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At least 19 recordsLinked to original sources
PubMed1980

Reconstitution of lipoproteins. II. Lipid-protein interaction between dimyristoyl-lecithin and dimyristoyl-lecithin:cholesterol vesicles and purified apolipoprotein C-I and C-III2 studied by isomeric spin-labelled lecithins.

The reconstitution of purified apolipoprotein C-I and C-III2 with sn-3-dimyristoyl-lecithin and sn-3-dimyristoyl-lecithin:cholesterol (10:1) vesicles was studied by electron spin resonance spectroscopy using isomeric 5'-, 12'-, and 16'-(N-oxyl-4",4"-dimethyloxazolidine)stearoyl spin-labelled lecithin probes. Results obtained from the temperature-induced changes of lipoprotein recombinants showed the hydrophilic nature of the lipid-protein interactions. The temperature-induced phospholipid phase transition, as measured by 5'-(N-oxyl-4",4"-dimethyloxazolidine)stearoyl spin-labelled lecithin probe in recombinants containing apoprotein C-1 or apoprotein C-iii2, is very broad and has a small cooperative unit indicative of extensive lipid-protein interactions occurring at the head group region of the phospholipid bilayer. When 12"- and 16'-(N-oxyl-4",4"-dimethyloxazolidine)stearoyl spin-labelled lecithins are used as probes in the same system, similar sharper and more cooperative lipid phase changes are detected. These results indicate a surface location for both apoprotein C-I and apoprotein C-III2 with respect to the phospholipid bilayer in lipoprotein recombinants with and without cholesterol.

Amino Acids↗
PubMed1983

Cholesterol gallstone dissolution in bile. Dissolution kinetics of crystalline cholesterol monohydrate by conjugated chenodeoxycholate-lecithin and conjugated ursodeoxycholate-lecithin mixtures: dissimilar phase equilibria and dissolution mechanisms.

Using compressed discs and microcrystals of cholesterol monohydrate, we evaluated the mechanisms and kinetics of dissolution in conjugated bile salt-lecithin solutions. In stirred conjugated ursodeoxycholate-lecithin and cheno-deoxycholate-lecithin solutions, dissolution of 10,000-psi discs was micellar and linear with time for 10 hours. The dissolution rate constants (k) decreased in proportion to the lecithin content and dissolution rates and k values were appreciably smaller in conjugated ursodeoxycholate-lecithin solutions. After dissolution for 5 to 10 days the discs incubated with ursodeoxycholate-lecithin systems became progressively transformed into macroscopic liquid crystals. Unstirred dissolution of 3,000-psi discs in "simulated" human bile containing physiological lecithin concentrations gave apparent k values that decreased in the following order: ursodeoxycholate-rich >/= chenodeoxycholate-rich > normal. In most cases the discs incubated with ursodeoxycholate-rich bile became covered with a microscopic liquid-crystalline layer. With 20-25 moles % lecithin, these layers eventually dispersed into the bulk solution as microscopic vesicles. During dissolution of microcrystalline cholesterol in conjugated ursodeoxycholate-lecithin systems, a bulk liquid-crystalline phase formed rapidly (within 12 hours) and the final cholesterol solubilities were greater than those in conjugated chenodeoxycholate-lecithin micellar systems. Prolonged incubation of cholesterol microcrystals with pure lecithin or lecithin plus bile salt liposomes did not reproduce these effects. Condensed ternary phase diagrams of conjugated ursodeoxycholate-lecithin-cholesterol systems established that cholesterol-rich liquid crystals constituted an equilibrium precipitate phase that coexisted with cholesterol monohydrate crystals and saturated micelles under physiological conditions. Similar phase dissolution-relationships were observed at physiological lecithin-bile salt ratios for a number of other hydrophilic bile salts (e.g., conjugated ursocholate, hyocholate, and hyodeoxycholate). In contrast, liquid crystals were not observed in conjugated chenodeoxycholate-lecithin-cholesterol systems except at high (nonphysiological) lecithin contents. Based on these and other results we present a molecular hypothesis for cholesterol monohydrate dissolution by any bile salt-lecithin system and postulate that enrichment of bile with highly hydrophilic bile salts will induce crystalline cholesterol dissolution by a combination of micellar and liquid crystalline mechanisms. Since bile salt polarity can be measured and on this basis the ternary phase diagram deduced, we believe that the molecular mechanisms of cholesterol monohydrate dissolution as well as the in vivo cholelitholytic potential of uncommon bile salts can be predicted.-Salvioli, G., H. Igimi, and M. C. Carey. Cholesterol gallstone dissolution in bile. Dissolution kinetics of crystalline cholesterol monohydrate by conjugated chenodeoxycholate-lecithin and conjugated ursodeoxycholate-lecithin mixtures: dissimilar phase equilibria and dissolution mechanisms.

Bile↗
PubMed2001

Final report on the safety assessment of Lecithin and Hydrogenated Lecithin.

Lecithin is a naturally occurring mixture of the diglycerides of stearic, palmitic, and oleic acids, linked to the choline ester of phosphoric acid, commonly called phosphatidylcholine. Hydrogenated Lecithin is the product of controlled hydrogenation of Lecithin. Bilayers of these phospholipids in water may form liposomes, a spherical structure in which the acyl chains are inside and not exposed to the aqueous phase. Lecithin and Hydrogenated Lecithin are used in a large number of cosmetic formulations as skin conditioning agents-miscellaneous and as surfactant-emulsifying agents. Hydrogenated Lecithin is also used as a suspending agent-nonsurfactant. Historical data on concentration of use of Lecithin reveals that 0.1% to 1.0% is the concentration range most frequently seen, with concentrations up to 50% reported for two moisturizing products. A solution of 65% Lecithin is currently reported to be used at concentrations up to 3% in cosmetics. Nonocclusive application of Lecithin-containing liposomes to murine skin resulted in 30% penetration to the subdermis. In piglet skin, the same application resulted in 99% accumulating in the stratum corneum. In general, liposomes are considered effective in capturing other compounds inside their spherical structure and delivering any such captured compound through the skin barrier. As a result, caution should be exhibited in formulating cosmetic products that contain these ingredients in combination with other ingredients whose safety is based on their lack of absorption or where dermal absorption is a concern. Lecithin is virtually nontoxic in acute oral studies, short-term oral studies, and subchronic dermal studies in animals. Lecithin is not a reproductive toxicant, nor is it mutagenic in several assays. In an oral carcinogenicity study, brain neoplasms were found in mice exposed to Lecithin. In a subcutaneous carcinogenicity study, no neoplasms were found in mice and rats exposed to Lecithin. Adverse reactions to Lecithin in a metered-dose inhaler have been reported. Lecithin and Hydrogenated Lecithin were generally nonirritating and nonsensitizing in animal and human skin. Based on the available data, Lecithin and Hydrogenated Lecithin are safe as used in rinse-off cosmetic products; they may be safely used in leave-on products at concentrations up to 15%, the highest concentration tested in clinical irritation and sensitization studies; but the safety of use could not be substantiated in cosmetic products likely to be inhaled. Because of the possibility of formation of nitrosamines, these ingredients should not be used in cosmetic products in which N-nitroso compounds may be formed.

Administration, Inhalation↗
PubMed1992

Two different allelic mutations in the lecithin-cholesterol acyltransferase gene associated with the fish eye syndrome. Lecithin-cholesterol acyltransferase (Thr123----Ile) and lecithin-cholesterol acyltransferase (Thr347----Met).

We have elucidated the genetic defect in a 66-yr-old patient with fish eye syndrome (FES) presenting with severe corneal opacities and hypoalphalipoproteinemia. The patient's plasma concentration of high density lipoprotein (HDL) cholesterol was reduced at 7.7 mg/dl (35.1-65.3 mg/dl in controls) and the HDL cholesteryl ester content was 31% (60-80% in controls); however, total plasma cholesteryl esters were similar to normal (60% of total cholesterol vs. a mean of 66% in controls). The patient's plasma cholesterol esterification rate was slightly reduced at 51 nmol/ml per h (control subjects: 61-106 nmol/ml per h), whereas lecithin-cholesterol acyltransferase (LCAT) activity, assayed using a HDL-like exogenous proteoliposome substrate, was virtually absent (0.9 nmol/ml per h vs. 25.1-27.9 nmol/ml per h in control subjects). DNA sequence analysis of the proband's LCAT gene revealed two separate C to T transitions resulting in the substitution of Thr123 with Ile and Thr347 with Met. The mutation at codon 347 created a new restriction site for the enzyme Nla III. Analysis of the patient's polymerase chain reaction-amplified DNA containing the region of the Thr347 mutation by digestion with Nla III confirmed that the proband is a compound heterozygote for both defects. The patient's daughter, who is asymptomatic despite a 50% reduction of LCAT activity, is heterozygous for the Thr123----Ile mutation. Our data indicate that the regions adjacent to Thr123 and Thr347 of LCAT may play an important role in HDL cholesterol esterification, suggesting that these regions may contain a portion of the LCAT binding domain(s) for HDL.

Aged↗
PubMed2000

Lecithin for dementia and cognitive impairment.

BACKGROUND: People with Alzheimer's disease have been found to have a relative lack of the enzyme responsible for converting choline into acetylcholine within the brain. Lecithin is a major dietary source of choline, so extra consumption may assist in the production of acetylcholine and reduce some of the symptoms of dementia. OBJECTIVES: To determine the efficacy of lecithin in the treatment of dementia or cognitive impairment. SEARCH STRATEGY: The Cochrane Dementia and Cognitive Impairment Group Register of Clinical Trials has been searched, as have the electronic databases MEDLINE, EMBASE, Psychlit, ISI and Current Contents. Reference lists and relevant books have been examined. SELECTION CRITERIA: All unconfounded, randomised trials comparing lecithin with placebo in a treatment period longer than one day, in patients with dementia of the Alzheimer type, vascular dementia, mixed vascular and Alzheimer's disease, unclassified or other dementia or unclassified cognitive impairment not fulfilling the criteria for dementia are eligible for inclusion. DATA COLLECTION AND ANALYSIS: Data are extracted by two independent reviewers and cross checked. Meta-analyses are performed when more than one trial provide data on a comparable outcome on sufficiently similar patients. Random effects analyses are performed whenever heterogeneity between results appears to be present. Standardised mean difference are used due do the use of different scales and periods of treatment. Odds ratios for dichotomous data are pooled using the Mantel-Haenszel or DerSimonian and Laird methods. MAIN RESULTS: Eleven randomised trials have been identified involving patients with Alzheimer's disease (265 patients) and Parkinsonian dementia (21 patients). No trials reported any clear clinical benefit of lecithin. Few trials contributed data to meta-analyses. The only statistically significant result was in favour of placebo for adverse events, based on one trial, which appears likely to be a spurious result. REVIEWER'S CONCLUSIONS: Evidence from randomised trials does not support the use of lecithin in the treatment of patients with dementia or cognitive impairment. A moderate effect cannot be ruled out, but results from the small trials to date do not indicate priority for a large randomised trial.

Alzheimer Disease↗
PubMed1980

The influence of paraquat on the in vivo incorporation of lecithin precursors in lung tissue and 'alveolar' lecithin.

Rats were injected with paraquat (1,1'-dimethyl-4,4'-bipyridyliumdichloride, 35 mg/kg) and killed 14 or 48 h later. Twelve hours prior to sacrifice labelled choline or palmitic acid was injected. Immediately after sacrifice alveolar lavage was performed in situ and the lungs were removed and homogenized. Lipid extracts from lavage fluid and lung homogenates were prepared and their lecithin content analysed by thin layer chromatography. Lecithin was quantitated by phosphorous determination, the incorporation rate of the lecithin precursors in 'alveolar' and lung tissue lecithin was measured by liquid scintillation, and the fatty acid composition of lecithin was determined by gas liquid chromatography. In comparison with controls, the content of lecithin was reduced in lavage fluid from paraquat-injected rats. These animals also had reduced incorporation of choline in alveolar lecithin. The rate of incorporation of palmitic acid was the same in experimental animals and controls, so was the incorporation of choline in lung tissue lecithin. The findings suggest that paraquat interferes with the synthesis of alveolar lecithin by the phosphocholine transferase pathway, but not with the formation of lung tissue lecithin.

Animals↗
PubMed1978

Equilibrium studies of lecithin-cholesterol interactions I. Stoichiometry of lecithin-cholesterol complexes in bulk systems.

The maximum molar ratio of lecithin:cholesterol in aqueous dispersions has been reported to be 2:1, 1:1, or 1:2. The source of the desparate results has been examined in this study by analyzing (a) the phase relations in anhydrous mixtures (from which most dispersions are prepared) and (b) various methods of preparing aqueous dispersions, with the purpose of avoiding the formation of metastable states that may be responsible for the variability of the lecithin-cholesterol stoichiometry. Temperature-composition phase diagrams for anhydrous mixtures of cholesterol (CHOL) with dimyristoyl (DML) and with dipalmitoyl (DPL) lecithin were obtained by differential scanning calorimetry (DSC). Complexes form with molar ratios for lecithin:CHOL of 2:1 and 1:2; they are stable up to 70 degrees C. When x(CHOL) < 0.33, two phases coexist: complex (2:1) plus pure lecithin; when 0.33 < x(CHOL) < 0.67 complexes (2:1) and (1:2) coexist as separate phases. The corresponding phase diagram in water for these mixtures was determined by DSC and isopycnic centrifugation in D(2)O-H(2)O gradients. Aqueous dispersions were prepared by various methods (vortexing, dialysis, sonication) yielding identical results except as noted below. The data presented supports the following phase relations. When x(CHOL) < 0.33, two lipid phases coexist: pure lecithin plus complex (2:1) where the properties of the lecithin phase are determined by whether the temperature is below or above T(c), the gel-liquid crystal transition temperature. Therefore, complex (2:1) will coexist with gel state below T(c) and with liquid crystal above T(c). The densities follow in the order gel > complex (2:1) > liquid crystal. The density of complex (2:1) is less sensitive to temperature in the range 5 degrees -45 degrees C compared to the temperature dependence for DML and DPL where large changes in density occur at T(c). When x(CHOL) > 0.33, CHOL phase coexists with complex (2:1); anhydrous complex (1:2) is apparently not stable in H(2)O. The results are independent of the method and temperature used for preparing the lipid dispersions. However, when dispersions are prepared by sonication or with solvents at T > T(c), an apparent 1:1 complex is formed. Evidence suggests the 1:1 complex is metastable.

Calorimetry, Differential Scanning↗
PubMed1992

Interaction of rat lecithin-cholesterol acyltransferase with rat apolipoprotein A-I and with lecithin-cholesterol vesicles.

The interaction of rat plasma lecithin-cholesterol acyltransferase with lecithin-cholesterol vesicles and with rat apo-A-I was studied in comparison with that of human plasma lecithin-cholesterol acyltransferase to clarify the reaction mechanism of rat plasma lecithin-cholesterol acyltransferase. The interaction of both human and rat lecithin-cholesterol acyltransferase with lecithin-cholesterol vesicles was investigated by gel permeation chromatography on Superose 12. Both enzymes had almost the same affinity to the vesicles. The affinity of rat enzyme to rat apo-A-I was stronger than that of human enzyme to human apo-A-I when estimated on the apo-A-I-Sepharose 4B column. When human apo-A-I was added to the human enzyme/vesicle mixture which contained the enzyme-vesicle complex, the enzyme was effectively dissociated from the complex. But when rat apo-A-I was added to the rat enzyme/vesicle mixture, apo-A-I-enzyme-vesicle complex was still recognized by its elution pattern on gel permeation chromatography. This suggests that the mixture of rat enzyme, rat apo-A-I, and vesicles, which are the major components in the rat lecithin-cholesterol acyltransferase reaction, forms a stronger complex than do the components of the human reaction.

Animals↗
PubMed1978

Inhibition of lecithin:cholesterol acyltransferase in human plasma by dicarboxylic lecithins.

The effect of dicarboxylic lecithins on the lecithin:cholesterol acyltransferase [LCAT] activity was studied with a partially purified preparation [approximately 24-fold]. The presence of dicarboxylic lecithins is followed by the inhibition of LCAT. The inhibition is proportional to the concentration of glutaryl-lecithin and is about 50% with 0.16 mM glutaryl-lecithin. For a higher concentration, the inhibition is total. The inhibition of LCAT activity was of a mixed type. It can be explained by a combination of competitive inhibition and interaction of glutaryl-lecithin with phospholipid, which changes the physical properties of lipid, making it less available for conversion into cholesteryl ester.

Humans↗
PubMed1980

Low density lipoprotein-activated lysolecithin acylation by human plasma lecithin-cholesterol acyltransferase. Identity of lysolecithin acyltransferase and lecithin-cholesterol acyltransferase.

There is in normal plasma an enzyme activity which converts labeled lysolecithin to lecithin by an energy-independent low density lipoprotein-activated pathway. Studies were undertaken to compare the identity of this enzyme with lecithin-cholesterol acyltransferase. During purification of the enzyme by ultracentrifugation and by chromatography on high density lipoprotein affinity column, DEAE-Sepharose column, and hydroxylapatite column, both the lysolecithin acyltransferase activity and the lecithin-cholesterol acyl transferase activity were found in the same fractions and were enriched to the same extent at each step. The final purified preparation which had 16,000- to 24,000-fold higher specific activities than starting plasma gave a single protein band on polyacrylamide gel electrophoresis and this single band contained both the activities. Also, the effects of pH, heat, and chemical inhibitors on the enzyme activities were similar. Plasma from patients with familial lecithin-cholesterol acyltransferase deficiency also lacked lysolecithin acyltransferase activity. These results indicate that a single enzyme carries out both lecithin-cholesterol acyltransferase and lysolecithin acyltransferase activities. The purified enzyme required apolipoprotein A-I for lecithin-cholesterol acyltransferase activity, but required low density lipoprotein for lysolecithin acyltransferase activity.

1-Acylglycerophosphocholine O-Acyltransferase↗
PubMed1979

Lecithin : cholesterol acyl transfer (LACT) and fatty acid composition of lecithin and cholesterol esters in young male myocardial infarction survivors.

Lecithin : cholesterol acyl transfer (LCAT) and relative fatty acid composition of serum lecithin and cholesterol esters were studied in 20 young male survivors of myocardial infarction (MI). Comparisons were made with controls matched for serum cholesterol. There was no difference in LCAT rate between MI patients and controls. The relative content of arachidonic acid in cholesterol esters was higher in MI patients. The fatty acid composition of lecithin and cholesterol esters suggests an equal transfer of linoleic and oleic acids from lecithin to cholesterol. Furthermore negative correlations were found between LCAT and linoleic acid content of lecithin (r = --0.43, P less than 0.01) and cholesterol esters (r = --0.45, P less than 0.01). This inverse relationship does not seem to be linked to substrate specificity, but rather to be mediated by influences in common on serum lipid content and turnover.

Adult↗
PubMed1976

Billiary lecithin secretion. II. Effects of dietary choline and biliary lecithin synthesis.

Choline which is absorbed from the intestine isne produced no change in bile salt pool size or secretion rate. However, with each increment in dietary choline, biliary lecithin as well as cholesterol secretion rates were significantly increased. The results demonstrate that although bile salt is required for biliary lecithin secretion, the magnitude of secretion is principally dependent upon the extent of biliary lecithin synthesis, which in turn may be regulated by the amount of dietary choline. Results further indicate that biliary cholesterol secretion is more closely linked to lecithin than to bile salt secretion. These findings would therefore suggest that lecithin secretion might be independently manipulated when bile salt is deficient to achieve enhanced biliary cholesterol transport.

Animal Nutritional Physiological Phenomena↗
PubMedDate not supplied

[Thermotropic behavior of liposomes from egg yolk lecithin, hydrogenized egg yolk lecithin and their mixtures].

The thermotropic properties of multilamellar liposomes from egg yolk lecithin, hydrogenized egg yolk lecithin and several mixtures of these two lipids were studied with the application of excimer--forming optical probe pyrene and microcalorimetry. It was discovered that when the proportion of the egg yolk lecithin in the lipid mixture was raised the temperature of the main phase transition reduced. For all this, independent of the lipid mixture composition when the temperature was raised, apparently, polarity of pyrene microenvironment in the liposomes bilayers decreased. On the basis of the analysis of solidus and liquidus curves obtained from calorimetric studies of the lipid mixtures and bend points of Arrhenius anamorphose obtained during the pyrene excimer formation measurements some conclusions were made about the role of unmodified and hydrogenized egg yolk lecithin cluster formation in the determination of thermotropic properties of the liposomes from the above two lipids mixtures. High temperature phase transition discovered for the egg yolk lecithin while measuring the pyrene excimer formation is proposed to be closely connected with temperature-dependent changes in the organization of phospholipid heads on the interphase bilayer/H2O solution.

Calorimetry↗
PubMed1977

[Prevention and therapy of the respiratory distress syndrome in premature infants using lecithin. Distribution of 14C--labeled lecithin after intravenous and intraamnial administration in pregnant miniature pigs?].

The aim of our researches was to point out a new therapeutical possibility to prevent a respiratory distress syndrome of prematures by application of 14C-lecithine. The experiments were carried out at Göttinger mini-pigs. Examining the placental passage it could be determined that an intravenous application was not efficient, while after intraamnial application of lecithine a rapid resorption in the fetal organism was proved. Of special interest was a high accumulation of lecithine in the fetal lung-tissue. These results indicate a possible therapeutical way to prevent a respiratory distress syndrome by lecithine substitution.

Amnion↗
PubMed1976

Molecular motion and order in single-bilayer vesicles and multilamellar dispersions of egg lecithin and lecithin-cholesterol mixtures. A deuterium nuclear magnetic resonance study of specifically labeled lipids.

Deuterium (2H) nuclear magnetic resonance (NMR) quadrupole splittings and relaxation times have been measured for a variety of specifically deuterated lipids intercalated in lamellar-multibilayer dispersions and single-bilayer vesicles of egg lecithin and lecithin-cholesterol mixtures. The deduced order parameters and relaxation times vary with position of deuteration, acyl chain length, unsaturation, and temperature. The order parameters and spinlattice relaxation times T1 indicate rapid intramolecular motions of restricted amplitude in both the choline head group and hydrocarbon chains. The ordering profile for the acyl chains is similar to that predicted by statistical-mechanical theory. The order parameters yield estimates of the bilayer thickness and linear coefficient of expansion in close agreement with the x-ray determinations. A comparison of the deuterium and electron spin resonance spinprobe order parameters demonstrates the perturbation of the bilayer by the bulky nitroxide probe. The transverse relaxation time T2 for single-bilayer vesicles is quantitatively accounted for by a simple modification of classical relaxation theory which takes into account the modulation of the static quadrupole interaction by rapid local molecular motions and the modulation of the residual quadrupole interaction by the slower overall tumbling of the vesicle. It is unambiguously demonstrated that molecular motion and order in single-bilayer vesicles are very similar to those in lamellar multibilayers. Significant differences occur only for a few segments near the terminal methyl groups of the acyl chains, where the order parameters for vesicles are 10-30% smaller than those found for lamellae. The incorporation of cholesterol in lecithin bilayers is shown to increase the degree of orientational order in vesicles and lamellae, and to increase the hydrodynamic radius of vesicles. Thus, single-bilayer vesicles and multilamellar dispersions of phospholipids are equally useful models for biological membranes. They yield equivalent information about the internal organization and mobility of lipid bilayers, when the spectral manifestations of overall vesicle motion are correctly taken into account.

Binding Sites↗