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PubMed1981

Effect of meconium contamination on amniotic fluid lecithin: sphingomyelin ratio.

Studies on the lecithin: sphingomyelin (L:S) ratio in amniotic fluid were made before and after the addition of meconium in 130 normal pregnancies. The meconium was collected from premature and term infants after delivery. That which was collected from premature neonates had no significant effect on the mean L:S ratio of amniotic fluid; in 28% (17 of 60), however, the L:S ratio was elevated by 0.1 to 0.2, though in none by more than 0.2. When meconium collected from term neonates was added to amniotic fluid, it significantly increased the mean L:S ratio of amniotic fluid when the baseline L:S ratio was between 1.0 and 1.9 (P less than .01); in 56% (39 of 70), the L:S ratios were elevated by 0.1 to 0.5, though none increased by more than 0.5. This study suggests that when amniotic fluid is contaminated with meconium, an L:S ratio of 2.2 in premature pregnancies and 2.5 or greater in term pregnancies retains its original predictive value.

Amniotic Fluid↗
PubMedDate not supplied

X-ray studies on phospholipid bilayers. I. Polymorphic forms of dimyristoyl lecithin.

A structural study of the synthetic phospholipid, L-alpha-dimyristoyl lecithin (DML), habs been made by X-ray fiber diffraction methods. Three different types of oriented specimens were prepared. They were X-ray photographed under the same conditions, including temperature and relative humidity. Three different types of diffraction patterns, corresponding to different conformations and/or packing arrangements, were found. They are characterized by their unit cell dimensions, space group, molecular conformations, and packing arrangements.

Dimyristoylphosphatidylcholine↗
PubMed1981

Concanavalin A receptor capping and blastogenesis in human lymphocytes: inhibition by egg lecithin.

Egg lecithin may arrest blastogenic response of human peripheral blood lymphocytes mediated by different mitogenic lectins. Previous studies suggested that the inhibition may occur after lectin binding but before the cells are committed to the response. This was confirmed when it was presently shown that the lipid does not affect 125l-concanavalin A binding to lymphocytes nor does the lipid interact significantly with the lectin. The presence of the lipid however inhibits concanavalin A receptor capping and this occurred at similar concentration of the lipid as that required to arrest mitogenic response.

Cell Division↗
PubMed1980

Isolation of 1,3-distearoyl-glycero-2-phosphocholine (beta-lecithin) from commercial 1,2-distearoyl-sn-glycero-3-phosphocholine.

Different batches of 1,2-distearoyl-sn-glycero-3-phosphocholine (DSPC) had varying amounts of contaminants which appeared to affect systematic biological studies. This contaminant was separated by silica gel column chromatography followed by high performance liquid chromatography and identified as 1,3-distearoyl-glycerol-2-phosphocholine (beta-lecithin.

Chemical Phenomena↗
PubMed1980

Simultaneous measurement of lecithin, sphingomyelin, phosphatidylglycerol, phosphatidylinositol, phosphatidylethanolamine, and phosphatidylserine in amniotic fluid.

A one-dimensional thin-layer chromatographic method is described by which the ratios and proportions of lecithin, sphingomyelin, phosphatidylglycerol, phosphatidylinositol, phosphatidylethanolamine, and phosphatidylserine in amniotic fluid may be simultaneously determined. Commercial chromatographic plates, 10 X 7.5 cm, pretreated with cupric chloride, are used. The solvent system is chloroform/methanol/ammonium hydroxide (30/17/1.5 by vol). The plates are sprayed with a cupric acetate (350 g/L)/phosphoric acid (80 mL/L) reagent and charred on a hot plate to make the phospholipids visible. The percentage of each phospholipid present is determined by direct reflectance or transmission densitometry. The correlation coefficients for the lecithin/sphingomyelin, phosphatidylinositol/sphingomyelin, and phosphatidylglycerol/sphingomyelin ratios of the two scanning methods are 0.971, 0.980, and 0.955, respectively, for between-day analyses.

Amniotic Fluid↗
PubMed1980

[Change in the state of a lecithin molecular layer at the heptane-aqueous KCl solutions interface on the introduction of the ionophore, valinomycin].

The influence of ionophore--valinomycin on the organization of the lipid layer located between a heptane solution of lecithin and KCl water solutions of different concentrations has been shown by measurements of the interfacial tension. Specific changes in the interfacial tension found at high KCl concentrations are related to the transition of valinomycin into a form of its complex with K+-ion. A conclusion on the difference in the lipid layer organisation in the presence of the neutral ionophore and its charged complex has been made.

Cations, Monovalent↗
PubMedDate not supplied

[Lecithin-cholesterol acyltransferase activity and lipid composition of high density lipoprotein subfractions in hyperalphalipoproteinemia].

In blood plasma of men activity of lecithin-cholesterol acyl transferase /LCAT/ was elevated when the cholesterol concentration was increased in the fraction of high density lipoproteins /HDL/; the enzymatic activity was evaluated by the rate of 3H-cholesterol esterification in endogenous HDL. The phenomenon observed was accompanied by an increase in content of HDL2 subfraction: The content of free cholesterol was found to increase in the HDL2 fraction obtained from persons with hyper-alpha-lipoproteinemia. Analysis of the data obtained showed that LCAT activity was preferentially dependent on HDL3 cholesterol concentration in persons with low and middle content of HDL cholesterol, and--on HDL2 cholesterol concentration in patients with hyper-alpha-lipoproteinemia.

Adult↗
PubMed1980

The effect of propranolol treatment on total cholesterol, HDL cholesterol, triglycerides. Postheparin lipolytic activity and lecithin:cholesterol acyltransferase in hypertensive individuals.

Administration of 120 mg propranolol per day to hypertensive patients is followed by decreased plasma concentrations of total cholesterol and HDL cholesterol and increased concentrations of triglycerides. Postheparin lipolytic activity was reduced when measured 5 min after heparin administration. The activity of lecithin:cholesterol acyltransferase is diminished. Reduced activity of this enzyme by propranolol could be demonstrated in vitro as well.

Adolescent↗
PubMed1978

A rapid method for lecithin:cholesterol acyltransferase estimation in human serum.

All the described procedures for lecithin:cholesterol acyltransferase (LCAT) determination in the plasma have raised criticisms: Lack of sensitivity for methods using colorimetric determination of unesterified cholesterol or phosphatidyl-choline in plasma before and after incubation at 37 degrees C. Incomplete isotopic equilibrium of the free cholesterol substrate between the different lipoproteins in radioassay procedures. Gas-liquid chromatography methods cannot be used when LCAT activity is low. A new method, easier, more sensitive and accurate has been developed in our laboratory:plasma samples are delipoproteinized by coprecipitation with Intralipid, dextran sulphate, and calcium chloride. Cholesterol esterification is assayed by a short incubation (30 min) of 100 microliter delipoproteinized plasma and a 30 microliter of 3H-cholesterol-labelled substrate. About 15% of cholesterol is esterified in these conditions in 30 min (35 +/- 7 micromole/h/l). The LCAT reaction is linear for about one hour.

Calcium Chloride↗
PubMed1978

Phosphatidylcholine substrate specificity of lecithin:cholesterol acyltransferase.

Lecithin:cholesterol acyltransferase (LCAT) has been partially purified by the combined method of ultracentrifugation and dextranblue-2000 4 B affinity chromatography. The enzyme was incubated with liposomes consisting of phosphatidylcholine-cholesterol in a molar ratio of 10/1. Chemically synthesized phosphatidylcholine substrates with labeled fatty acids in 1-and 2-position were chosen to evaluate the degree of transesterification. It was found that the fatty acid in the 1-position of phosphatidylcholine significantly influences cholesteryl ester formation, both by its direct involvement in the LCAT reaction and its contribution to the physico-chemical properties of phosphatidylcholine.

Chemical Phenomena↗
PubMed1978

Lecithin:cholesterol acyltransferase activation and lipid binding by synthetic fragments of apolipoprotein C-I.

Peptide fragments of apolipoprotein C-I (apoLP-C-I) have been synthesized by solid phase methodology. After purification, each peptide showed the correct amino acid analysis and was a single band by polyacrylamide gel electrophoresis. In density gradient ultracentrifugation with vesicles of dimyristoyl phosphatidylcholine, peptide fragments 32-57, 24-57, and 17-57 formed stable complexes while 39-57 did not. With mixed vesicles of dimyristoyl phosphatidylcholine-cholesterol 20 micrometer of the fragments 32-57, 24-57 and 17-57 stimulated lecithin:cholesterol acyltransferase (LCAT) activity 50, 60, and 100%, respectively, of the value found for apolipoprotein C-I, while fragment 39-57 was inactive. The results indicate that residues 17-57 contain the structural requirements for LCAT activation by apoLP-C-I, and that residues 32-57 represent one of the major phospholipid-binding regions of apoLP-C-I.

Amino Acid Sequence↗
PubMed1981

Changes in the lecithin:sphingomyelin ratio during labor and the associated fetal heart rate patterns.

Serial samples of amniotic fluid were taken from 38 patients in spontaneous labor and the lecithin:sphingomyelin (L:S) ratios were estimated. The fetal heart rate (FHR) pattern for each patient was analyzed, and the baseline rate, long-term variability, and periodic changes wee determined. It was found that changes in the L:S ratios were significantly correlated with the duration of labor and FHR long-term variability. Very low L:S ratios were observed in some patients whose infants did not subsequently develop respiratory distress syndrome. This raises the possibility that during labor the amniotic fluid is no longer representative of lung fluid, perhaps because of reduced tracheal fluid efflux, a process which may operate when the fetus is under stress.

Amniotic Fluid↗
PubMed1995

Specificity of lecithin:cholesterol acyltransferase and atherogenic risk: comparative studies on the plasma composition and in vitro synthesis of cholesteryl esters in 14 vertebrate species.

To determine whether the specificity of lecithin: cholesterol acyltransferase (LCAT) influences the susceptibility to atherosclerosis, we compared the composition and in vitro synthesis of cholesteryl ester (CE) in the plasmas of 14 vertebrate species with varying predisposition to atherosclerosis. The susceptible species (Group I) had significantly higher ratios of 16:0 CE/20:4 CE in their plasma than the resistant species (Group II). The in vitro formation of labeled CE species in native plasma from labeled cholesterol correlated highly with the mass composition, showing that the LCAT reaction is the predominant source of plasma CE in all the animal species examined. Isolated LCATs from Group I species also synthesized CE with higher ratios of 16:0/20:4 than LCATs from Group II when egg phosphatidylcholine (PC) was used as the acyl donor. In addition, the Group I LCATs exhibited lower specificity towards sn-2-20:4 and sn-2-22:6 PCs, and higher specificity towards sn-2-18:2 PC species than Group II LCATs. With 16:0-20:4 PC as the substrate, all Group I LCATs synthesized more 16:0 CE than 20:4 CE, whereas all Group II LCATs, with the exception of dog enzyme, synthesized predominantly 20:4 CE, showing that the two types of LCAT have different positional specificities towards this PC. These results suggest that there are two classes of LCAT in nature that differ from each other in their substrate and positional specificities, possibly because of differences in their active-site architectures. We propose that the presence of one type of LCAT, which cannot efficiently transfer certain long chain polyunsaturated acyl groups and which consequently synthesizes more saturated CE, may increase the risk of atherosclerosis.

Animals↗
PubMed1993

Apolipoprotein A-I domains involved in the activation of lecithin:cholesterol acyltransferase. Importance of the central domain.

The reaction of highly purified lecithin:cholesterol acyltransferase (LCAT) with defined reconstituted discoidal apoA-I-containing lipoproteins (LpA-I) with 2, 3, or 4 apoA-I molecules/particle (Lp2, 3, or 4A-I) has been studied in the presence of a number of specific anti apoA-I antibodies. Among nine anti-apoA-I monoclonal antibodies (mAbs) reacting with epitopes distributed over 80% of the sequence, three significantly inhibit the LCAT reaction with all particles. The position of their epitopes located in the middle to COOH-terminal region between residues 96-121 (3G10), 135-148 (A03), and 149-186 (A44) is compatible with an inhibition by steric hindrance over a central domain. Antibody 4H1 binding to the NH2 terminus (residues 2-8) profoundly increases (5-fold) the LCAT reaction with Lp2A-I (7.8 nm), but not with other particles. Other mAbs, A11 and 5F6, binding to epitopes (residues 99-139 and 118-141) enhance LCAT reactivity with the small Lp2A-I (7.8 nm) and Lp3A-I (10.8 nm) but not with their larger counterparts. Most mAbs have similar effects on LCAT reaction with native high density lipoprotein3 as with LpA-I. The inhibitory or enhancing effects of these mAbs are also observed with Fab fragments and not related to their binding affinity for apoA-I containing reconstituted lipoprotein particles. The intercalation of epitopes for mAbs that inhibit or enhance LCAT reaction with small LpA-I is compatible not with steric hindrance but with conformational modifications of apoA-I and indirectly of the lipids in small particles. We propose that enhancing mAbs act by stabilization of an apoA-I conformation which is not favored in small LpA-I, i.e. by increasing binding of amphipathic helices to lipids or by interfering with the mobility of a hinged domain. The epitopes for the inhibitory mAbs can be shown to overlap on several LpA-I models, indicating that steric hindrance over a single site is a possible mechanism of inhibition.

Antibodies, Monoclonal↗
PubMed1993

Effects of pravastatin on lipid transfer protein and lecithin cholesterol acyltransferase in heterozygous familial hypercholesterolemia.

The effects of HMG CoA reductase inhibitor PRAVASTATIN on plasma lipoprotein levels, lipid transfer protein (LTP) activity and lecithin cholesterol acyltransferase (LCAT) activity were investigated in 20 patients with heterozygous familial hypercholesterolemia. Plasma total cholesterol decreased from 299.2 +/- 45.2 to 245.9 +/- 45.1 (mean +/- SD in mg/dl) (p < 0.0001), low density lipoprotein (LDL) cholesterol from 221.1 +/- 47.6 to 164.9 +/- 48.1 (p < 0.0001) and LDL-triglycerides from 38.0 +/- 10.2 to 30.2 +/- 8.8 (p < 0.0001). High density lipoprotein (HDL) cholesterol increased from 60.1 +/- 13.9 to 63.1 +/- 17.0 (p = 0.0264). The HDL-cholesterol: HDL-triglycerides ratio increased from 3.91 +/- 1.14 to 4.91 +/- 1.65 (p = 0.0029). Lipid transfer protein (LTP) activity (as % of transferred cholesteryl ester (CE)) decreased from 4.68 +/- 2.47 to 3.70 +/- 2.31 (p = 0.0024) and LCAT activity decreased from 113.1 +/- 29.9 (U/L) to 97.0 +/- 22.7. There was a negative correlation between LTP/LCAT ratio and HDL-C levels. These results suggested that the changes in plasma HDL-cholesterol concentrations during treatment with pravastatin may be related to the decreases in LTP and LCAT activity due to this drug.

Adult↗
PubMedDate not supplied

[A study of the physico-chemical properties of lecithin membranes using hydrophobic and hydrophilic spin probes].

Some physico-chemical properties of lecithin lyposomes and the effects of pH, temperature and ionic strength changes are studied by ESR using hydrophobic and hydrophylic nitroxyl radicals as spin probes. The structure differences between outer and inner layers of bilayer liposomes are observed using auxiliary water soluble paramagnetic complex and attributed tentatively to the different curvature signs of both layers. Lower estimates of transversal diffusion rates of both probes throught the membrane are obtained using exchange broadening technique and water soluble reducing agent. The limiting step in this diffusion is revealed, caused by the transport of a charged group of the diffusing molecule through the hydrophobic membrane space.

Electron Spin Resonance Spectroscopy↗
PubMed1995

Dietary fatty acid modification of HDL phospholipid molecular species alters lecithin: cholesterol acyltransferase reactivity in cynomolgus monkeys.

In the following report, cynomolgous monkeys, fed atherogenic diets containing either saturated, monounsaturated, polyunsaturated (n-6 Poly) or fish oil (n-3 Poly) fat as 35% of total calories, provide a model for the study of dietary fat effects on plasma lipoproteins and atherosclerosis. We have previously described the ability of polyunsaturated fat diets to lower plasma described the ability of polyunsaturated fat diets to lower plasma high density lipoprotein (HDL) cholesterol levels and alter HDL subpopulation distribution in the primate model. These experiments investigate possible mechanisms responsible for such modifications. Animals fed polyunsaturated fat had significantly lower plasma concentrations of HDL cholesterol, total plasma cholesterol, and apolipoprotein A-I. Such changes were reflected in the distribution of protein among HDL subfractions, with the most remarkable modification in subclass distribution being the preponderance of small HDL particles in the n-3 Poly-fed animals. Striking alterations were also observed in the distribution of phosphatidylcholine (PC) molecular species (diet effect P < 0.0001 for all major molecular species). Phosphatidylcholine isolated from lipoproteins were used to make recombinant HDL (rHDL) particles. The reaction rate of purified lecithin:cholesterol acyltransferase (LCAT) with particles made from n-3 Poly-derived PC was 50% of that determined using rHDL formed with PC from other dietary groups (P < 0.0001). When the distribution of LCAT-derived rHDL cholesteryl esters was analyzed, LCAT demonstrated little selectivity for certain PC molecular species except in n-3 Poly-derived rHDL where 18:2-containing PC was selectively utilized. These data demonstrate that differences in dietary fat intake can significantly alter HDL PC concentration and molecular species distribution. We suggest that diet-induced alterations in HDL PC molecular species modify the type of cholesteryl esters produced during the LCAT reaction thereby affecting the plasma cholesteryl ester pool. We also propose that dietary n-3 Poly affects cholesteryl ester metabolism in part via LCAT by lowering PC (LCAT substrate) availability, altering the rate of the LCAT reaction, and decreasing HDL cholesterol concentrations; however, n-6 Poly dietary fat effects on HDL concentration appear to be through some mechanism other than LCAT.

Animals↗
PubMed1995

Copper and gas-phase cigarette smoke inhibit plasma lecithin:cholesterol acyltransferase activity by different mechanisms.

Cigarette smokers have reduced levels of plasma high density lipoprotein (HDL) compared to nonsmokers and are at risk of premature cardiovascular disease. Previous work from this laboratory has shown that exposure of human plasma to gas-phase cigarette smoke (CS) inhibited the activity of lecithin:cholesterol acyltransferase (LCAT), the enzyme that catalyzes the formation of cholesteryl ester in HDL and thereby promotes HDL maturation. As CS contains free radicals that could potentially oxidize plasma lipoproteins, we examined the involvement of lipid peroxidation in LCAT inhibition. Results obtained with CS were compared with those obtained by initiating lipid peroxidation with copper ions. Exposure of dialyzed human plasma to an equivalent of one-eighth of a cigarette at 15-min intervals resulted in a progressive loss of LCAT activity (50 and 90% reductions by 1 and 6 h, respectively). A similar pattern of LCAT inhibition was produced with copper (0.5 mM) where 50 and 97% reductions were observed at 1 and 6 h, respectively. To determine whether LCAT inhibition was related to lipid peroxidation, lipoprotein fractions corresponding to VLDL-IDL, LDL, and HDL were isolated from plasma exposed to CS or copper and analyzed for changes in TBARS, the polyunsaturated fatty acid arachidonate relative to palmitate (20:4/16:0 ratio), and vitamin E concentrations. Exposure of plasma for 6 h to CS had no effect on the levels of TBARS and 20:4/16:0 ratio; however, 6 h copper treatment (0.5 mM) caused a 3.0-, 4.0-, and 1.4-fold increase in TBARS and a 17, 25, and 13% reduction in the 20:4/16:0 ratio in VLDL-IDL, LDL, and HDL fractions, respectively. In addition, a complete depletion of lipoprotein vitamin E was observed with CS, whereas copper decreased vitamin E levels by approximately 50% in each fraction. Supplementation of plasma with either vitamin C (85 microM) or butylated hydroxytoluene (BHT, 0.45 mM) was unable to protect LCAT from CS. In contrast, BHT completely protected LCAT activity from inhibition by copper. We conclude that unlike copper, CS-induced inhibition of plasma LCAT activity was unrelated to free radical-induced lipid peroxidation. The inhibition of LCAT activity by cigarette smoke may contribute to the development of atherosclerosis by impairing HDL metabolism and the reverse cholesterol transport process.

Ascorbic Acid↗