with lecithin: cholesterol acyltransferase deficiency, free cholesterol was markedly increased, and esterified cholesterol was diminished. In the patient's plasma, an increase in phosphatidylcholine (PC) and a decrease in sphingomyelin were observed. Concomitantly, an increase in a shorter acyl chain 16:0 was noted in PC, sphingomyelin and phosphatidylethanolamine (PE). In contrast to these results, longer chains such as 22:0 and 24:0 were decreased, especially in sphingomyelin. Unsaturated double bonds such as 18:1 was also increased in PC and PE. In the red-cell membrane lipids, the increase in free cholesterol was counteracted by an increase in PC and by a decrease in sphingomyelin and PE, reflecting changes in the patient's plasma lipids. Increased 16:0 (in PC) and decreased 18:0 and 24:0 were observed. The increased plasma free cholesterol due to metabolic defect (lecithin: cholesterol acyltransferase deficiency) led to decreased red-cell membrane fluidity. This effect appeared to be counteracted by changing phospholipid composition (increased PC and decreased sphingomyelin and PE), by increasing shorter chains (16:0), by decreasing longer chains (18:0 and 24:0) and by increasing unsaturated double bonds (18:2). These results can be interpreted as a self-adaptive modification of lecithin: cholesterol acyltransferase deficiency-induced red-cell membrane abnormalities, to maintain normal membrane fluidity. This speculation was supported by the ESR spin-label studies on the patient's membrane lipids. The normal order parameters in intact red cells and in total lipid liposomes were decreased if cholesterol-depleted membrane liposomes were prepared. Thus, the hardening effect of cholesterol appeared to be counteracted by the softening effects described above. Overall membrane fluidity in intact red cells of the lecithin: cholesterol acyltransferase-deficient patient was maintained normally, judged by order parameters in ESR spin-label studies.

Cholesterol↗
PubMed1984

Demonstration of intact intracellular cholesterol esterification and normal low-density lipoprotein pathway in fibroblasts from a patient with lecithin:cholesterol acyltransferase deficiency.

There was a 6-46-fold increase in intracellular cholesterol esterification in response to 25-hydroxycholesterol and low-density lipoproteins in normal and lecithin:cholesterol acyltransferase-deficient fibroblasts. Uptake and degradation of 125I-labelled low-density lipoproteins were similar in the two cell lines. Low-density lipoproteins caused a doubling of the mass of cholesteryl ester in the mutant cells. These findings indicate that: (a) acyl-CoA:cholesterol acyltransferase exhibits normal activity in mutant cells; (b) lecithin:cholesterol acyltransferase and acyl-CoA:cholesterol acyltransferase are different enzymes and are probably not products of the same gene; (c) the low-density lipoprotein-pathway is intact in fibroblasts from a patient with lecithin:cholesterol acyltransferase deficiency; (d) acyl-CoA:cholesterol acyltransferase is probably responsible for the small amount of cholesteryl ester found in plasma from patients with lecithin:cholesterol acyltransferase deficiency.

Cell Line↗
PubMed1984

A study of the small spherical high density lipoproteins of patients afflicted with familial lecithin: cholesterol acyltransferase deficiency.

We studied the effects of the lecithin:cholesterol acyltransferase reaction on the size and composition of the small spherical high density lipoproteins of patients afflicted with familial lecithin:cholesterol acyltransferase deficiency. We isolated these lipoproteins by preparative ultracentrifugation and rate zonal ultracentrifugation, determined their diameter by gradient gel electrophoresis, and then calculated their composition by relating measurements of their lipid and apolipoprotein content to particle volume. Our results revealed lipoprotein particles 6.0-6.2 nm in diameter that contained approximately 2 molecules of apolipoprotein A-I, 37-38 molecules of phospholipid, 3-9 molecules of unesterified cholesterol, 1-2 molecules of cholesteryl ester, and 1-2 molecules of triacylglycerol. Upon being incubated with lecithin:cholesterol acyltransferase and a source of additional unesterified cholesterol, these lipoproteins increased in content of total cholesterol and in particle size to form discrete lipoprotein products 6.6-8.6 nm in diameter. The increase in size occurred despite a net decrease in product unesterified cholesterol and phospholipid and though the net change in total lipid volume was small. Moreover, specific product lipoproteins, isolated by rate zonal ultracentrifugation, contained an increased amount of apolipoprotein A-I. These results seem best explained by a process involving lecithin:cholesterol acyltransferase-induced particle rearrangement reactions. The possibility that a similar process normally occurs in vivo deserves to be explored.

Electrophoresis, Polyacrylamide Gel↗
PubMedDate not supplied

Kinetics and thermodynamics of dissolution of lecithin by bile salts.

The kinetics of dissolution of dispersions of egg phosphatidylcholine (lecithin) by bile salts was studied by observing the decrease in turbidity as mixed micelles of lecithin and bile salts were formed. The rate of dissolution of lecithin corresponding to formation of mixed micelles was studied in the presence of dihydroxy bile salts, sodium deoxycholate, sodium chenodeoxycholate, sodium ursodeoxycholate and one trihydroxy bile salt, sodium cholate. The rate of dissolution of lecithin and mixed micelle formation decreased in the order: chenodeoxycholate greater than deoxycholate greater than cholate greater than ursodeoxycholate. Kinetic solvent isotope studies in D2O, along with measurement of enthalpies of mixed micelle formation both in H2O and D2O, suggest that formation and stabilization of mixed micelles are related to "hydrophobicity" as estimated by high performance liquid chromatography retention factors.

Bile Acids and Salts↗
PubMed2004

Possible neuroprotective effects of lecithin and alpha-tocopherol alone or in combination against ischemia/reperfusion insult in rat brain.

A close correlation exists between ischemia/reperfusion (I/R)-induced insult and the release of free radicals. Lecithin is a polyunsaturated phosphatidylcholine that corresponds to the phosphatidylcholine molecule. Phosphatidylcholines are high-energy functional and structural elements of all biologic membranes. alpha-Tocopherol is the major lipid-soluble chain-breaking antioxidant in the body tissues and effectively protects against neuronal damage. Therefore, we studied the effect of lecithin (300 mg/kg, p.o., 14 days) and alpha-tocopherol (200 mg/kg, p.o., 14 days), alone or in combination, on the brain redox state during I/R. Adult male Wistar rats were subjected to global ischemia by the occlusion of the two carotid arteries 24 h after the last dose of drug administration. Reperfusion was carried out 1 h after induction of ischemia and lasted for another hour. Brain lipid peroxides (MDA) and glutathione (GSH) contents, as well as superoxide dismutase (SOD) and catalase (CAT) activities were assessed. The results showed that I/R elevated brain lipid peroxides content which was accompanied by a reduction in both antioxidant enzyme activities, however, brain GSH level remained unaltered. Lecithin, alpha-tocopherol and their combination restored MDA content, as well as CAT activity with a slight tendency to normalize SOD activity. We conclude that lecithin has a possible neuroprotective effect partly through its antioxidant action which is comparable to that of alpha-tocopherol.

Animals↗
PubMed1979

Enthalpy of bile salt-lecithin mixed micelle formation.

The enthalpies for the dissolution of lecithin by sodium salts of cholic, deoxycholic, and chenodeoxycholic acids and their glycine and taurine conjugates are reported. Exothermic enthalpies were found in each case. It is suggested that heat evolution is due to a bile salt-lecithin interaction other than hydrophobic interactions. These results provide strong support for the "mixed disk" model for the complex lecithin-bile salt micelle, which requires that a substantial fraction of the bile salt molecules be incorporated within a lecithin bilayer where hydrogenbonded pair formation can occur. Calorimetric studies of the interaction between sodium cholate and nonionic, cationic, and anionic detergents yielded exothermic heats. These results suggest that these bile salt molecules partition into the detergent micelle interior as hydrogenbonded pairs.

Bile Acids and Salts↗
PubMed1985

Examination of the Sephadex G10 beads uptake method for determination of bile salt monomer concentration in taurocholate-lecithin solutions.

Experiments have been undertaken to examine the validity of the method of Ammon and Walter for the determination of bile acid monomer concentrations in taurocholate-lecithin (TC-L) solutions. The procedure involves, basically, the uptake of the bile acid monomer by Sephadex G10 beads (exclusion limits 700 Da) in the presence of a suitable aqueous phase marker (raffinose). Several of the experimental variables involved in the bead-washing technique have been critically studied, and good precision in data (SD in the range of +/- 2-5% of the mean value) has been obtained. Monomer concentrations determined in the absence of lecithin over a wide range (10-70 mM) of TC were found to be in agreement with those obtained by Ammon. Most important, however, is the finding that TC monomer concentrations at constant NMBS were found to be constant in all solutions containing or not containing lecithin [here, the nonmixed micelle bile salt (NMBS) is the total bile salt concentration, but not including species involving lecithin, and is determined by dialysis equilibrium experiments].

Bile Acids and Salts↗