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PubMed1993

Fatty acid composition of lecithin is a key factor in bile metastability in supersaturated model bile systems.

We studied the effect of fatty acid saturation of biliary lecithin on bile metastability, determined by nucleation time, using model bile solutions with identical lipid compositions except for the lecithin species (total lipid concentration, 9 g/dl; cholesterol, 12 mM; lecithin, 31 mM, bile salts, 116 mM). Gel permeation chromatographic studies revealed that nonmicellar cholesterol distribution was inversely related to the degree of unsaturation of the lecithin species. Differential interference contrast microscopy and cholesterol crystal growth assay showed that a lower degree of saturation of the lecithin species was associated with a faster nucleation time and crystal growth rate. These results suggest that vesicular lecithin containing more unsaturated fatty acyl chains binds less tightly to cholesterol as compared with lecithin containing predominantly saturated fatty acids and that the biliary lecithin species modulates cholesterol crystal nucleation in bile. Also, the high ratio of cholesterol to lecithin (more than 1.0) was found in the crystal forming model biles, although the vesicle aggregation was not always observed prior to the cholesterol crystal formation. These findings indicated that there are different processes in cholesterol crystal nucleation, with or without vesicle aggregation, and that such processes depend, in part, on lecithin species in vesicles.

Bile↗

PubMed1981

Cholesterol solubilization by short-chain lecithins: characterization of mixed micelles and cholesterol oxidase activity.

The synthetic short-chain lecithins diheptanoylphosphatidylcholine and dioctanoylphosphatidylcholine solubilize cholesterol up to 10 and 18 mol %, respectively. The half-time for diheptanoylphosphatidylcholine solubilization of solid cholesterol is 80 (+/- 30) min. This is much faster than Triton X-100 micelle or egg lecithin vesicle solubilization of solid cholesterol. Both the broadening of lecithin and [4-13C]cholesterol carbon resonances by Mn2+ and the observation of surface dilution kinetics for phospholipase A2 (Naja naja naja) and phospholipase C (Bacillus cereus) hydrolysis of the lecithins indicate that the cholesterol 3 beta-hydroxyl group resides at the particle surface exposed to solvent. Analysis of lecithin 13C chemical shifts suggests that cholesterol causes the short-chain lecithin acyl chains to become slightly more trans, although to a lesser extent than it affects egg lecithin chains in liposomes. Lecithin motion as characterized by 13C T1s and line widths is unaffected by the incorporation of cholesterol. [3,4-13C2]Cholesterol line widths are 5-10-fold narrower in these mixed micelles than in egg lecithin sonicated vesicles, while T1s in the two systems are comparable. These mixed micelles serve as substrates for cholesterol oxidase (Nocardia erythropolis) with a 40-fold rate increase over comparable cholesterol concentrations in egg lecithin vesicles. Part of this rate enhancement can be understood as an increase in interfacial area available to cholesterol oxidase in the micellar systems. These studies suggest that cholesterol oxidase has a weaker affinity for interfaces than other surface active enzymes.

3-Hydroxysteroid Dehydrogenases↗

PubMed1996

Lecithin hydrophobicity modulates the process of cholesterol crystal nucleation and growth in supersaturated model bile systems.

The present study was performed to determine whether the degree of lecithin hydrophobicity regulates bile metastability and, therefore, affects the process of cholesterol crystallization. Supersaturated model bile (MB) solutions were prepared with an identical composition on a molar basis (taurocholate/lecithin/cholesterol, 73:19.5:7.5; total lipid concentration 9 g/dl) except for the lecithin species; egg yolk phosphatidylcholine, soybean phosphatidylcholine, 1-palmitoyl-2-linoleoyl-sn-phosphatidylcholine, dilinoleoyl phosphatidylcholine and dipalmitoyl phosphatidylcholine. Each MB solution was incubated and sequentially examined. Video-enhanced contrast microscopy demonstrated that the rate of vesicular aggregation and fusion correlated with the degree of lecithin hydrophobicity, and that the rate of cholesterol crystal nucleation correlated with the degree of lecithin hydrophilicity. In MBs containing less hydrophobic lecithin, needle-like crystals developed and transformed into mature plate-like crystals, whereas classical plate-like crystals were consistently observed in MBs composed of hydrophobic lecithin. Laser-diffraction particle size analysis demonstrated that the increase in lecithin hydrophobicity enlarged the vesicle dimension, enhancing its cholesterol-holding capacity. Correlation between vesicular cholesterol packing density and lecithin hydrophobicity suggests that the process of bile cholesterol nucleation and growth is regulated, in part, by acyl chain unsaturation in lecithin. Since the composition of biliary lecithins is responsive to dietary manipulations, this study provides new insights into the prevention of cholesterol gallstones.

Bile↗

PubMed2003

Lecithin decreases human milk fat loss during enteral pumping.

BACKGROUND: The fat content of human milk provides the majority of calories for infants. However, large fat losses in human milk have been observed using enteral pump systems, causing poor growth in infants. The fat may adhere in the pump system. Lecithin, a phospholipid, has been used in the food industry as a lipophilic emulsifier of fats. OBJECTIVE: The purpose of this study was to evaluate the effects of lecithin on the delivery of human milk fat from an enteral pump. It is hypothesized that the addition of lecithin would decrease the fat loss during human milk delivery. METHODS: Six mothers at a mature stage of lactation (>4 weeks of lactation) donated human milk. The human milk samples were stored separately at -20 degrees C before analysis and evaluated individually. The fat content of the milk samples was estimated by the creamatocrit method, in which the samples were centrifuged in a standard hematocrit tube and the fat layer read with vernier calipers and expressed as a percentage of the length of the milk column to the nearest 0.5%. The accuracy of this method is 92%. The Kangaroo 324 Feeding Pump (Sherwood Medical, St. Louis, MO) was used as the continuous pump system. The human milk samples were divided into either control samples without lecithin or with lecithin (1 or 0.5 g soy lecithin dissolved in 50 mL milk). All samples were pumped at 10 to 50 mL/h for at least 4 hours. The pumped milk was collected in an iced container, and creamatocrits were determined in duplicate. RESULTS: There was significant fat loss in the control milk samples compared with the milk samples with added lecithin. The average fat loss was 58% +/- 13% for control samples and 55% +/- 26% for the milk with 0.5 g soy lecithin. Milk with 1 g soy lecithin averaged 2% +/- 2% fat loss. The pumping rate had no effect on fat loss. The greatest fat loss (70% +/- 6%)occurred during the first 4 hours of pumping. CONCLUSIONS: The addition of 1 g soy lecithin per 50 mL milk decreased the human milk fat loss during intermittent pumping and may help infants receive more calories from human milk administered by pump.

Energy Intake↗

PubMed1975

Ion-binding to phospholipids. Interaction of calcium and lanthanide ions with phosphatidylcholine (lecithin).

Surface chemical and nuclear magnetic resonance (NMR) techniques have been used to study the interaction of Ca2+ and lanthanides with lecithins. With both methods positive reactions were detected at metal concentrations greater than 0.1 mM. 1H and 31P high-resolution NMR spectra obtained with single bilayer vesicles of lecithin were invariant up to Ca2+ concentrations of 0.1 M indicating that there is only a loose association between Ca2+ and the phospholipid. The weak interaction between Ca2+ and lecithin is confirmed by both surface chemical and NMR techniques showing that the packing of egg lecithin molecules present in bilayers does not change up to Ca2+ concentrations of about 0.1 M. The packing was also independent of pH between 1--10. Contradictory results have been reported in the literature concerning the question of Ca2+ binding to lecithins. The conflicting results are shown to have arisen from differences in the experimental conditions and differences in the sensitivity of the physical methods used by various authors to study Ca2+ -lecithin interactions. An estimate of the strength of binding and molecular details of the interaction were derived using paramagnetic lanthanides as isomorphous replacements for Ca2+. From the changes in chemical shifts induced in the presence of lanthanides an apparent binding constant KA approximately 30 l/mol was calculated at lanthanide concentrations greater than 10 mM. Using surface chemical methods it was shown that this KA is up to 10 times larger than that for Ca2+ binding. The complete assignment of the 1H NMR spectrum of lecithin, including the resonances from the relatively immobilized glycerol group, was determined to derive molecular details of the cation-lecithin interaction. From spin-lattice relaxation-time measurements and line broadening in the presence of GdCl3 it is concluded that the cations are bound to the phosphate group and that this is the only binding site. The absolute proton shifts induced by paramagnetic lanthanides depended on the nature of the ion, but the shift ratios standardised to the shift of the O3POCH2 (choline) signal were invariant throughout the lanthanide series indicating that the shifts are purely pseudocontact. In contrast the 31P shifts were found to contain significant contact contributions. These findings are consistent with a weak interaction and with the phosphate group being the binding site. The absolute shifts but not the shift ratios depended on the anion present indicating that the cation binding may be accompanied by binding of anions. Contrary to negatively charged phospholipids the interaction of lanthanides with lecithins was enhanced as the ionic strength was increased by adding NaCl. This was explained in terms of steric hindrance due to the extended conformation of the lecithin polar group.

Binding Sites↗

PubMed2001

Identification of IgE-binding proteins in soy lecithin.

BACKGROUND: Soy lecithin is widely used as an emulsifier in processed foods, pharmaceuticals and cosmetics. Soy lecithin is composed principally of phospholipids; however, it has also been shown to contain IgE-binding proteins, albeit at a low level. A few clinical cases involving allergic reactions to soy lecithin have been reported. The purpose of this investigation is to better characterize the IgE-binding proteins typically found in lecithin. METHODS: Soy lecithin proteins were isolated following solvent extraction of lipid components and then separated on sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). The separated lecithin proteins were immunoblotted with sera from soy-sensitive individuals to determine the pattern of IgE-binding proteins. The identity of IgE-reactive bands was determined from their N-terminal sequence. RESULTS: The level of protein in six lecithin samples obtained from commercial suppliers ranged from 100 to 1,400 ppm. Lecithin samples showed similar protein patterns when examined by SDS-PAGE. Immunoblotting with sera from soy-sensitive individuals showed IgE binding to bands corresponding to 7, 12, 20, 39 and 57 kD. N-terminal analysis of these IgE-binding bands resulted in sequences for 3 components. The 12-kD band was identified as a methionine-rich protein (MRP) and a member of the 2S albumin class of soy proteins. The 20-kD band was found to be soybean Kunitz trypsin inhibitor. The 39-kD band was matched to a soy protein with unknown function. CONCLUSIONS: Soy lecithin contains a number of IgE-binding proteins; thus, it might represent a source of hidden allergens. These allergens are a more significant concern for soy-allergic individuals consuming lecithin products as a health supplement. In addition, the MRP and the 39-kD protein identified in this study represent newly identified IgE-binding proteins.

Adolescent↗

PubMed1975

The choline incorporation pathway: primary mechanism for de novo lecithin synthesis in fetal primate lung.

The two pathways of de novo lecithin synthesis, choline incorporation (I) and phosphatidylethanolamine methylation (II), were examined in lung slices from rhesus monkey fetuses throughout the last half of gestation. Incorporation rates of pathway-specific radioactive precursors were used as a measure of lecithin production. At all stages of development studied, pathway I incorporated 10-50 times more precursor ([14C]choline) into lecithin than did pathway II ([14C]methionine or [14C]ethanolamine). In addition, although methylation activity did not change significantly during gestation, choline incorporation showed three distinct phases: (1) a stable, relatively low rate in early gestation, (2) an abrupt, twofold increase at approximately 90 percent of term, and (3) a return to lower activity levels in late gestation. This correlates with reports that lung lecithin concentration in fetal primates increases significantly in the last 10 percent of gestation. The lecithin to spingomyelin (L/S) ratios measured in amniotic fluid samples obtained at abdominal delivery were compared with pathway activities in lung slices from the same fetuses. Significant correlation was found between the amniotic fluid L/S ratio and pathway I activity (r = 0.77, P less than 0.001); in contrast, pathway II activity showed no relationship to the amniotic fluid L/S ratio. Thus, the L/S ratio appears to be a reflection of lung lecithin synthesis through the choline pathway. The conclusion that the choline pathway is the primary route of de novo lecithin synthesis in the nonhuman fetal primate lung is supported by three lines of evidence, (1) the predominance of choline incorporation into lecithin, (2) the late gestational rise in conversion of choline to lecithin, and (3) the correlation between pathway I activity and both lung lecithin concentration and amniotic fluid L/S ratio.

Adenosine Triphosphate↗

PubMed1979

[Effect of lecithin on liver microsomal lipid peroxidation].

The effect of exogeneous (egg) lecithin on peroxidation of microsomal lipids was studied with the view of elucidating the role of various components of lipid substrate in the overall oxidation rate of the lipids. The following processes were studied a) NADPH-dependent microsomal lipid peroxidation in the presence of lecithin; b) ascorbate-dependent microsomal lipid peroxidation in the presence of lecithin; c) oxidation of lipid mixture, isolated from the microsomes, and that of lecithin in the presence of the Fe2+ + ascorbate system; 4) oxidation of lecithin induced by the Fe2+ + ascorbate system. It was found that in the presence of exogeneous lecithin the oxidation of microsomal lipids in inhibited, which is probably due to the peculiarities of lecithin oxidation. It was shown that the specific rate of lecithin oxidation is decreased with an increase in lecithin concentration. Possible mechanisms of lecithin effect on microsomal lipid peroxidation are discussed.

Animals↗

PubMed1967

Studies in the biosynthesis of hepatic and biliary lecithins.

Male rats with biliary cannulae were injected with linoleate-1-(14)C, stearate-1-(14)C, palmitate-9-10-(3)H, phosphate-(32)P, l-methionine-methyl-(14)C, and choline-methyl-(3)H in various combinations and the incorporation of these isotopes into the phospholipids of liver, bile, and plasma was determined for 1-4 hr. The results summarized below favor the view (a) that exchange of saturated fatty acids plays a role in the formation of lecithins; (b) that the unsaturated fatty acids do not undergo significant exchange and determine the pathway of biosynthesis of lecithins; and (c) that there is either more than one pool of CDP-choline in liver or a pathway of biosynthesis of lecithin from choline not involving CDP-choline as an intermediate. Linoleoyl lecithin of liver attained higher specific activity with respect to phosphate-(32)P and choline-methyl-(3)H than did arachidonoyl lecithin. Lecithin in bile attained higher specific activities with respect to phosphate-(32)P, choline-methyl-(3)H, and linoleate-1-(14)C than the corresponding hepatic lecithins. Stearate-1-(14)C and palmitate-9-10-(3)H attained highest specific activities in the hepatic lecithin fraction rich in arachidonic acid. The specific activity of hepatic phosphatidyl ethanolamine was lower with respect to saturated fatty acids, but much higher with respect to (32)P than any lecithin. The ratio of specific activity of (3)H in methyl groups from choline to (14)C in methyl groups from methionine in hepatic sphingomyelin was lower than in hepatic linoleoyl lecithin.

Animals↗

PubMed2001

Lecithinized Cu, Zn-superoxide dismutase limits the infarct size following ischemia-reperfusion injury in rat hearts in vivo.

Covalent binding of 4 molecules of phosphatidylcholine palmitoyl to human recombinant superoxide dismutase (SOD) results in a compound (lecithinized SOD) that has a longer half-life and greater affinity to the cell membrane than unmodified SOD. We investigated whether lecithinized SOD played a protective role against myocardial ischemia-reperfusion injuries in rats. Rats underwent 45 min of myocardial ischemia by occluding the left coronary artery followed by 120 min of reperfusion. They were randomly assigned to receive either lecithinized SOD, polyethylene glycol conjugated SOD (PEG-SOD), unmodified SOD, free lecithin derivative, or PBS intravenously at 5 min prior to reperfusion. Myocardial infarct area assessed by TTC staining was smaller in lecithinized SOD group than PEG-SOD, unmodified SOD, free lecithin derivative or control group. Blood pressure and heart rate was similar in each group. ELISA demonstrated SOD level in the heart was significantly high in lecithinized SOD group, especially in the heart of ischemia at risk. Although serum SOD level of PEG-SOD was as high as lecithinized SOD, SOD level of the heart was low. These data suggested lecithinized SOD had a protective effect in myocardial ischemia-reperfusion injuries through its increased bioavailability.

Animals↗

PubMed1985

Intestinal cholesterol uptake: comparison between mixed micelles containing lecithin or lysolecithin.

The aim of our study was to define the mechanism by which cholesterol uptake is inhibited by lecithin but not by lysolecithin. The work compared the cholesterol uptake by everted rat jejunal sacs from bile salt-lecithin-cholesterol or bile salt-lysolecithin-cholesterol micelles. The micellar size and the cholesterol saturation were measured. The size or molecular weight increases when the lecithin concentration rises, and the cholesterol uptake decreases and leads to zero when the micelles contain more than 30% lecithin. The size of bile salt-lysolecithin-cholesterol micelles is smaller than that of lecithin micelles in comparable molar ratios. Consistent with this result is the fact that, for a given phospholipid concentration, cholesterol uptake is greater in the presence of lysolecithin than in the presence of lecithin. The diffusion rate of the micelles through the unstirred water layer decreases when micellar size increases. However, the comparison of uptakes from lecithin or lysolecithin micelles similar in size and in cholesterol saturation showed that the cholesterol uptake is still lower for lecithin micelles. This shows that with larger micelles some factor other than micellar size and cholesterol content of the micelles is important. We observe that lysolecithin absorption is 15-fold greater than lecithin absorption. We suggest that lysolecithin absorption results in a rapid supersaturation with cholesterol leading to cholesterol absorption.

Animals↗

PubMed2001

Lecithinized copper, zinc-superoxide dismutase ameliorates ischemia-induced myocardial damage.

We have reported that lecithin-conjugated recombinant human Cu, Zn-superoxide dismutase (lecithinized SOD) has greater pharmacological potency than unmodified SOD through an increase in cell membrane affinity and half-life in plasma. Recently, ischemia or hypoxia alone has been suggested to result in increased superoxide anions, which lead to apoptosis in cardiomyocytes. We tested the effect of lecithinized SOD in reducing the infarct size following prolonged myocardial ischemia without reperfusion. Rats were subjected to a 24-h left coronary occlusion. Lecithinized SOD, unmodified SOD, free lecithin derivative or PBS was administered intravenously 30 min before coronary occlusion. SOD concentration of the heart, measured by ELISA, was higher in the lecithinized SOD-treated group than in the other groups 24 h after administration. The infarct area ratio of the heart, assessed by TTC staining, in the lecithinized SOD-treated group was significantly smaller than those of the other groups. Both TUNEL-positive cardiomyocytes and DNA laddering were attenuated in the ischemic area of the heart treated with lecithinized SOD. Single bolus administration of lecithinized SOD had a cardioprotective effect against ischemia without reperfusion in the rat model of acute myocardial infarction, possibly due to its sustained high tissue concentration.

Animals↗

PubMed1986

Interaction of short-chain lecithin with long-chain phospholipids: characterization of vesicles that form spontaneously.

Stable unilamellar vesicles formed spontaneously upon mixing aqueous suspensions of long-chain phospholipid (synthetic, saturated, and naturally occurring phosphatidylcholine, phosphatidylethanolamine, and sphingomyelin) with small amounts of short-chain lecithin (fatty acid chain lengths of 6-8 carbons) have been characterized by using NMR spectroscopy, negative staining electron microscopy, differential scanning calorimetry, and Fourier transform infrared (FTIR) spectroscopy. This method of vesicle preparation can produce bilayer vesicles spanning the size range 100 to greater than 1000 A. The combination of short-chain lecithin and long-chain lecithin in its gel state at room temperature produces relatively small unilamellar vesicles, while using long-chain lecithin in its liquid-crystalline state produces large unilamellar vesicles. The length of the short-chain lecithin does not affect the size distribution of the vesicles as much as the ratio of short-chain to long-chain components. In general, additional short-chain decreases the average vesicle size. Incorporation of cholesterol can affect vesicle size, with the solubility limit of cholesterol in short-chain lecithin micelles governing any size change. If the amount of cholesterol is below the solubility limit of micellar short-chain lecithin, then the addition of cholesterol to the vesicle bilayer has no effect on the vesicle size; if more cholesterol is added, particle growth is observed. Vesicles formed with a saturated long-chain lecithin and short-chain species exhibit similar phase transition behavior and enthalpy values to small unilamellar vesicles of the pure long-chain lecithin prepared by sonication. As the size of the short-chain/long-chain vesicles decreases, the phase transition temperature decreases to temperatures observed for sonicated unilamellar vesicles. FTIR spectroscopy confirms that the incorporation of the short-chain lipid in the vesicle bilayer does not drastically alter the gauche bond conformation of the long-chain lipids (i.e., their transness in the gel state and the presence of multiple gauche bonds in the liquid-crystalline state).

Animals↗

PubMed1987

Noncooperative vs. cooperative reactivation of D-beta-hydroxybutyrate dehydrogenase: multiple equilibria for lecithin binding are determined by the physical state (soluble vs. bilayer) and composition of the phospholipids.

D-beta-Hydroxybutyrate dehydrogenase (BDH) is a lecithin-requiring mitochondrial enzyme that catalyzes the interconversion of beta-hydroxybutyrate and acetoacetate. The purified soluble enzyme devoid of lipid (i.e., the apodehydrogenase) can be reactivated with soluble lecithin or by insertion into phospholipid vesicles containing lecithin. Lipid activation curves have a sigmoidal shape, and two models have been proposed to explain them. We have previously reported that the kinetics of reactivation with short-chain lecithins in the soluble state is consistent with a model in which the enzyme enzyme contains two identical, noninteracting lecithin binding sites, both of which must be occupied to activate the enzyme [noncooperative mechanism; Cortese, J.D., Vidal, J.C., Churchill, P., McIntyre, J.O., & Fleischer, S. (1982) Biochemistry 21, 3899-3908]. More recently a kinetic model involving cooperative interactions between lecithin binding sites was proposed for the reactivation of the membrane-bound enzyme [Sandermann, H., Jr., McIntyre, J.O., & Fleischer, S. (1986) J. Biol. Chem. 261, 6201-6208]. This study reinvestigates the basis for the different conclusions in these two studies. The previous study with soluble lecithins was limited to about 34% of maximal activation compared with mitochondrial phospholipid, due to inactivation of the enzyme at the critical micellar concentration. We could now extend this study to 91% activation by increasing the ethanol concentration. This experimental evidence confirms that the soluble system follows a noncooperative equation. We provide a new kinetic approach to test the cooperative model. A velocity equation is derived for a Hill-type cooperative ligand binding system interacting with a mixture of ligands. This equation predicts a proportionality between an overall weighted cooperative dissociation constant [Kcoop(w)] and a dissociation constant for a single lecithin (PC) species from interacting sites (KPC), regulated by the PC molar fraction (XPC): 1/Kcoop(w) = XPC/KPC. The equation was applied to the data of Sandermann et al. [Sandermann, H., Jr., McIntyre, J.O., & Fleischer, S. (1986) J. Biol. Chem. 261, 6201-6208] as well as to newly obtained data. The results obtained over a wide range of PC molar fractions and different mixtures of bilayer phospholipids fit this equation, confirming the cooperative behavior. We conclude that BDH has a different mode of reactivation depending on the nature of the lipid environment. With soluble lecithin, the activation is noncooperative, whereas in the bilayer, mixtures of phospholipids give cooperative behavior that fits a Hill equation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1990

Sizing of lecithin-bile salt mixed micelles by size-exclusion high-performance liquid chromatography.

Size-exclusion high-performance liquid chromatography with a TSK 5000 PW column was shown to be a fast and relatively inexpensive method for the size determination of lecithin-bile salt mixed micelles. Perturbation of the equilibrium between aqueous soluble and micellar bile salts during elution was avoided by preequilibration of the column with buffer containing the aqueous soluble concentration of the bile salt. Elution volumes were converted to size dimensions from a calibration curve produced from the elution volumes of proteins and small unilamellar vesicles of known size. Micelle sizes determined for several different lecithin-bile salt mixtures were consistent with those obtained by other techniques. The well-known hyperbolic increase in mixed micelle size as the lecithin to bile salt ratio approaches the micellar-vesicle phase limit was reproduced with this chromatographic technique. On the basis of these data and the recent observation by small-angle neutron scattering that lecithin-bile salt micelles increase in size by the elongation of constant-diameter rods [Hjelm et al. (1988) J. Appl. Crystallogr. 21, 858-863], a new model for the mixed micelle structure is proposed. According to this model, separation of the lecithin head groups by bile salts inserted along the rod surface produces a radial orientation of lecithin molecules along the length of the rod. Each end of the rod is sealed off by a lecithin-bile salt configuration that is richer in bile salts than the rod portion of the micelle. A simple mathematical description of this model predicts the observed changes in micellar size as a function of the lecithin-bile salt ratio with parameters that are consistent with lecithin and bile salt molecular dimensions.

Bile Acids and Salts↗

PubMed1977

Effect of age on the saturated lecithin contents of human and rat lung tissues.

Changes with age in the lecithin (especially saturated lecithin) content of human and rat lung and in lecithin synthetic activities in rat lung were examined to obtain information on lecithin metabolism in the lung in old age. In lung tissues of humans and rats, the content of saturated lecithin as a percentage of total lecithin was fairly constant (about 35%) throughout adult and old age; The percentage content in bronchial wash was 55--60% in both young and old rats. The radioactivities incorporated into lung tissue per milligram total and saturated lecithin after intravenous administration of palmitic acid3-H were similar in young and old rats. These results suggest that lung tissue contains a rather constant amount of saturated lecithin throughout adult and old age and that lecithin synthesis in the lung is still active in old age.

Adult↗

PubMed1990

Evidence that polyunsaturated lecithin induces a reduction in plasma cholesterol level and favorable changes in lipoprotein composition in hypercholesterolemic rats.

For 30 d adult rats were fed a hypercholesterolemic (H) diet (25% saturated fat, 1% cholesterol and 0.5% cholic acid) containing different amounts of saponins (1% or 0.2%) and/or purified polyunsaturated lecithin (2.5% or 0.7%). Lecithin induced a striking reduction in the plasma levels of very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and low density lipoprotein (LDL) cholesterol as well as an increase in the level of high density lipoprotein (HDL) cholesterol. Saponins had only a very slight effect in lowering the level of VLDL cholesterol. Apoprotein A-I was unexpectedly present in VLDL, IDL and LDL after feeding rats the H diet and disappeared only after lecithin feeding. The activity of plasma lecithin-cholesterol acyltransferase was higher when the two lecithin diets were fed than when the other diets were fed. Fecal excretion of neutral sterols was unmodified by the various diets whereas acid steroid excretion increased after lecithin feeding. Saponins, when added with lecithin to the diet, reduced the beneficial effect of lecithin. The results indicate that polyunsaturated lecithin induced a reduction in plasma cholesterol, possibly through an increased formation of HDL particles.

Animals↗

PubMed1979

Effect of fatty acyl group and sterol composition on sensitivity of lecithin liposomes to imidazole antimycotics.

The specific affinity for membrane lipids and the membrane selectivity of three imidazole derivatives, clotrimazole, miconazole, and econazole, were studied using various types of liposomes with respect to the lecithin fatty acyl group composition and the liposome content and composition of sterol as membrane models. The sensitivity of liposomes to these drugs was primarily dependent upon the lecithin fatty acyl group composition. With sterol-free liposome systems, each imidazole induced maximum release of trapped glucose as a marker from the unsaturated dioleoyl lecithin liposomes, minimum release from the saturated dipalmitoyl lecithin liposomes, and intermediate release from egg lecithin liposomes. The sensitivity of the dipalmitoyl lecithin liposomes to any imidazole drug was not influenced by the incorporation of cholesterol or ergosterol. On the other hand, clotrimazole-induced permeability changes of liposomes prepared from unsaturated dioleoyl lecithin or egg lecithin were greatly enhanced by the incorporation of ergosterol, whereas they were suppressed by cholesterol incorporation. The sensitivity of liposomes prepared from these unsaturated lecithins to miconazole and econazole was also augmented by ergosterol incorporation, although it was scarcely altered by cholesterol incorporation. Negatively charged liposomes were more sensitive to the three imidazole drugs than positively charged liposomes.

Antifungal Agents↗