Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LECITHINS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources

The origin of amnitoic fluid lecithin.

Lecithin has been measured in amniotic fluid, pharyngeal aspirate, fetal and maternal plasma and fetal membranes from the same pregnancy. In the amniotic fluid from a term pregnancy 79 per cent of the lecithin is found in the reconstituted precipitate of centrifuged fluid. It is suggested that the lecithin of amniotic fluid may originate from sources other than fetal lung and that lecithin concentration is therefore a measure of overall fetal maturity.

Amniotic Fluid↗

Calorimetric study on the solubilization of butanol by alkylphosphate and alkylphosphate-lecithin systems.

Microcalorimetric studies on alkylphosphate-butanol and alkylphosphate-butanol-lecithin systems were carried out as a first step to study the role of butanol (used as cosurfactant) in the formation of microemulsions. The enthalpy of solubilization; delta H, of the same amount of butanol (1.806 mol kg-1) in aqueous sodium monoalkyl-phosphates, with a hydrocarbon chain varying from 6 to 10 carbon atoms, was investigated as a function of alkylphosphate concentration. Measurements were performed in the presence and in the absence of lecithin. The enthalpy values measured upon addition of butanol to the mixtures were negative in all cases. Below the critical micelle concentration (CMC) of the alkylphosphates, the heats of butanol dissolution were found to decrease upon increasing the concentration of the alkylphosphate. This behaviour was related to the dissolution of butanol in water and to the formation of mixed butanol-alkylphosphate and butanol-alkylphosphate-lecithin micelles. Above the CMC essentially constant delta H values were found. The delta H measured may be the sum of simultaneous effects--heat of alcohol dissolution and the simple alkylphosphate micelle dissociation or alkylphosphate-lecithin mixed aggregate dissociation and the heat of mixed micelle formation. The delta H at the plateaus were linearly related to the corresponding CMC values of the alkylphosphates.

Butanols↗

Binding of DDT to lecithin.

An interaction between DDT and lecithin is indicated by the reciprocal effects of each compound on the proton magnetic resonance spectrum of the other. The phosphoryl choline moiety of the lecithin and the benzylic proton of the DDT seem to be involved. The most pronounced response in the proton magnetic resonance spectrum of the lecithin produced by increasing concentration s of DDT was a change in the chemical shift of the resonance peak due to the protons of the choline methyl groups. Increasing concentrations of lecithin produced changes in the chemical shift of the resonance peaks of the benzylic proton and adjacent ring protons of the DDT. Equilibrium constant of 0.597 +/-0.015 molal(-1) was obtained for this interaction.

DDT↗

Elution of enteric viruses from Mississippi estuarine sediments with lecithin-supplemented eluents.

Isoelectric casein supplemented with lecithin was tested for its ability to recover enteric viruses from estuarine sediments of varied sand, silt, and clay composition. Recoveries were higher when lecithin was incorporated into an eluent as compared with trials with only the casein solution. Semipurified soybean lecithin (3%) allowed the highest overall recovery of virus from all sediments tested; crude soybean lecithin produced the lowest recovery. A difference in the percentage of virus able to be recovered from a sediment was related to the percentage of clay in the sample. Correlational statistics indicated a trend toward lower virus recovery as the clay composition of a sediment increased. Virus adsorption to the four sediments tested revealed differences between poliovirus, coxsackievirus, and echovirus adsorption that could not be explained on the basis of the clay content of a sediment.

Aluminum Silicates↗

Lecithin supplementation in healthy volunteers: effect on cholesterol esterification and plasma, and bile lipids.

Plasma and bile lipids and in vitro cholesterol esterifying activity of plasma (mg CE/dl/6 h) were determined in healthy volunteers who supplemented their regular diets with 7.5 g doses of soya lecithin three times daily for a 4-week period. Lecithin ingestion by the 4 male and 6 female subjects did not produce any significant changes either in total plasma cholesterol (TC) level or cholesterol esterification. A small but significant reduction was observed in the plasma triglyceride (TG) and total phospholipid (TPL) levels after supplementation. The molar percent of bile acids (BA), TC and TPL as well as the lithogenic index (LI = TC/BA + TPL) in both hepatic and gallbladder bile were also unaltered by 4 weeks of lecithin supplementation. In vitro cholesterol esterification was found linearly related to plasma-free cholesterol (r = 0.60, p less than 0.01) cholesterol ester (r = 0.50, p less than 0.05), total phospholipid (r = 0.50, p less than 0.05), lecithin (r = 0.45, p less than 0.05), and triglyceride (r = 0.57, p less than 0.025) levels.

Adult↗

Formation of disaturated lecithin through the lysolecithin pathway in the lung of the developing rabbit.

The formation of disaturated lecithin in slices of developing rabbit lung was studied using 14C-CDP-choline, 3H-S-adenosylmethionine, and doubly labeled lecithin, lysolecithin and phosphatidylethanolamine as precursors. The labeling patterns suggest that some of the unsaturated lecithin becomes deacylated and subsequently reacylated to form disaturated surface-active lecithin. The rate of this pathway (lysolecithin 'loop') increases as a function of gestation and may contribute to the functional maturation of the lung.

Age Factors↗

Lung lecithin biosynthesis in the nonhuman primate fetus: determination of the primary pathway in vivo.

The two pathways for de novo lecithin (phosphatidylcholine) biosynthesis, choline incorporation (1) and phosphatidylethanolamine methylation (II), were examined simultaneously in lung and other tissues of Rhesus monkey fetuses. Cannulation of interplacental fetal vessels permitted studies on the intrauterine fetus without disruption of fetal-placental-maternal-amniotic fluid anatomic integrity. In contrast to observations with indirect techniques in the same species, direct measurement of the incorporation of isotopic precursors (3H-choline and 14C-ethanolamine) into lecithin indicated that pathway I predominates by 100-fold over PE methylation in pulmonary lecithin synthesis. Fetal liver, brain, and kidney also showed 10--70-gold greater choline incorporation that methylation activity. Measurement of lung phosphatidylcholine production via the two pathways in acidemic fetuses (umbilical venous pH less than 7.20) demonstrated marked inhibition of pathway I, but not II. It is concluded that the choline pathway is the major mechanism of lung lecithin synthesis in fetal primates and that this pathway is pH sensitive in vivo.

Acid-Base Equilibrium↗

Betamethasone-induced lecithin release in vitro from the fetal membranes.

Lecithin release from fetal membranes and placental tissue was assayed in basal conditions as well as under betamethasone administration. In the absence of the steroid, amnion and chorion released lecithin as a function of incubation time. Both tissues responded to betamethasone by increasing the lecithin release, the amnion exhibited a higher basal level and a greater responsiveness to the hormone than the chorion. Basal lecithin release from placental tissue was unaffected by any steroid concentration.

Amnion↗

Relative fatty acid composition of serum lecithin in the normal puerperium.

21 women who had been followed regularly during their normal pregnancies were examined in the puerperium. The relative fatty acid composition of serum lecithin was analyzed by means of gas-liquid chromatography. Palmitic acid decreased and stearic acid increased, which indicates a shift to more pathway II-synthesized lecithin in the puerperal period. Linoleic acid increased and the longer polyunsaturated fatty acids decreased. These changes were slow as compared to the changes in the saturated fatty acids. No correlations were found between the saturated fatty acids and linoleic acid dominating the polyunsaturated fatty acids. The results indicate different incorporational ways into the lecithin molecule of these fatty acid groups. It is suggested that the deacylation-reacylation cycle is responsible for the high content of longer polyunsaturated fatty acids still 1 week after delivery. 6 weeks after delivery normal values were recorded. Breast-feeding did not seem to influence the fatty acid pattern of serum lecithin.

Adult↗

Influence of long-term beta-mimetic therapy on the lecithin content of amniotic fluid.

The lecithin content of 157 amniotic fluid samples taken from 60 patients who had been treated with Fenoterol over a long period of time (longer than 30 mg/daily per os for 14 days; intravenous infusion for longer than 7 days) was calculated thin-layer chromatographically according to Kynast and Saling. These lecithin levels were statistically compared with the levels in a control (Wilcoxon test). It emerged that the lecithin levels in the long-term beta-mimetic therapy group were significantly lower, i.e., from 33/0 to 39/6 (33/0-34/6, p less than 0.05; 35/0-39/6, p less than 0.01). The answer to the question how often levels occur in the long-term group which are below the as critical described level of 3 mg Lec/100 ml amniotic fluid appears to be clinically important. It is shown that values below the critical level from 33/0 to 39/6 are much more frequent in the long-term beta-mimetics therapy group than in the control group. There is no known explanation for this. It was concluded that the application of beta-mimetics in cases of long-term tocolysis should only be discontinued when the lecithin content of the amniotic fluid lies above the critical limit of 3 mg Lec/100 ml.

Administration, Oral↗

Change of catalytic properties of erythrocyte acetylcholinesterase after binding to lecithin liposomes.

Phosphatidylcholine and phosphatidylserine + phosphatidylcholine liposomes were prepared with cholate and erythrocyte acetylcholinesterase (EC 3.1.1.7). Dipalmitoyllecithin- and egg lecithin-acetylcholinesterase complexes exhibit an affinity for acetylthiocholine different from that of the free enzyme. The binding to lecithin apparently abolishes the excess substrate inhibition of acetylcholinesterase; the affinity constants of acetylthiocholine, acetylcholine and acetylcarnitine for the lecithin-bound enzymes are higher than the ones found for the free enzyme. Binding to lecithin decrease the optimum pH value for acetylcholinesterase, increase the resistance of the enzyme to heat denaturation and reduces the extent of activation by Ca2+.

Acetylcarnitine↗

Effects of substrate fatty acids on products of lecithin hydrolysis and acyl-CoA-independent transacylation with cholesterol by aortic enzyme preparations.

The acyl composition of substrates and products of enzymatic hydrolysis and transacylation of lecithin with cholesterol in the arterial wall was investigated. Saturated acyl residues predominated in lysolecithin and unsaturated ones in acids released by hydrolysis of egg lecithin. In the reaction system with cholesterol, saturated acyls predominated in both lysolecithin and acids released whereas unsaturated ones were more abundant in newly formed acylcholesterols. Mainly unsaturated acyls were present in the hydrolysis products from soybean lecithin in the reaction systems with and without cholesterol. For acylcholesterols formed in the presence of either lecithin, the percent values are in the numerical order of C18:2 greater than C18:1 greater than C16:0 greater than or equal to C18:0. It It is concluded that acyl preferences and interactions in the enzyme-catalyzed reactions studied may contribute to the different accumulation and removal of the compounds involved from the artery.

Acylation↗

Plasma lipoproteins in familial lecithin: cholesterol acyltransferase deficiency: lipid composition and reactivity in vitro.

Plasma lipoproteins from patients with familial lecithin:cholesterol acyltransferase (LCAT) deficiency have been fractioned by preparative ultra-centrifugation and gel filtration and their lipid content and reactivity studied. All of the lipoproteins are abnormal with respect to lipid concentration or relative lipid content. The low density lipoproteins (LDL) and high density lipoproteins (HDL) appear to react normally with partially purified LCAT from normal plasma. Also, the lipids of the very low density lipoproteins (VLDL) and LDL, like those of the corresponding lipoproteins of normal plasma, are indirectly altered by the action of LCAT on normal HDL. Thus, during incubation in vitro VLDL cholesteryl ester is increased and VLDL triglyceride is decreased, as described by others for VLDL from hyperlipemic plasma, and both the unesterified cholesterol and lecithin of the VLDL and LDL are decreased. The patients' VLDL and LDL are abnormal, however, in that they lose unesterified cholesterol and lecithin to normal HDL in the absence of LCAT. Also, the patients' HDL lose these lipids to erythrocyte membranes in the absence of the enzyme. Our results provide further evidence that the abnormal cholesterol and phospholipid composition of the patients' lipoproteins is caused by the LCAT deficiency. They support the postulate that an excess of unesterified cholesterol and lecithin develops as VLDL are converted to LDL and HDL and suggest that in the absence of LCAT this excess lipid distributes among plasma lipoproteins and plasma membranes. They further suggest that LCAT normally reduces this excess lipid through a combination of direct and indirect effects.

Acyltransferases↗

Effect of glycine-conjugated bile acids with and without lecithin on water and glucose absorption in perfused human jejunum.

Perfusion studies were performed in healthy volunteers to test whether the secretory effect of conjugated bile acids, previously shown for the colon, was also present in the jejunum. A perfusion system with a proximal occlusive balloon (and continuous aspiration of duodenal secretions) was used; isotonic test solutions contained glycine-conjugated bile acids with or without lecithin. Fluid movement was measured by changes in the concentration of polyethylene glycol (PEG, mol wt 4,000). Conjugated dihydroxy bile acids inhibited electrolyte and fluid absorption and, at higher concentrations, evoked secretion of an isotonic fluid. Glucose absorption continued, despite fluid secretion, but its rate decreased. The secretory effects of bile acids were abolished by the addition of lecithin to the bile acid solutions. A trihydroxy bile acid (cholylglycine) had no effect on jejunal absorption. Small amounts (6-9%) of conjugated bile acids were absorbed in the jejunum; lecithin was well absorbed (72-90%). The results indicate that dihydroxy bile acids influence salt and water transport in the human jejunum but that this effect may be abolished when a polar lipid such as lecithin is present. We speculate that this effect of bile acids may modify fluid movement in the small intestine postprandially after fat absorption has occurred.

Bile Acids and Salts↗

Low levels of apolipoprotein A1 are not contributors to the low lecithin-cholesterol acyl transferase activity in premature newborn infants.

Umbilical cord sera were obtained from three groups of newborn infants; group I (n = 8) and group II (n = 12) weighed less than 1500 g and between 1500 and 2500 g, respectively. Group III (n = 16) was full term and weighed more than 2500 g. Lecithin-cholesterol acyl transferase activities, determined as the rates of esterification of [3H]cholesterol, were 0.13 +/- 0.01, 0.17 +/- 0.01, and 0.26 +/- 0.01 (mean +/- SEM) nmol/h/ml for groups I, II, and III, respectively. The adult value (n = 8) was 0.96 +/- 0.01 nmol/h/ml. The respective apolipoprotein A1 (apo-A1) levels were 52 +/- 6, 59 +/- 4, and 67 +/- 4 (mean +/- SEM) mg/dl. Serum level of apo-A1 in adults was 137 +/- 6 mg/dl. Plasma high-density lipoprotein cholesterol levels increased with gestational age. However, in newborn infants, high-density lipoprotein apo-lipoprotein B, total cholesterol, and triglyceride levels, were significantly lower than in adults. These data indicate that serum levels of lecithin-cholesterol acyl transferase activity significantly (p less than 0.01) increase whereas the levels of apo-A1 do not significantly change with the gestational age. Also, in full-term newborns, lecithin-cholesterol acyl transferase activity is only 27%, whereas apo-A1 levels are 49% of adult values. Therefore, lower levels of apo-A1 do not account for the significantly lower activity of lecithin-cholesterol acyl transferase in preterm as compared to full-term newborn infants.

Apolipoproteins A↗

The relationship of cortisol and cortisone to saturated lecithin concentration in ovine amniotic fluid and fetal lung liquid.

Cortisol and cortisone concentrations in ovine amniotic fluid and fetal lung liquid were analyzed with respect to gestational age and fetal lung maturation as reflected by saturated lecithin concentration. In amniotic fluid, the cortisol concentration rises as a function of gestational age while that of cortisone falls (P less than 0.001). The ratio of cortisol/cortisone is significantly related to gestational age (r=0.693, P less than 0.001), and shows an even stronger correlation with saturated lecithin concentration (r=0.832, P less than 0.001). When examined independently of gestational age, the correlation of the cortisol/cortisone ratio to saturated lecithin concentration remains highly significant (r=0.641, P less than 0.001). Similar findings were observed in fetal lung liquid, except that in this fluid both the saturated lecithin concentration and the ratio of cortisol/cortisone are significantly higher than simultaneously determined values in amniotic fluid. These observations provide further evidence that the process of fetal lung maturation is closely linked to the fetal hormonal milieu.

Amniotic Fluid↗

A double blind cross-over study on the effects of ORG OD14 compared to estradiol valerate and placebo on the fatty acid composition of serum lecithin and cholesterol ester in oophorectomized women.

Twenty-two women, oophorectomized in connection with surgical treatment for cervical carcinoma in clinical stage IB or IIA, were given ORG OD14 [(7 alpha,17 alpha)17-hydroxy-7-methyl-19-norpregn-5-(10)20-yn-3-one; 2.5 mg/day], a placebo, and estradiol valerate (2 mg/day), six weeks each, in a double blind, cross-over study. ORG OD14 is a synthetic steroid for continuous treatment of climacteric symptoms which in traditional bioassays has been shown to have weak estrogenic and progestogenic as well as very weak androgenic-anabolic properties. The aim of this study was to evaluate its effects on serum lecithin as well as on the relative fatty acid composition of serum lecithin and serum cholesterol ester. In serum lecithin, OD14 induced an increase in palmitic acid and a decrease in stearic acid, effects typical of 17-C-alkylated steroids, compared to both placebo and estradiol valerate. Furthermore, there was an increase in linoleic acid and a decrease in both arachidonic and dihomo-gamma-linolenic acid after OD14 administration. This decrease is interpreted as an inhibitory action of the steroid on the mechanisms of elongation and desaturation of linoleic acid and is considered to be an androgenic influence. The relative decrease is further accentuated by the decrease in total serum lecithin induced by OD14. Since these fatty acids are the major precursors for prostaglandin synthesis, these findings might have relevance in that context.

Adult↗

Enhancement of oral bioavailability of d-alpha-tocopherol acetate by lecithin-dispersed aqueous preparation containing medium-chain triglycerides in rats.

In order to evaluate oral dosage forms of d-alpha-tocopherol acetate (VEA), d-alpha-tocopherol (VE) concentration in the plasma was examined following oral administration of three VEA preparations; lecithin-dispersed aqueous preparation, polysorbate 80 (PS-80)-solubilized aqueous solution and soybean oil solution. The lecithin-dispersed preparation gave the highest Cmax and the largest AUC0-24h, while Tmax was delayed. In the thoracic duct fistula rat, no increase in VE plasma concentration was observed after intraduodenal administration of lecithin-dispersed VEA preparation via the lymphatic route. The delayed Tmax and prolonged VE plasma concentration obtained with the lecithin-dispersed preparation in comparison with PS-80-solubilized aqueous solution could be explained by the different route of absorption.

Administration, Oral↗