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PubMed1982

[Enzymatic lecithin determination in amniotic fluid for antepartal diagnosis of lung maturity - a multi-center study (author's transl)].

A new test-combination for the enzymatic determination of lecithin in amniotic fluid for the assessment of fetal lung maturity has been developed by Boehringer Mannheim. This test was evaluated by 12 hospitals and has been compared with the L/S ratio, the foam-test or the densitometric determination of lecithin. The assay is based on the hydrolysis of lecithin by phospholipase C which starts an enzymatic chain reaction in which NADH consumption if measured photometrically. The intra- and interassay precision were characterized by CV values below 10%. Average recoveries of lecithin were 95-102%. It is recommended to centrifuge the samples (10 min, 700 g) and to start the analysis as soon as possible after receipt of the specimen. The total amount of time required is 2 hours for a single determination. Batches of up to 10 samples require little extra time. An opened test-combination can be used for a maximum of 30 single determinations. Comparison of the quantitative enzymatic lecithin determination with other methods showed that the critical value for lecithin is 5.0 mg/100 ml. Above 5.1 mg/100 ml no case respiratory distress syndrome was observed. The good precision accuracy and the simple handling make the enzymatic lecithin determination suitable for routine use.

Amniotic Fluid↗
PubMed1980

Studies on plasma lipoproteins during absorption of exogenous lecithin in man.

Human subjects were infused intraduodenally with either lecithin (150 mg/kg/hr) or safflower oil (100 mg/kg/hr)of similar fatty acid composition, and plasma lipoproteins were studied when constant plasma lipid levels were reached. Both types of fat induced increases of lipoproteins of Sf > 400 (chylomicrons) and Sf 20--400 (VLDL). Lecithin infusions produced increases predominantly in VLDL, whereas infusion of safflower oil induced mainly chylomicrons. Chylomicrons derived from lecithin were generally smaller and had a high phospholipid:triglyceride ratio (mean 0.15) than those produced during safflower oil infusions (mean 0.08). The increases in VLDL from both lipids occurred mainly in larger particles of this density range. This "incremental VLDL" had a lower cholesterol:triglyceride ratio (0.098) than preinfusion VLDL (0.283) and probably represented "small chylomicrons" of gut origin. The differences in lipoproteins resulting from infusion of lecithin and safflower oil in human subjects were not observed in rats; in the latter, lecithin induced large chylomicrons to the same extent as did safflower oil. Lecithin absorption measured over 50- or 100-cm intestinal segments averaged 41%, but was probably greater over the whole of the small intestine. Lecithin infusion unexpectedly was found to decrease markedly the absorption of cholesterol in the upper part of the small intestine.

Cholesterol↗
PubMed1996

Fish meal lecithin as alternative precursor of docosahexaenoate and choline.

Choline and docosahexaenoate (DHA) are essential nutrients for maintaining normal brain function. However, their existence in fish lecithin is ignored and excluded during the degumming step of conventional fish oil manufacturing process. The study aims to introduce fish lecithin as alternative precursor of choline and omega-3 fatty acids especially DHA for nutritional supplements. Four grades of Thai fish meals with protein contents ranging from 60-70% were used. Their lipid characteristics were examined. Fish meal's fats and lecithin were 9-15 and 2-3 g/100 g, respectively. Total fatty acids constitute 23-27% monoenes without erucic acid and 24-28% polyenes including 15-19% DHA. Lecithin with 50% purity was prepared from grade-1 fish meal by means of consecutive methanol/n-hexane/acetone extraction. The obtained lecithin contains choline upto 66-70 mole% with DHA reaches to 20-23%. Its peroxide value of 57 and acid value of 9 are accepted for food grade lecithin preparation, however, the further refinery process is still suggested. Since the world consumption of nutritional supplement foods is increasing steadily, the results of our study implies that fish lecithin is probably a promising source of choline and omega-3 fatty acids especially DHA for such an objective.

Choline↗
PubMed2001

[Curative effect of soybean lecithin on cerebral infarction].

OBJECTIVE: To investigate the clinical curative effect of soybean lecithin on cerebral infarction. METHODS: 542 patients with cerebral infarction within 48 h after the onset with the nervous function defect scores of 31-35 were divided into 3 groups: basic treatment group, 60 cases, with conventional treatment; citicoline group, 122 patients, with conventional treatment and citicoline; and soybean lecithin group, 360 patients, with conventional treatment and soybean lecithin 10 g tid. For all patients, treatment began sometime within 48 hours after the onset. The treatment course lasted 28 days. RESULTS: When the course was over, the infarct volumes in basic group citicoline group, and soybean lecithin group, were 7.6 cm3 +/- 2.9 cm3, 7.3 cm3 +/- 3.1 cm3, and 6.4 cm3 +/- 2.7 cm3 respectively (F = 7.371, P = 0.0007). The basic group and citicoline group being compared with the soybean group by Dunnett test, t = 4.387 and 3.969 respectively, P < 0.01. The nervous function defect integral in the 3 groups decreased 14.2 +/- 10.93, 15.0 +/- 9.0, and 18.5 +/- 10.9 respectively. Two-way analysis of variance of drug kind and beginning time of treatment showed the value of F in drugs as 6.250, P = 0.0021, and value of F in times as 0.9417, P = 0.4201. In the order of death,deterioration, no improvement, improvement, significant improvement, and recovery, the Ridit values for the comprehensive curative effect in the 3 groups were 0.4003, 0.4118, and 0.54 5 respectively; chi2 = 27.89, P < 0.001. CONCLUSION: Soybean lecithin is effective in treatment of acute cerebral infarction. The mechanism may be that soybean lecithin lowers the decrease of brain phospholipid content in brain ischemia.

Cerebral Infarction↗
PubMedDate not supplied

Bile salt structure and phase equilibria in aqueous bile salt and bile salt-lecithin systems.

The hydrophilic-hydrophobic balance of bile salt monomers can be readily quantified by their elution sequence during reverse-phase high-performance liquid chromatography. Such studies have demonstrated that subtle variations in bile salt structure have profound effects on the hydrophilic-hydrophobic balance of this important family of detergent-like molecules. The common trihydroxy bile salt, cholate, is more hydrophilic than dihydroxy bile salts with alpha-oriented OH groups. In contrast, dihydroxy bile salts with one equatorial OH function are more hydrophilic than cholate. Hydrophilic bile salts have, in general, higher critical micellar concentrations than do hydrophobic bile salts and their primary micelles polymerize less readily to form secondary micelles either with increasing bile salt concentrations or with increases in ionic strength. Hydrophilic bile salts also disperse lecithin into mixed micelles at a slower rate than do hydrophobic bile salts. The structure of mixed bile salt-lecithin micelles is more complex than previously believed and varies with bile salt-to-lecithin ratio. These micelles are disc-like in which bile salts saturate the lecithin bilayer "core" presumably as reverse micelles, as well as coating the perimeter as a bilayered "ribbon". The ratio of bile salt to lecithin in the bilayer and the intermicellar monomeric bile salt concentration (critical micellar concentration) determines the macroscopic phase limit. With the common bile salt species, the lecithin-to-bile salt phase limit does not correlate closely with the hydrophilic-hydrophobic balance of the bile salt monomers.(ABSTRACT TRUNCATED AT 250 WORDS)

Bile Acids and Salts↗
PubMed1990

Attenuation of alcohol-induced hepatic fibrosis by polyunsaturated lecithin.

Characteristic features of alcoholic liver injury include fibrosis and striking membrane alterations, with associated phospholipid changes. To offset some of these abnormalities, a 10-yr study was conducted in baboons: 12 animals (eight females, four males) were fed a liquid diet supplemented with polyunsaturated lecithin (4.1 mg/kcal) for up to 8 yr, with either ethanol (50% of total energy) or isocaloric carbohydrate. They were compared with another group of 18 baboons fed an equivalent amount of the same diet (with or without ethanol), but devoid of lecithin. In the two groups, comparable increases in lipids developed in the ethanol-fed animals, but striking differences in the degree of fibrosis were seen. Whereas at least septal fibrosis (with cirrhosis in two) and transformation of their lipocytes into transitional cells developed in seven of the nine baboons fed the regular diet with ethanol, septal fibrosis did not develop in any animals fed lecithin (p less than 0.005). They did not progress beyond the stage of perivenular fibrosis (sometimes associated with pericellular and perisinusoidal fibrosis) and had a significantly lesser activation of lipocytes to transitional cells. Furthermore, when three of these animals were taken off lecithin, but continued on the same amount of the ethanol-containing diet, they rapidly (within 18 to 21 mo) progressed to cirrhosis, accompanied by an increased transformation of their lipocytes to transitional cells. These results indicate that some component of lecithin exerts a protective action against the fibrogenic effects of ethanol. Because we had previously found that choline, in amounts present in lecithin, has no comparable action, the polyunsaturated phospholipids themselves might be responsible for the protective effect.

Animals↗
PubMed1993

The influence of lecithin on plasma choline concentrations in triathletes and adolescent runners during exercise.

An investigation was carried out on the effect of lecithin (phosphatidylcholine, 90%) on the plasma choline concentrations during continuous strain in 10 top level triathletes (4 women and 6 men), trial I, and 13 excellent adolescent runners (3 girls and 10 boys), trial II. Venous blood, collected before and immediately after the race, was separated and plasma was assayed by an improved high performance liquid chromatography method for choline. Each study comprised three experiments. In trial I the triathletes performed two periods of bicycle exercise each lasting 2 h at an average speed of 35 km.h-1, and in the second study (trial II) the subjects were subjected to severe physical stress on two occasions during cross-country races of durations between 30-60 min according to their ages. The participants received either a placebo or 0.2 g lecithin.kg body mass-1, 1 h before each exercise. As a control the same dose of lecithin was administered without any exercise (both trials I and II). Bicycle exercise without lecithin supply decreased plasma choline concentrations in all the triathletes, on average by 16.9% (P < or = 0.01). When lecithin was given before exercise, average plasma choline concentrations remained at the same level as the initial values. The supply of lecithin without exercise led to a significant increase of the plasma choline concentrations, on average by 26.9% (P < or = 0.01). In trial II, when running without a supply of lecithin, the mean plasma choline concentrations in the adolescent runners remained stable which may have been due to the duration of the physical stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1979

Effect of lecithin on jejunal absorption of micellar lipids in man and on their monomer activity in vitro.

The effect of lecithin on jejunal absorption of fatty acids and octadecenoylglycerol was studied in healthy volunteers with a jejunal perfusion system which excluded pancreatic and biliary secretions from the test segment. Lecithin significantly reduced the absorption of oleic acid (P less than 0.05) and octadecenoylglycerol (P less than 0.01), while it had no effect on the absorption of ricinoleic acid. In vitro, lecithin reduced monomer activities of all three lipids; the changes were greater for oleic acid and octadecenoylglycerol than for ricinoleic acid (P less than 0.02). From these data it is concluded that lecithin reduces monomer activity of fatty acids in mixed micellar solutions and that it can thereby reduce the absorption rates of micellar lipids. Intact lecithin is not absorbed under these conditions. Maldigestion of lecithin in pancreatic insufficiency may, therefore, aggravate the steatorrhea observed in this condition.

Adult↗
PubMed1980

A simple chromatographic method for purification of egg lecithin.

Egg lecithin was purified from the CdCl2-lecithin complex by column chromatography on Alumina. The yield from 5 eggs was 2.8 g. The purified lecithin had correct chemical values for pure lecithin and a fatty acid composition similar to lecithin prepared by other methods. The method probably can be adapted for purification of other lipids containing the phosphocholine moiety and for purification of synthetic lecithin.

Aluminum Oxide↗
PubMed2006

Highly sensitive spectrofluorimetric determination of trace amounts of lecithin.

A new spectrofluorimetric method was developed for the determination of trace amounts of lecithin using the ciprofloxacin (CIP)-terbium (Tb3+) ion complex as a fluorescent probe. In a buffer solution at pH = 5.60, lecithin can remarkably reduce the fluorescence intensity of the CIP-Tb3+ complex at lambda = 545 nm. The reduced fluorescence intensity of the Tb3+ ion is proportional to the concentration of lecithin. Optimum conditions for the determination of lecithin were also investigated. The linear range and detection limit for the determination of lecithin were 1.0 x 10(-6) - 3.0 x 10(-5) mol L(-1) and 3.44 x 10(-7) mol L(-1), respectively. This method is simple, practical, and relatively free of interference from coexisting substances. Furthermore, it has been successfully applied to assess lecithin in serum samples.

Hydrogen-Ion Concentration↗
PubMed1982

Evidence that reverse cholesterol transport occurs in vivo and requires lecithin-cholesterol acyltransferase.

The transport of cholesterol from extrahepatic tissues into plasma (reverse cholesterol transport) and the possible requirement for lecithin:cholesterol acyltransferase was examined in the rat. One hour after removal of the liver plasma cholesterol ester concentrations were significantly increased by 20%, whereas free cholesterol concentrations were unchanged. The lecithin:cholesterol acyltransferase inhibitor, 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB) was administered to eviscerated rats. It inhibited plasma lecithin:cholesterol acyltransferase activity by 90% which in turn totally prevented the increase in plasma cholesterol ester concentrations. In addition, heat-inactivated plasma from DTNB-treated eviscerated rats was 50% more reactive toward a standard source of lecithin:cholesterol acyltransferase compared to plasma from control or untreated eviscerated rats. These data suggest that in the rat a reactive lecithin:cholesterol acyltransferase substrate is formed extrahepatically. Together with lecithin:cholesterol acyltransferase, this reactive substrate removes cholesterol from peripheral tissues.

Animals↗
PubMed1982

Study of the lecithin: cholesterol acyltransferase reaction with liposome and high density lipoprotein substrates.

The activity of highly purified preparations of human plasma lecithin: cholesterol acyltransferase were stabilized by precipitating the enzyme with ammonium sulfate and using the dilutions of the particulate lecithin: cholesterol acyltransferase suspension for enzyme assays. Ammonium sulfate concentrations in the assay mix up to 0.1 M had no significant effect on lecithin: cholesterol acyltransferase activity. The basic enzymatic properties of lecithin: cholesterol acyltransferase were investigated using liposomes and high density lipoprotein (HDL) substrates. pH optima for both substrates was approximately 8.0. The temperature dependence of lecithin: cholesterol acyltransferase activity resulted in non-linear Arrhenius plots with both substrates. The activity vs. temperature (degrees C) curves showed slight inflections at 30 degrees C, which may have been due to the relatively rapid inactivation of the enzyme above this temperature. HDL3 was found to be a better substrate than HDL or HDL2. HDL3 was also considerably better than egg phosphatidylcholine/cholesterol liposomes as an lecithin: cholesterol acyltransferase substrate. Addition of HDL2 to a reaction mix of enzyme and HDL3 indicated that HDL2 acts as an inhibitor of cholesterol esterification in this system.

Apolipoprotein A-I↗
PubMed1983

Evidence that lecithin:cholesterol acyltransferase acts on both high-density and low-density lipoproteins.

In incubations of plasma containing lipoproteins at physiological concentrations it has been confirmed that high-density lipoproteins (HDL) are the major initial recipients of the esterified cholesterol formed in the reaction catalysed by lecithin:cholesterol acyltransferase. It has also been confirmed, however, that a small proportion of the esterified cholesterol of lecithin:cholesterol acyltransferase origin is incorporated directly into low-density lipoproteins (LDL), via a pathway that bypasses the HDL. This direct incorporation of esterified cholesterol into LDL is compatible with either of two general models. Model A proposes that lecithin:cholesterol acyltransferase does not interact directly with LDL but rather that it acts only on lipoproteins outside the LDL fraction. According to model A, while most of the esterified cholesterol so formed is incorporated into HDL, a small proportion is transferred directly to LDL. Model B, by contrast, proposes that a direct incorporation of esterified cholesterol into LDL is the result of a direct action of lecithin:cholesterol acyltransferase on the free cholesterol associated with LDL. To differentiate between these two models, experiments have been performed in which incubation mixtures containing LDL, HDL and a source of lecithin:cholesterol acyltransferase were supplemented with free [3H]cholesterol which had previously been incorporated into either LDL or HDL. It was found that, of the esterified [3H]cholesterol which was subsequently formed, the proportion recovered in the LDL fraction was much greater in the incubations to which the free [3H]cholesterol had been added as a component of LDL than in those to which it had been added as a component of HDL. This essentially excluded model A but was consistent with model B. It has been concluded that, while most of the lecithin:cholesterol acyltransferase may interact with particles in the HDL fraction, a small proportion of the enzyme interacts directly with LDL.

Adolescent↗
PubMed1985

A rapid large-scale procedure for purification of lecithin-cholesterol acyltransferase from human and animal plasma.

A rapid and convenient procedure was developed for large-scale purification of lecithin-cholesterol acyltransferase from the plasma of humans, pigs, dogs, goats and rabbits. The procedure included dextran sulfate-Mg2+ precipitation, Phenyl-Sepharose column, Affi-gel blue column, DEAE-Sepharose column, DEAE-Affi-gel blue column and hydroxyapatite column. Lecithin-cholesterol acyltransferase was purified approx. 20 000-fold with about 14% yield from human plasma. A similar result of purification was obtained from pigs, dogs, goats and rabbits. The final enzyme preparation from all five mammalian species was homogeneous as judged by SDS-polyacrylamide gel electrophoresis and high-performance gel filtration in the presence of SDS. The apparent molecular weight of the purified enzymes from humans, pigs, dogs, goats and rabbits were 65 000, 66 000, 65 000, 65 000 and 66 000, respectively, as determined by SDS-polyacrylamide gel electrophoresis and were 67 000, 67 000, 66 000, 66 000 and 67 000, respectively, by high-performance gel filtration. Studies with DEAE-Sepharose columns demonstrated that lecithin-cholesterol acyltransferase from these mammalian species was similar in molecular charge. The pH optimum for activity of purified enzyme ranged from 7.4 to 8.0 among these species. All purified lecithin-cholesterol acyltransferase species were activated by human apolipoprotein A-I and were similarly inhibited by p-hydroxymercuribenzoate and phenylmethylsulfonyl fluoride. We concluded that this purification scheme is suitable for rapid isolation of lecithin-cholesterol acyltransferase from the plasma of humans, pigs, dogs, goats and rabbits and, by inference, from other mammalian species. The availability of purified active lecithin-cholesterol acyltransferase from various animal species should facilitate phylogenetic and comparative studies of the enzyme.

Animals↗
PubMed1986

Phospholipase A2-treated human high-density lipoprotein and cholesterol movements: exchange processes and lecithin: cholesterol acyltransferase reactivity.

Human HDL3 (d 1.125-1.21 g/ml) were treated by an exogenous phospholipase A2 from Crotalus adamenteus in the presence of albumin. Phosphatidylcholine hydrolysis ranged between 30 and 90% and the reisolated particle was essentially devoid of lipolysis products. (1) An exchange of free cholesterol was recorded between radiolabelled erythrocytes at 5-10% haematocrit and HDL3 (0.6 mM total cholesterol) from 0 to 12-15 h. Isotopic equilibration was reached. Kinetic analysis of the data indicated a constant rate of free cholesterol exchange of 13.0 microM/h with a half-time of equilibration around 3 h. Very similar values of cholesterol exchange, specific radioactivities and kinetic parameters were measured when phospholipase-treated HDL replaced control HDL. (2) The lecithin: cholesterol acyltransferase reactivity of HDL3, containing different amounts of phosphatidylcholine, as achieved by various degrees of phospholipase A2 treatment, was measured using a crude preparation of lecithin: cholesterol acyltransferase (the d 1.21-1.25 g/ml plasma fraction). The rate of esterification was determined between 0 and 12 h. Following a 15-30% lipolysis, the lecithin: cholesterol acyltransferase reactivity of HDL3 was reduced about 30-40%, and then continued to decrease, though more slowly, as the phospholipid content was further lowered in the particle. (3) The addition of the lecithin: cholesterol acyltransferase preparation into an incubation medium made of labelled erythrocytes and HDL3 promoted a movement of radioactive cholesterol out of cells, above the values of exchange, and an accumulation of cholesteryl esters in HDL. This reflected a mass consumption of free cholesterol, from both the cellular and the lipoprotein compartments upon the lecithin: cholesterol acyltransferase action. As a consequence of a decreased reactivity, phospholipase-treated HDL (with 2/3 of phosphatidylcholine hydrolyzed) proved much less effective in the lecithin: cholesterol acyltransferase-induced removal of cellular cholesterol.

Cholesterol↗
PubMed1987

Effects of dietary cholesterol and fat, sex and sire on lecithin-cholesterol acyltransferase activity in baboons.

We analyzed the effects of dietary cholesterol, type of dietary fat, sex and sire progeny family on lecithin-cholesterol acyltransferase activity in 80 adult baboons. The animals were the progeny of 80 dams and 6 sires and were randomly assigned at birth to breast feeding or to one of three formulas containing 0.02, 0.30 or 0.60 mg cholesterol/ml. After weaning at 4 months of age the animals were fed one of four diets that were either high or low in cholesterol with 40% of the calories from either saturated or unsaturated fat. The fractional and molar rates of lecithin-cholesterol acyltransferase activity were measured at 7-8 years of age by an HPLC method. Infant diet (breast vs. formula feeding or level of cholesterol in formula had no effect on enzyme activity later in life. The adult diets that were high in cholesterol decreased the fractional lecithin-cholesterol acyltransferase rate by 20% / compared to diets low in cholesterol (7.89 vs. 9.84%/h, P less than 0.002), but dietary cholesterol did not affect the molar activity. Animals fed the high cholesterol diets had higher unesterified cholesterol concentrations compared to those fed the low cholesterol diets (38.1 mg/dl vs. 31.6 mg/dl, P less than 0.0001). The molar lecithin-cholesterol acyltransferase rate was increased 13% by saturated compared to unsaturated fat (83.3 vs. 73.6 nmol/h per ml plasma, P less than 0.07), but no effect of dietary fat was observed on the fractional enzyme activity. Females compared to males had significantly higher fractional (10.9 vs. 7.14%/h, P less than 0.0001) and molar lecithin-cholesterol acyltransferase activities (99.3 vs. 61.7 nmol/h per ml plasma, P less than 0.0001). After adjustment for the effects of diet and sex we observed differences in the fractional activity (range, 7.2-10.8%/h, P less than 0.04) and in the molar rate (range, 63.6-99.8 nmol/h per ml plasma, P less than 0.07) among the six sire progeny groups. The differences among sire progeny groups are evidence for genetic differences in lecithin-cholesterol acyltransferase activities among the baboon families.

Animals↗
PubMed1975

Permeability and integrity properties of lecithin-sphingomyelin liposomes.

The properties of multibilayered liposomes formed from mixtures of sphingomyelin and phosphatidylcholine in varying mole ratio (all containing one mole dicetylphosphate per 10 moles of phospholipids) have been studied. The principal findings are: (1) Over the range 0 to 1 mole fraction sphingomyelin the liposomes exhibit multibilayer structure as visualized by electron microscopy using negative staining. (2) The two phospholipids differ in their interaction with dicetylphosphate in a bilayer structure. In mixtures of the two the effect of sphingomyelin is dominant. (3) The ability of sphingomyelin to form osmotically active liposomes depends on its fatty acid's composition. (4) Liposomes of all mole fractions of sphingomyelin are osmotically active if the C24: 1 fatty acid content of sphingomyelin exceeds 10% of the total acyl residues. The degree of osmotic activity, however, depends upon the molar ratio between the two phospholipids. The highest initial rate of water permeability was found for lecithin liposomes. The maximal change of volume by osmotic gradients was obtained for liposomes composed of 1:1 lecithin to sphingomyelin (mole ratio). (5) Permeability to glucose increased with increasing lecithin mole fraction. (6) Liposomes composed of 1:1 lecithin to sphingomyelin have the largest aqueous volume per mole of phospholipid as measured by glucose trapping. (7) The osmotic fragility of liposomes made of sphingomyelin is higher than for those made of lecithin but the highest osmotic fragility was obtained for liposomes containing lecithin and sphingomyelin in 1:1 molar ratio. (8) When the temperature is abruptly lowered to about 2 degrees C, lipsomes formed from phosphatidylcholine release about 20% of trapped glucose during a transient increase in permeability. Liposomes containing 0.5 mole fraction sphingomyelin release about 30% of the trapped glucose under these conditions. Liposomes composed of sphingomyelin alone do not exhibit this phenomenon.

Animals↗
PubMed2005

Thermal analysis of the crystallization and melting behavior of lipid matrices and lipid nanoparticles containing high amounts of lecithin.

Lipid nanoparticles (LNP) based on triglycerides containing high amounts of the amphiphilic lipid lecithin have been proposed as a promising alternative drug delivery system with regard to drug loading capacity. Aim of the present study is to evaluate the influence of lecithin within the lipid matrix (LM) on the crystallization behavior by thermoanalysis and wide angle X-ray diffraction (WAXD). The crystallinity of LM and LNP is mainly determined by the triglyceride content. However, lecithin influences the crystallization behavior significantly. WAXD shows an accelerated polymorphic transition of the LM to the beta-modification upon storage with increasing lecithin content. Both, the melting point and the crystallization temperature are not affected by the lecithin concentration and are comparable to recrystallized triglyceride bulk. However, the crystallinity indices (CI) of LM show a general decrease by 10% suggesting an incomplete crystallization. For the formation of LNP at least 10% lecithin is necessary and all systems are present in the stable beta-modification. In comparison to the undispersed LM, the crystallization temperature of LNP is significantly decreased by about 20 degrees C whereas the melting point is reduced by about 5 degrees C only. Melting enthalpy is comparable to the untreated triglyceride bulk and elevated in comparison to the undispersed LM. Isothermal heat-conduction microcalorimetry (IMC) enables the determination of crystallization kinetics after fitting of the heat flow volume according to the Avrami equation.

Calorimetry, Differential Scanning↗