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PubMed1978

Interaction of an amine oxide detergent with lecithin vesicles as studied by nuclear magnetic resonance.

The interaction of an amine oxide detergent with single bilayer lecithin vesicles was investigated with proton and phosphorus magnetic resonance. The addition of the detergent micelles to vesicles suspensions leads to rapid detergent incorporation into the vesicle bilayer, resulting in a heterogenous vesicle population. Initially, some vesicles take up the equivalent of one detergent micelle, whereas others contain no detergent. Subsequently, the detergent is distributed between the vesicles by vesicle-vesicle collisions. This can be followed by the change in the Pr3+-shifted spectral positions of the detergent and lecithin head groups with time. From the intensity of the head-group signals, it can be concluded that after about 20 h the detergent is almost equally distributed between the outer and inner vesicle membrane monolayers. Vesicles obtained by cosonication of the detergent and lecithin take up metal ions. This ion permeability depends on the vesicle concentration and can be attributed to vesicle-vesicle or vesicle-mixed micelle collisions. Egg lecithin vesicles are stable against the detergent up to molar ratios of detergent to lecithin of 0.2--0.3. At larger ratios mixed micells and multibilayers are formed. Measurements of proton spin-lattice relaxation times confirmed that the internal architecture of the vesicle bilayer is almost unaffected by the incorporated detergent.

Detergents↗
PubMed2003

Influence of environmental conditions on the stability of oil in water emulsions containing droplets stabilized by lecithin-chitosan membranes.

Oil-in-water emulsions containing cationic droplets stabilized by lecithin-chitosan membranes were produced using a two-stage process. A primary emulsion containing anionic lecithin-coated droplets was prepared by homogenizing oil and emulsifier solution using a high-pressure valve homogenizer (5 wt % corn oil, 1 wt % lecithin, 100 mM acetic acid, pH 3.0). A secondary emulsion containing cationic lecithin-chitosan-coated droplets was formed by diluting the primary emulsion with an aqueous chitosan solution (1 wt % corn oil, 0.2 wt % lecithin, 100 mM acetic acid, and 0.036 wt % chitosan). The stabilities of the primary and secondary emulsions with the same oil concentration to thermal processing, freeze-thaw cycling, high calcium chloride concentrations, and lipid oxidation were determined. The results showed that the secondary emulsions had better stability to droplet aggregation during thermal processing (30-90 degrees C for 30 min), freeze-thaw cycling (-10 degrees C for 22 h/30 degrees C for 2 h), and high calcium chloride contents (</=500 mM CaCl(2)) and exhibited less lipid oxidation (peroxide formation) than primary emulsions. The interfacial engineering technology used in this study could lead to the creation of food emulsions with improved stability to environmental stresses.

Calcium Chloride↗
PubMed2005

Use of differential scanning calorimetry to study lipid oxidation. 1. Oxidative stability of lecithin and linolenic acid.

The oxidation of linolenic acid (LNA) and soy lecithin was studied by differential scanning calorimetry (DSC) with linear programmed heating rates (non-isothermal mode). The interpretation of the shape of DSC curves is discussed, and it has been concluded that temperatures of the extrapolated start of heat release are the most reliable data for the rapid estimation of the oxidative stability of lipid materials. The Ozawa-Flynn-Wall method was used to calculate the kinetic parameters of the process: for LNA autoxidation the activation energy, Ea, and pre-exponential factor, Z, are 66 +/- 4 kJ/mol and 1.5 x 10(7) s(-1), respectively, and the autoxidation of lecithin is described by Ea = 98 +/- 6 kJ/mol and Z = 9.1 x 10(10) s(-1). Values of Ea and Z can be applied for calculation of the overall first-order rate constant of autoxidation at various temperatures, k(T). For the two studied lipids the comparison of k(T) values shows the inversion of their oxidative stabilities; that is, below 167 degrees C lecithin is more stable than LNA, k(T)lecithin < k(T)LNA, and above that temperature (termed the isokinetic temperature) k(T)lecithin > k(T)LNA. The calculated inversion of oxidative stabilities can be an explanation of similar observations for other pairs of lipids if the results of accelerated tests measured at temperatures above 100 degrees C are compared with the results obtained at temperatures below 100 degrees C.

Calorimetry, Differential Scanning↗
PubMed1967

Stability of unimolecular films of 32P-labeled lecithin.

1. The stability of monolayers of a highly unsaturated yeast lecithin labelled with (32)P has been investigated by a surface radioactivity technique. 2. Lecithin films on distilled water at all surface pressures between 6 and 48dynes/cm. were completely stable on rapid perfusion of the subphase and on addition of ionic amphipathic substances to the film. 3. Ultrasonically treated lecithin added to the subphase caused a slow loss of surface radioactivity but little pressure change. 4. The addition of proteins to the subphase caused negligible changes in the film even when conditions were favourable for electrostatic heterocoagulation and penetration. 5. Lecithin films were not hydrolysed by a strongly acid subphase at room temperature. The very low rate of hydrolysis produced by alkali was proportional to the subphase OH(-)ion concentration: the apparent activation energy and temperature coefficient (Q(10)) of the reaction were 14250 cal. and 2.37 respectively. 6. Alkaline hydrolysis of lecithin monolayers was markedly stimulated by adding methanol (10-20%, v/v) to the subphase. The addition of ionic amphipaths to the monolayer had the expected type of effect on the hydrolysis rate, but its magnitude was far less than that suggested by an application of the Poisson-Boltzmann equation for ion distribution at a charged interface (Davies & Rideal, 1963).

Chemical Phenomena↗
PubMed1981

Evidence for a lipoprotein carrier in human plasma catalyzing sterol efflux from cultured fibroblasts and its relationship to lecithin:cholesterol acyltransferase.

Immunoaffinity chromatography has been used to study the determinants of sterol efflux and net transport from cultured fibroblasts to human plasma medium. Sterol efflux was highly (approximately 80%) dependent upon a minor lipoprotein fraction containing apolipoprotein A-I unassociated with other apolipoproteins. The remaining activity was associated with the lipoprotein-free fraction of plasma and could be replaced by apoprotein-free albumin. Efflux was independent of lecithin:cholesterol acyltransferase (EC 2.3.1.43) activity. Net transport (i.e., the excess of efflux over influx) was completely inhibited by inhibition of lecithin:cholesterol acyltransferase or its removal by affinity chromatography on immobilized antibodies to apolipoprotein A-I or D (components of the transfer complex in human plasma). In uninhibited plasma, efflux and net transport rates had similar kinetics, suggesting that these were linked functions and that net transport was initiated by a carrier-dependent efflux step that, in the absence of lecithin:cholesterol acyltransferase activity, was associated with an equivalent influx of free sterol to the cells and that, in the presence of lecithin:cholesterol acyltransferase, was associated with esterification and transfer protein activity. The cholesterol carrier lipoprotein function (approximately 5% of plasma apolipoprotein A-I) appears to be the first step of lecithin:cholesterol acyltransferase-linked sterol transport from cells.

Apolipoproteins↗
PubMed1976

Positional fatty acid composition in total and acetone-precipitated amniotic fluid lecithin.

The fatty acid composition of lecithin has been determined separately at the 1- and 2-position in 22 samples of amniotic fluid. Palmitic acid (16:0) was the main fatty acid present at both carbon atom positions throughout the last trimester. Myristic acid (14:0) was present in very small amounts only. There was no evidence of 1-palmitoyl/2-myristoyl lecithin being present in more than trace amounts before 35 weeks of gestation. The positional specificity of the methylation pathway is therefore doubtful. Acetone precipitation of lecithin did not alter the observed fatty acid composition at either position, indicating that this procedure precipitates the different lecithin subspecies in equal proportion, without any preference for disaturated species. This method therefore fails to isolate a lecithin fraction with a specific fatty acid composition.

Acetone↗
PubMed2002

Antistress and adaptogenic activity of lecithin supplementation.

OBJECTIVE: Investigation of lecithin administration in rats for its antistress and adaptogenic activity. DESIGN: Lecithin was administered orally (1 mg/g body weight) to rats 0.5 hour, 1.5 hours, 3.0 hours, and 6.0 hours prior to cold (5 degrees C)-hypoxia (428 mm Hg)-restraint (C-H-R) exposure and serum choline estimation. The rectal temperature (T(rec)) of the rats was monitored during the exposure and the recovery periods. The time for decrease of T(rec) to 23 degrees C and its recovery to 37 degrees C were used as indices of antistress and adaptogenic activity. RESULTS: Lecithin administration 3-6 hours prior to C-H-R exposure was found to have significant adaptogenic activity that correlated with increased serum choline levels. Lecithin administration prior to C-H-R exposure increased the stress tolerance of the rats by delaying the time for decrease of T(rec) to 23 degrees C during C-H-R exposure. It also helped shorten poststress recovery as observed by decreased time to attain T(rec) of 37 degrees C from C-H-R-induced hypothermia (T(rec), 23 degrees C). CONCLUSIONS: The results suggested that lecithin supplementation acted as an antistress and adaptogenic functional food. It improved resistance during C-H-R exposure and enhanced recovery from hypothermia.

Adaptation, Physiological↗
PubMed1983

Amniotic fluid lecithin, phosphatidylglycerol, L/S ratio, and foam stability test in predicting respiratory distress in the newborn.

Amniotic fluid phospholipids (lecithin, sphingomyelin, phosphatidylglycerol) were extracted and separated by the method of Gluck and associates. In addition, these lipids were quantified against standards that were concurrently developed in three adjacent thin layer chromatography (TLC) channels. A log-log transformation of the reflectance and concentration values provided rectilinear plots for quantification. A foam stability assay (FS) of 0.48 or greater was associated with high values of L/S ratio and lecithin concentration, and values of 0.44 or less almost always were associated with low values. Lecithin values of 12 micrograms/mL or more were associated with L/ S ratios of 2.0 or greater. Phosphatidylglycerol was detected consistently only when lecithin levels were 40 micrograms/mL or greater and L/S ratios 4.0 or greater. Case reviews indicated that: (1) FS test of 0.48 almost always was associated with pulmonary maturity in the newborn; (2) that a pulmonary maturity index combining the lecithin concentration and L/S ratio was a better predictor of pulmonary maturity in the newborn then either one alone; (3) that phosphatidylglycerol added little to this discrimination; and (4) that these assays showed no significant interpretative differences between diabetic and non-diabetic mothers.

Amniotic Fluid↗
PubMed1976

Effect of cholesterol sulfate and sodium dodecyl sulfate on lecithin-cholesterol acyltransferase in human plasma.

The effects of cholesterol sulfate and sodium dodecyl sulfate (SDS) on the esterification of cholesterol in sonicated dispersions of lecithin-cholesterol mixtures by lecithin-cholesterol acyltransferase [EC 2.3.1.43] (LCAT) in human plasma were studied in vitro. The acyltransferase activity was inhibited at concentrations of cholesterol sulfate higher than 1 X 10(-4) M. This inhibition was not eliminated by the addition of bovine serum albumin or CaC12. On the contrary, the acyltransferase activity was stimulated at concentrations of SDS ranging from 1 X 10(-5) M to 1 X 10(-3) M, and maximum stimulation was obtained at 5 X 10(-4) M. The maximum stimulation disappeared on the addition of bovine serum albumin (30 mg per ml of incubation medium), 1 X 10(-3) M CaC12 or 1 X 10(-4) M cholesterol sulfate. On the other hand, the extent of inhibition of the acyltransferase by cholesterol sulfate was not affected by the amount of lecithin in the dispersion added as a substrate, but the maximum stimulation (5 X 10(-4) M SDS) of the acyltransferase was interfered with when a large amount of lecithin was present in the dispersion. In addition, the amount of SDS required for maximum cholesterol esterification was not affected by the amount of lecithin present in the dispersion. These results suggest that the action of cholesterol sulfate on the acyltransferase is different from that of SDS.

Acyltransferases↗
PubMed1986

Stimulation of lecithin:cholesterol acyltransferase activity by apolipoprotein A-II in the presence of apolipoprotein A-I.

Various combinations of incorporation and addition of apolipoprotein A-I (apo A-I) and apolipoprotein A-II (apo A-II) individually or together to a defined lecithin-cholesterol (250/12.5 molar ratio) liposome prepared by the cholate dialysis procedure were used to study the effect of apo A-II on lecithin:cholesterol acyltransferase (LCAT, EC 2.3.1.43) activity of both purified enzyme preparations and plasma. When apo A-I (0.1-3.0 nmol/assay) alone was incorporated or added to the liposome, apo A-I effectively activated the enzyme. By contrast, when apo A-II (0.1-3.0 nmol/assay) alone was incorporated into or added to the liposome, apo A-II exhibited minimal activation of LCAT activity, approximately 1% of the activity obtained by an equal amount of apo A-I. Addition of apo A-II (0.1-3.0 nmol/assay) together with apo A-I (0.8 nmol/assay) to the liposome reduced the LCAT activity to approximately 30% of the level obtained with addition of apo A-I alone. On the other hand, addition of apo A-II (0.1-3.0 nmol/assay) or addition of lecithin-cholesterol liposome containing apo A-II (0.1-3.0 nmol/assay) to lecithin-cholesterol liposome containing apo A-I (0.8 nmol/assay) did not significantly alter apo A-I activation of LCAT activity. However, when the same amounts (0.1-3.0 nmol/assay) of apo A-II were incorporated together with apo A-I (0.8 nmol/assay) into the liposome, apo A-II significantly stimulated LCAT activity as compared to activity obtained with incorporation of apo A-I alone. The maximal stimulation was obtained with 0.4 nmol apo A-II/assay for both purified and plasma enzyme. At this apo A-II concentration, approximately 4-fold and 1.8-fold stimulation was observed for purified enzyme and plasma enzyme, respectively. These results indicated that apo A-II must be incorporated together with apo A-I into lecithin-cholesterol liposomes to exert its stimulatory effect on LCAT activity and that apo A-II in high-density lipoprotein may play an important role in the regulation of LCAT activity.

Apolipoprotein A-I↗
PubMedDate not supplied

Estimation of lecithin in rabbit tissues.

1. A simple method for lecithin estimation was developed. Phospholipids in rabbit tissues were extracted with chloroform and methanol. 2. The samples were chromatographed with eluting solvent system; chloroform:methanol:glacial acetic acid:water (100:25:8:1.1). Lecithin was identified by the spray reagent as blue spots and the intensities were quantitated with a densitometer. 3. The concentration of lecithin in the various rabbit tissues varied from 2.8 to 10 mg/g tissue. The sequence of increasing lecithin concentration was heart less than kidney less than lung less than liver less than brain. 4. Recovery experiments of added lecithin into the tissues showed a recovery of 91-104%.

Animals↗
PubMed1997

Lecithinization of IL-6 enhances its thrombopoietic activity in mice.

This study was conducted to assess the merit of lecithinization of recombinant human interleukin-6 (IL-6) as a drug delivery system. IL-6 was lecithinized by covalently binding it with a phosphatidylcholine (lecithin, PC) derivative. The in-vivo thrombopoietic potency of lecithinized IL-6 (PC-IL-6) was greater than that of native IL-6 when administered subcutaneously, although the in-vitro bioactivity of PC-IL-6 was markedly reduced by lecithinization. When PC-IL-6 and native IL-6 were given in doses that produced the same level of thrombopoietic activity, the former stimulated less production of IgG1, a marker of the adverse effects of IL-6, than did the latter. Furthermore, PC-IL-6 persisted in the blood longer than native IL-6. Based on the above, PC-IL-6 appears to be useful as a drug delivery system and may also be useful in the treatment of drug-induced thrombocytopenia.

Animals↗
PubMed1973

The effect of lecithin on intestinal cholesterol uptake by rat intestine in vitro.

1. Sacs 20 cm long were obtained from the upper half of the small intestine of bile fistula rats (bile duct cannulated 48 hours previously). The sacs were everted, filled with oxygenated phosphate buffer and incubated 1 hr at 37 degrees C in 25 ml. of a buffered micellar solution of oleic acid (0.6 mM), mono-olein (0.3 mM), sodium taurocholate (4.8 mM) and (3)H-labelled cholesterol (0.15 mM) plus glucose (28 mM).2. After incubation the amount of [(3)H]cholesterol taken up by the mucosal tissue was measured. It averaged 200 n-mole/hr.g tissue wet wt. +/- 6 (S.E.).3. Adding 3 ml. whole rate bile with other factors unchanged caused cholesterol uptake to decrease by 50% in confirmation of previous studies.4. Adding purified lecithin obtained from rat liver tissue, and from egg yolks, similarly decreased cholesterol uptake. A significant response was obtained with 2.5 mg liver lecithin (concentration 0.13 mM) and a near maximum response with 15 mg (concentration 0.80 mM). 10 mg lecithin decreased uptake by an amount equivalent to that obtained with 3 ml. whole bile.5. Lecithin is an active component of whole bile causing reduced intestinal cholesterol uptake from micelles.6. The decreased uptake of cholesterol in the presence of lecithin may have been the result of expansion of the cholesterol-containing micelles with consequent reduction in cholesterol permeability.

Animals↗
PubMed1973

Selective membrane toxicity of the polyene antibiotics: studies on lecithin membrane models (liposomes).

In the absence of sterol, amphotericin B at 5 x 10(-6) M caused maximum marker release from the saturated dipalmitoyl lecithin liposomes, minimum release from the unsaturated dioleoyl lecithin liposomes, and an in-between response from egg lecithin liposomes. Nystatin at 2.5 to 4.0 x 10(-5) M induced appreciable marker release from all three types of sterol-free liposomes. The amphotericin B- and nystatin-induced permeability changes in dipalmitoyl lecithin liposomes were drastically suppressed by the incorporation of cholesterol or stigmasterol (with identical Delta5 sterol nuclei), but were unaffected by the incorporation of ergosterol or 5,7-cholestadien-3beta-ol (with identical Delta5,7 sterol nuclei). The nystatin sensitivity of dioleoyl lecithin liposomes remained low after the incorporation of cholesterol or stigmasterol, but was greatly enhanced by the incorporation of ergosterol or 5,7-cholestadien-3beta-ol. Digitonin, a compound known to interact specifically with membrane sterol, induced marker release from liposomes in proportion to the amount of either cholesterol or ergosterol incorporated; epicholesterol did not sensitize to digitonin. These results lead to the following conclusions: (i) polyene-induced permeability alteration in model membrane systems is effected by the composition of membrane phospholipid fatty acyl chains; (ii) the distribution of double bonds in the sterol nucleus is related to the selective toxicity of the polyenes toward natural sterol-containing membranes; and (iii) polyenes differ in membrane selectivity.

Amphotericin B↗
PubMed1973

Influence of amniotic fluid volume on lecithin estimation in prediction of respiratory distress.

One hundred samples of amniotic fluid were obtained by amniocentesis from 82 patients at different stages of normal and abnormal pregnancies. The concentration of lecithin was estimated together with the volume of the amniotic fluid, using the dilution technique. Thus the total quantity of lecithin in any amniotic sac could be calculated. While confirming the findings of others that concentrations of lecithin below 3.5 mg/100 ml in the liquor immediately before delivery suggested that the baby was likely to develop respiratory distress syndrome, we found that in borderline cases the total amount of lecithin in the sac was of greater prognostic significance than the lecithin concentration.

Amniocentesis↗
PubMed1985

A double-blind, placebo controlled trial of high-dose lecithin in Alzheimer's disease.

The first long-term double-blind placebo controlled trial of high dose lecithin in senile dementia of the Alzheimer type is reported. Fifty one subjects were given 20-25 g/day of purified soya lecithin (containing 90% phosphatidyl plus lysophosphatidyl choline) for six months and followed up for at least a further six months. Plasma choline levels were monitored throughout the treatment period. There were no differences between the placebo group and the lecithin group but there was an improvement in a subgroup of relatively poor compliers. These were older and had intermediate levels of plasma choline. It is suggested that the effects of lecithin are complex but that there may be a "therapeutic window" for the effects of lecithin in the condition and that this may be more evident in older patients.

Aged↗
PubMed1982

Lipid metabolic studies in oophorectomized women: effects of synthetic progestogens on individual serum phospholipids and serum lecithin fatty acid composition.

Norethisterone acetate (NET), levonorgestrel (NORG) and medroxyprogesterone acetate (MPA) were administered to oophorectomized women to evaluate the effects on individual serum phospholipids as well as serum lecithin and cholesterol ester fatty acid composition. Blood samples were drawn after a 3-week period without hormonal replacement therapy and after 3 weeks on each progestogen. NORG reduced cepahlin and lecithin with a concomitant increase in lysolecithin. This shift in individual phospholipids has previously been induced by exogenous androgens. The 17C-alkylated synthetic progestogens NET and NORG but not the non-alkylated MPA caused a redistribution among the 1-position fatty acids of serum lecithin with an increase in palmitic concomitant with a decrease in stearic acid. These findings indicate differences between 19-nortestosterone derivatives and 17-hydroxyprogesterone derivatives in effect on individual serum phospholipids and in influence on liver lecithin synthesis as judged from serum lecithin fatty acid composition.

Adult↗
PubMed1972

The appearance of lecithin- 32 P, synthesized from lysolecithin- 32 P, in phagosomes of polymorphonuclear leukocytes.

Rabbit polymorphonuclear leukocytes ingesting paraffin oil particles stabilized with albumin, converted more lysolecithin-(32)P (added to the medium as an albumin complex) to cellular lecithin than did control cells. Almost all of the increment in leukocyte lecithin-(32)P is found in association with the isolated phagocytic vacuoles. About half of lecithin-(32)P of granulocytes incubated first with lysolecithin-(32)P and then reincubated with paraffin particles in a nonradioactive medium is transferred from a sedimentable (presumably membrane) fraction to the phagosomes. Isolated phagosomes or granules by themselves are capable of acylating lysolecithin. The main source of lysolecithin-(32)P for synthesis of cellular lecithin-(32)P, however, appears to be extracellular rather than lysolecithin-(32)P within the cytoplasm or the phagocytic vacuole. We interpret our findings therefore as indicating that lecithin-(32)P in the phagosomes derives chiefly from the outer membrane.

Animals↗