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PubMed1982

Lecithin in the treatment of mania: double-blind, placebo-controlled trials.

The authors report double-blind, placebo-controlled trials of pure lecithin in the treatment of mania. As in preliminary trials, lecithin appeared to be nontoxic and effective. Improvement with lecithin was significantly greater than improvement with placebo in five of the six patients studied. The concurrent use of anticholinergic agents did not prevent the antimanic effect of lecithin. The authors discuss the possible mechanism of action of lecithin, including cholinergic and membrane-altering effects.

Adolescent↗
PubMed1983

Effect of lecithin on memory in normal adults.

In a double-blind, placebo-controlled, crossover study of the effect of lecithin on memory test performance, nine normal paid volunteers (age range = 22-55 years) took single oral doses of placebo and lecithin (20 g) 5 hours before cognitive testing. Lecithin raised plasma choline levels during the test session to nearly double the placebo levels, but a categorized serial learning task, a word recognition task, a paired associates learning task, and a test of retrieval by category demonstrated no significant change in memory performance. Lecithin did not selectively enhance memory for low-imagery words. Lecithin also had no effect on psychomotor speed.

Adult↗
PubMed1986

Cholinergic enhancement and REM sleep latency in the aged: lecithin does not reproduce physostigmine effect.

The administration of lecithin has failed to improve memory in aged or demented individuals. We studied the effect of lecithin on another cholinergic function, REM sleep latency. Intravenous doses of physostigmine shortened the latency to the first REM sleep period, but oral lecithin did not. In contrast to physostigmine, brain cholinergic function may not be enhanced by lecithin, which may explain why lecithin does not improve cognitive function.

Acetylcholine↗
PubMed1990

Interactions of lecithin and pig apolipoproteins of high density lipoproteins at the surface monolayer of reconstituted very small particles.

Cosonication of egg yolk lecithin and triolein with apolipoproteins isolated from pig high density lipoprotein (apoHDL) gave us reconstituted high density lipoprotein particles (r-HDLs) of 9 nm in average diameter. They were smaller than microemulsion particles (MEs) composed of the lipids (35 nm). The protein/egg yolk lecithin ratio in the fractionated r-HDLs was higher in the smaller particles. Binding of a hydrophobic probe, 2-p-toluidinylnaphthalene-6-sulfonate (TNS), to MEs, r-HDLs and apoHDL were evaluated on the basis of Halfman and Nishida's method. The reconstitution of apoHDL into MEs led to a 68% reduction in the binding of TNS and a small increase in the alpha-helix content as compared with free apoHDL. The binding experiments also showed the condensation of lecithin molecules at the r-HDL surface. The amphipathic helixes of apoHDL are located in the surface monolayer of egg yolk lecithin surrounding the triolein core. The intercalation of the hydrophobic residues of apoHDL between egg yolk lecithin molecules brings about a pronounced curvature of the surface and a decrease in the particle diameter.

Animals↗
PubMed1976

Human high denisty apolipoprotein A-I-lysolecithin-lecithin and sphingomyelin complexes. A method for high yield recombinations to lipoprotein complexes of reproducible stoichiometry.

High denisty apolipoprotein A-1 (apoLp A-I) has been prepared in a chromatographically and immunochemically homogeneous form. This apoprotein forms trimeric and tetrameric aggregates in aqueous solutions at higher concentrations. ApoLp A-I has been recombined in almost quantitative yield in the presence of lysolecithin with phosphatidylcholine and sphingomyelin to particles of reproducible stoichiometry. Lysolecithin is not required for the interactions of lecithin and sphingomyelin with the apoprotein A-I or for the stability of these complexes. Dialysis removes most of the lysolecithin without the loss of lecithin and sphingomyelin. ApoLp A-I-lecithin particles have a molecular weight of 200 000 and contain 50 molecules lecithin and 25 of lysolecithin. ApoLp A-I-sphingomyelin complexes contain 50 sphingomyelin and 13 lysolecithin molecules. The former particles show up as discs of 100 A diameter, and the latter particles are 250 A in diameter. Their thickness was estimated as 25 A in the apoLp A-I lecithin and 60 A in the apoLp A-I-sphingomyelin particles. ApoLp A-I and lysolecithin form complexes whose densities depend on the lysolecithin concentration. Lysolecithin enhances the binding of phosphatidylcholine to apoLP A-I, yielding lipoprotein complexes with decreasing density. The yield of apoLp A-I-sphingomyelin-lysolecithin complexes is proportional to the lysolecithin concentration. The ratio of apoLp A-I to sphingomyelin in all these complexes remains constant.

Apoproteins↗
PubMed1975

Metabolic heterogeneity of lecithins in intestine.

The incorporation of [2-3H]glycerol and lysolecithin labeled with [2-3H]glycerol into lecithin and its subspecies was investigated in epithelial and muscular layers of rat small intestine. The labeled compounds were administered in two wways: the intraduodenal injection and the injection into femoral vein. The incorporation of glycerol into lecithin was distinctly higher in epithelial layer than in muscular layer in both administration routes, but the incorporation of lysolecithin into lecithin showed no marked differences between both layers. Among lecithin species, dienoic and monoenoic species were highly labeled with the injection of labeled glycerol, and dienoic as well as tetraenoic specied were markedly labeled with the injecttion of labeled lysolecithin. Anyhow, no marked differences were found on the incorporation pattern of any labeled compounds into lecithin between both layers and between both administration routes.

Animals↗
PubMed1990

Effects of lecithin and corn oil on site of digestion, ruminal fermentation and microbial protein synthesis in sheep.

Six Hampshire wethers with ruminal and duodenal cannulas were fed three diets in a replicated 3 X 3 latin square to compare phospholipids with triglycerides for their effects on ruminal digestion. The diets (56% concentrate, 44% bermuda-grass hay, air-dried basis) contained either no added fat (control), 5.2% soybean lecithin or 2.4% corn oil on a DM basis. All diets were isonitrogenous and both fat-supplemented diets had similar fatty acid and energy contents. Fat added to the diet, regardless of source, reduced digestibilities of DM, energy, ADF and fatty acids in the rumen but had no effect on total tract digestibility coefficients. Lecithin slightly increased (P = .06) fatty acid digestion in the hindgut compared to corn oil (91.0 and 87.0%, respectively). Both fat sources decreased (P less than .01) ruminal ammonia concentration and increased (P less than .10) N flow to the duodenum. Added fat also reduced ruminal (P less than .01) and total tract (P less than .05) N digestibilities. Microbial N flow to the hindgut was not affected by diet, but adding fat increased (P less than .06) true efficiency of microbial protein synthesis. Overall, phospholipids from soybean lecithin inhibited ruminal fermentation similarly to triglycerides from corn oil. Despite ruminal degradation of lecithin by microbial phospholipases as shown in other studies, feeding lecithin tended to increase fatty acid digestion in the hindgut.

Animals↗
PubMed1994

Effect of lecithin on the apparent ileal and overall digestibility of crude fat and fatty acids in pigs.

Four barrows of approximately 40 kg initial body weight, fitted with post-valvular T-cecum cannulas, were used to study the effect of lecithin as an external emulsifier on apparent ileal and overall digestibility of crude fat, fatty acids, and other dietary nutrients (DM, N, GE, crude fiber [CF], P, Ca, and Mg), as well as the utilization of N, GE, Ca, P, and Mg. Two levels of lecithin (0 and .24%) and two levels of rendered fat (0 and 6%) in cereal-soybean meal-based diets were investigated according to a 4 x 4 Latin square design. No significant interactions were found between lecithin and rendered fat for apparent digestibility of crude fat as estimated at the end of the small intestine and the total digestive tract. Lecithin decreased the apparent ileal digestibility of C16:0 fatty acid (P < .1) and the apparent overall digestibility of C14:0 fatty acid (P < .05) and C18:2 fatty acid (P < .1). The apparent ileal and overall digestibility of crude fat (P < .001) and total fatty acids (P < .05) increased with the inclusion of rendered fat in diets. Furthermore, rendered fat increased the apparent ileal and overall digestibility of C14:0 (P < .01), C16:1 (ileal, P < .001; overall, P < .1), and C18:1 (P < .05) fatty acids and the apparent overall digestibility of C18:0 (P < .001) fatty acid. Lecithin had no impact on the apparent digestibility and retention (percentage of intake) of GE, N, total P, Ca, and Mg.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed1976

Amniotic fluid lecithin concentrations in pregnancies complicated by hypertensive disorders and intrauterine growth retardation.

Amniotic fluid lecithin has been measured in 92 samples from 75 patients with hypertensive disorders and in normotensive pregnancies complicated by intrauterine growth retardation (IUGR). For the group with hypertensive disorders the lecithin concentrations were not significantly different from a reference material at any stage in gestation. Pre-eclampsia associated with moderately elevated blood pressure and complicated by IUGR showed significantly higher lecithin concentrations than any other diagnostic subgroup. The lecithin concentrations showed no relationship to maternal urinary estrogen excretion. The value of serial estrogen measurements in predicting IUGR has been emphasized. An evaluation of the amniotic fluid lecithin concentration in relation to respiratory function has been made. Respiratory distress syndrome may occur even in growth retarded babies.

Amniotic Fluid↗
PubMedDate not supplied

Formation of positively charged microcapsules based on chitosan-lecithin interactions.

The formation of microcapsules which contain rosemary oil, is herewith described. The process is based on two steps: (a) formation of oil-in-water emulsions, by using lecithin as emulsifier, thus imparting negative charges on the oil droplets; (b) addition of a cationic biopolymer, chitosan, in conditions that favor the formation of an insoluble chitosan-lecithin complex. Zeta potential measurements revealed that addition of very low concentrations of chitosan to lecithin stabilized emulsions, led to reversal of charge. At a suitable pH range the chitosan precipitated around the oil droplets, forming positively charged microcapsules. The chitosan-lecithin insoluble complex is composed of a 1:1 molar ratio of the chitosan monomeric unit and lecithin, as evaluated by elementary analysis and turbidity measurements.

Capsules↗
PubMed1991

Effects of the nature of dietary proteins, lecithin and methionine on rat plasma lipids.

In order to study the complex interrelationships between on the one hand, dietary proteins, lecithin and methionine and, on the other, blood cholesterol and triglyceride levels, groups of .10 rats were fed for six weeks with diets only differing by the nature of proteins which comprised 10% of the diet. These diets were composed of egg white, heated soybean flour, casein, heated soybean flour supplemented with 1% methionine, or with 4% of the lipids replaced by soybean lecithin, heated 5-day germinated soybean supplemented or not with 1% methionine and casein with 4% of the lipids replaced by lecithin. Egg white caused no change in blood cholesterol compared to heated soybean meal (0.955 +/- 0.18 vs 0.83 +/- 0.14), but caused a significant increase in blood cholesterol levels compared to casein (0.955 +/- 0.18 vs 0.81 +/- 0.11 g/l). No effect was found on blood triglycerides levels. Lecithin caused no change when it partially replaced lipids in the soybean or casein diets thought it increased triglycerides with the casein diet (1.16 +/- 0.31 vs 0.84 +/- 0.24 g/l). Supplementation of the heated soybean diet with 1% methionine led to an increase in blood triglycerides (0.85 +/- 0.26 vs 1.18 +/- 0.34 g/l). After germination, this effect disappeared. The effects of the type of protein, partial replacement of dietary lipids by lecithin and supplementation with methionine are discussed.

Animals↗
PubMed1980

Fluorescence depolarization studies of phase transition and fluidity in lecithin liposomes containing alpha-tocopherol.

The effects of alpha-tocopherol and related compounds on the membrane fluidity of liposomes composed of dipalmitoyl-lecithin or egg lecithin were studied by measuring the fluorescence polarization of DPH(1,6-diphenyl-1,3,5-hexatriene), a hydrophobic fluorescent probe distributed in the hydrocarbon region of lipid bilayers. The transition temperature of dipalmitoyl-lecithin liposomes was lowered on incorporation of alpha-tocopherol into the membranes. A similar effect was observed on incorporation of phytol or phytanic acid into liposomes, but not on incorporation of 2,2,5,7,8-pentamethyl-1-hydroxychroman as an alpha-tocopherol model compound (TMC) which lacks an isoprenoid side chain. Above the phase-transition temperatures, incorporation of alpha-tocopherol or TMC dose-dependently increased the polarization values of DPH in dipalmitoyl-lecithin and egg lecithin liposomes, while incorporation of phytol or phytanic acid had little effect or slightly lowered the polarization. These results suggest that the effect of alpha-tocopherol in lowering the phase-transition temperature depends on its hydrophobic side chain, and that its effect in decreasing the membrane fluidity above the phase-transition temperature depends on its hydrophylic chroman ring portion. Cholesterol had an effect similar to alpha-tocopherol on membrane fluidity. alpha-Tocopherol and cholesterol had independent effects in increasing the polarization of DPH above the phase-transition temperature when the two compounds were incorporated together into liposomes.

Cholesterol↗
PubMed1976

[Effect of valinomycin on the structure of water-lecithin liposomes].

It has been established that water--lecithin liposomes in the heptane phase are formed in the course of equilibration of lecithin solution in heptane with water phase containing Na, K-picrate. The salts penetrate both the water nucleus of liposomes and their lecithin shell. The addition of valinomycin to this system does not change the water content in liposomes, but considerably increases the salt absorbed by the lipid shell of liposomes. A characteristic S-shape curve showing the relation between picrate extraction and the valinomycin concentration might be explained as an indication of a cooperative change of the structure of lecithin shell. This phase transition is induced by one valinomycin molecule per 10(3)--10(4) lecithin molecules.

Liposomes↗
PubMed2002

Effect of lecithin on epicutaneous absorption of diclofenac epolamine.

The epicutaneous application of nonsteroidal antiinflammatory drugs in localized rheumatic diseases results in a highly targeted antiinflammatory action and is associated with reduced systemic effects. The new diclofenac epolamine (DHEP) salt is much more soluble both in water and in lipid solvent than other diclofenac salts. The pharmaceutical addition of lecithin to DHEP leads to the formation of mixed micelles with high affinity to the cellular component, which guarantees the absorption of the active ingredient. We performed a bioavailability randomized, cross-over study to compare the plasma profiles of diclofenamic acid after repeated epicutaneous administration of the new topical formulation with those of the marketed DHEP formulation without lecithin. Based on a randomization list, 12 healthy volunteers were asked to apply one of the two formulations twice a day for 10 consecutive days. The other formulation was given after a washout period of 1 week. Blood samples were collected before the morning epicutaneous dose on days 1, 3, 5 and 8 of treatment and on day 10 at different sampling times until 24 h after the application. The pharmacokinetic analysis showed a significantly higher plasma concentration of diclofenamic acid after the application of DHEP lecithin, which indicates a better saturation of the subcutaneous tissues underlying the application site. This also indicates increased local availability of the active principle. In conclusion, the new DHEP formulation with lecithin should have a therapeutic advantage compared with the formulation without lecithin, even in cases of short- to medium-term treatments.

Adjuvants, Pharmaceutic↗
PubMed1976

Diminished pulmonary lecithin synthesis in acidosis: experimental findings as related to the respiratory distress syndrome.

Lung slices from term fetal rats were incubated in vitro at various pH values and the rates of the two de novo pathways for lecithin biosynthesis were determined by measuring the conversion of either 14C-choline (pathway 1) or 14C-methionine (pathway 2) to the phospholipid. It was observed that the choline pathway, but not phosphatidylethanolamine methylation, is pH-sensitive with maximum rates occurring at pH levels between 7.3 and 7.5; significantly less activity was found at pH levels between 7.0 and 7.2 and at pH levels between 7.6 and 8.0. Adjustment of the pH from 7.0 to 7.4 in vitro simulating the clinical correction of acidosis by alkali infusion was found to increase the conversion of choline to lecithin to a rate approximating that observed at pH 7.4. Since lecithins are the principal phospholipid components of pulmonary surfactant, and since pathway 1 is predominantly responsible for lung lecithin synthesis, the demonstration of impaired production with reduced pH offers a biochemical explanation for the pathophysiological effects of acidosis in the respiratory distress syndrome. A comparison of pH effects on choline pathway rate with the pH profiles of pathway enzymes suggests that these effects are mediated by the catalysts of lecithin synthesis.

Acidosis↗
PubMed1990

Use of 1H-NMR to determine the distribution of lecithin between the micellar and vesicular phases in model bile.

Biliary cholesterol/phospholipid vesicles play an important role in the pathogenesis of gallstone disease. A prerequisite for the study of the lipid composition and stability of these vesicles is a reliable method to quantify the amount of vesicular lipid. In the present report we show that NMR can be used to determine the distribution of biliary lecithin between the micellar and vesicular phases. The relatively large size of the vesicles leads to such a broadening of the lipid resonances that they are no longer visible in high resolution 1H-NMR spectra. Since micelles are much smaller, lipid present in the micellar phase does give rise to sharp peaks in 1H-NMR spectra. Micellar lecithin can easily be quantified in these spectra. The resonances of cholesterol are masked by the closely related bile acid that is present in a much higher concentration. By determining the difference between chemically and NMR estimated lecithin, the distribution of this phospholipid between the micellar phase and vesicular phase can be assessed. We have compared the results of NMR with gel permeation and density gradient ultracentrifugation. Using standard fractionation conditions, both gel permeation and density gradient ultracentrifugation lead to an underestimation of vesicular lecithin, the difference being minor at relatively high total lipid concentrations (10 g/dl) but large in diluted model bile. We conclude that 1H-NMR can be used to determine the distribution of lecithin in model bile.(ABSTRACT TRUNCATED AT 250 WORDS)

Bile↗
PubMed1989

Human plasma lecithin-cholesterol acyltransferase. Inhibition of the phospholipase A2-like activity by sn-2-difluoroketone phosphatidylcholine analogues.

Lecithin-cholesterol acyltransferase (LCAT) is a plasma enzyme which catalyzes the transacylation of the sn-2-fatty acid of lecithin to cholesterol, forming lysolecithin and cholesteryl ester. We have recently proposed a covalent catalytic mechanism for LCAT in which lecithin cleavage proceeds via the formation of a transition state tetrahedral adduct between the oxygen atom of the catalytic serine residue and the sn-2-carbonyl carbon atom of the substrate (Jauhiainen, M., Ridgway, N.D., and Dolphin, P.J. (1987) Biochim. Biophys. Acta 918, 175-188). This proposal is evaluated here by use of nonhydrolyzable sn-2-difluoroketone phosphatidylcholine analogues, known to inhibit calcium-dependent phospholipase A2. These compounds inhibited the calcium-independent phospholipase A2 activity of LCAT in a time and concentration dependent manner. The most potent analogues had a 100-fold higher affinity for the enzyme than the substrate, lecithin, when present within lecithin/apoA-I proteoliposomes. The inhibition was dependent upon the presence of a difluoromethylene group alpha to the sn-2-carbonyl carbon of the analogues. The inhibition is attributed to the formation of a tetrahedral adduct between the catalytic serine residue of LCAT and the sn-2-carbonyl carbon atom of the analogues which is stabilized by the electronegative fluorine atoms present upon the carbon atom alpha to the carbonyl carbon. This adduct mimics that proposed by us to occur during lecithin cleavage by LCAT, and the data substantiate the existence of this transition state adduct prior to the release of lysolecithin and formation of a fatty acylserine oxyester of the enzyme.

Humans↗
PubMed1988

Human plasma lecithin-cholesterol acyltransferase. The vicinal nature of cysteine 31 and cysteine 184 in the catalytic site.

Lecithin-cholesterol acyltransferase (LCAT) is a plasma enzyme which catalyzes the transacylation of the fatty acid at the sn-2 position of lecithin to cholesterol forming lysolecithin and cholesteryl ester. The substrates for and products of this reaction are present within the plasma lipoproteins upon which the enzyme acts to form the majority of cholesteryl ester in human plasma. We proposed a covalent catalytic mechanism of action for LCAT (Jauhiainen, M., and Dolphin, P. J. (1986) J. Biol. Chem. 261, 7032-7034) in which serine and histidine residues mediate lecithin cleavage and two cysteine residues cholesterol esterification. With the aid of sulfhydryl reactive trivalent organoarsenical compounds which are specific for vicinal thiols we have probed the geometry of the catalytic site. p-Aminophenylarsendichloride noncompetitively inactivates cholesterol esterification (Ki = 0.23 mM) by LCAT via alkylation of both catalytic cysteine residues. This reagent does not significantly inactivate lecithin cleavage by LCAT. Full enzyme activity is restored by treatment with 2,3-dimercapto-1-propanesulfonic acid. Treatment of LCAT with p-bromoacetylaminophenylarsenoxide blocks the subsequent incorporation of diisopropyl fluorophosphate and iodoacetamide and inactivates both cholesterol esterification and lecithin cleavage. These activities are not restored following 2,3-dimercapto-1-propanesulfonic acid treatment. However, the reduced cysteine thiols are regenerated and can catalyze cholesteryl arachidonate formation from arachidonyl-CoA. The control reagent, bromoacetylaniline, which lacks the sulfhydryl-reactive arsenical moiety, does not inactivate LCAT nor is this reagent incorporated into the LCAT protein. We conclude that the two catalytic cysteine residues of LCAT (Cys31 and Cys184) are vicinal with a calculated distance between their sulfur atoms of 3.50-3.62 A. The additional residue alkylated by the bifunctional reagent is within the catalytic site and may represent a previously identified catalytic serine or histidine residue.

Arachidonic Acid↗