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At least 793 records · Page 44Linked to original sources
PubMed1981

[Lysolecithin and lecithin. Influence in the etiopathogenesis of chronic and acute gastritis as related to bile reflux and duodenal juice. Experimental study].

The authors studied three groups of rats with had their stomachs exposed to lecithin, lisolecithin and salt solution action. They noticed through histopathologic methods and DNA dosages of the studied stomachs that lisolecithin can promote gastric inflammatory lesions as well the research method chosen has promoted acute erosive gastritis in various animals. They have also noticed, with gastric DNA dosages, a higher cell desquamation with the lisolecithin group. The authors have considered this method efficient to demonstrate precocious gastric lesions. The authors arise the question if lisolecithin present in duodenal juices (formed by the action of A phospholipase of the pancreatic juice with bilious lecithin) and the biliary salts constitute a substance of great importance to the gastric lesions produced by the alkaline reflux to the stomach.

Animals↗
PubMedDate not supplied

[Participation of lecithin-cholesterol-acyltransferase in the redistribution of high density lipoprotein subfractions in the blood of newborn infants].

Evidence was obtained in vitro for the participation of lecithin-cholesterol acyl transferase in redistribution of subfractions of high density lipoproteins (HDLP) in blood plasma of newborn children. Content of some HDLP subfractions (HDLP 2c and HDLP 2b) was decreased and content of the other subfractions (HDLP 2a) was increased after incubation of blood plasma of the newborn children with lecithin-cholesterol acyl transferase preparation purified 100-fold.

Adult↗
PubMedDate not supplied

[Apoprotein A-1 in high-density lipoprotein subfractions and lecithin-cholesterol-acyltransferase activity in hyperalphacholesterinemia].

Content of apolipoprotein (apo A-I) was studied in subfractions of high density lipoproteins (HDL) using quantitative "rocket" immunoelectrophoresis in two groups of men with the level of LPHD cholesterol within 70 mg/dl (27 patients) and above 70 mg/dl (15 patients). An increase in content of cholesterol from HDL2 subfraction and activation of lecithine-cholesterol acyltransferase in hyper-alpha-cholesterolemia (hyper-alpha-lipoproteinemia) were mainly due to elevation in both absolute amount of apo A-I containing in HDL2 of blood plasma and in relative part of apo A-I in HDL2 of blood plasma and in relative part of apo A-I in HDL2. But contrary to the observation, content of apo A-I from HDL3 subfraction was decreased in the impairment. In aggrement with the modern hypothesis on the antiatherogenic nature of hyper-alpha-lipoproteinemia, the impairment is related to intensification of the cholesterol-acceptor function of HDL due to the activating effect of apolipoprotein A-I (content of which is increased in HDL2) on lecithine-cholesterol acyltransferase in vivo.

Adult↗
PubMed1979

Enzymic assay for lecithin in amniotic fluid.

We describe an enzymic method for determining lecithin in amniotic fluid. Phospholipase D from savoy cabbage is used to liberate choline from lecithin, and the liberated choline is oxidized to betaine and hydrogen peroxide by choline oxidase from Arthrobacter globiformis. The hydrogen peroxide forms a colored complex with phenol and 4-aminoantipyrene in the presence of horseradish peroxidase, and this color is measured spectrophotometrically. The method is relatively easy, precise, and accurate, requires less time and sample than other methods, and offers a reliable alternative to the lecithin/sphingomyelin ratio techniques for assessing fetal lung maturity.

Alcohol Oxidoreductases↗
PubMed1993

Plasma lecithin cholesterol acyl transferase activity, high density lipoprotein cholesterol and cholesterol ester in cholestasis.

Lecithin cholesterol acyl transferase activity, cholesterol ester and high density lipoprotein cholesterol concentrations were determined in Nigerian subjects suffering from cholestatic jaundice. Plasma lecithin cholesterol acyl transferase activities in all the study groups were similar. High density lipoprotein cholesterol and cholesterol ester were significantly increased in extrahepatic cholestasis while reduced levels were found in intrahepatic cholestasis. Enhanced cholesterol esterification may occur in extrahepatic cholestasis.

Adolescent↗
PubMed1995

Comparison of the leishmanicidal activity of fungizone, liposomal AmB and amphotericin B incorporated into egg lecithin-bile salt mixed micelles.

We compared leishmanicidal activity of five formulations of amphotericin B (AmB). AmB used as Fungizone immediately caused cell lysis, at lower concentrations partial, and at higher concentrations total; the non-lysed cells reassuming growth. AmB formulated with egg-lecithin and bile salt at doses equivalent to those of Fungizone was not active, whereas at higher doses it resulted in a delayed but complete inhibition of cell growth. The activity of liposomal AmB was comparable to that of Fungizone. The time of initial leishmanicidal activity of the five formulations tested can be ascribed to the rate of free, monomeric AmB delivered. Features that are characteristic of the anticellular effect of AmB formulated with egg lecithin and bile salts, a delay in activity, a requirement for higher concentration and total inhibition of cell growth, were also noted.

Amphotericin B↗
PubMed1998

Trans unsaturated fatty acids inhibit lecithin: cholesterol acyltransferase and alter its positional specificity.

Although dietary trans unsaturated fatty acids (TUFA) are known to decrease plasma HDL, the underlying mechanisms for this effect are unclear. We tested the hypothesis that the decreased HDL is due to an inhibition of lecithin:cholesterol acyltransferase (LCAT), the enzyme essential for the formation of HDL, by determining the activity of purified LCAT in the presence of synthetic phosphatidylcholine (PC) substrates containing TUFA. Both human and rat LCATs exhibited significantly lower activity (-37% to -50%) with PCs containing 18:1t or 18:2t, when compared with the PCs containing corresponding cis isomers. TUFA-containing PCs also inhibited the enzyme activity competitively, when added to egg PC substrate. The inhibition of LCAT activity was not due to changes in the fluidity of the substrate particle. However, the inhibition depended on the position occupied by TUFA in the PC, as well as on the paired fatty acid. Thus, for human LCAT, 18:1t was more inhibitory when present at sn-2 position of PC, than at sn-1, when paired with 16:0. In contrast, when paired with 20:4, 18:1t was more inhibitory at sn-1 position of PC. Both human and rat LCATs, which are normally specific for the sn-2 acyl group of PC, exhibited an alteration in their positional specificity when 16:0-18:1t PC or 16:1t-20:4 PC was used as substrate, deriving 26-86% of the total acyl groups for cholesterol esterification from the sn-1 position. These results show that the trans fatty acids decrease high density lipoprotein through their inhibition of lecithin: cholesterol acyltransferase (LCAT) activity, and also alter LCAT's positional specificity, inducing the formation of more saturated cholesteryl esters, which are more atherogenic.

Animals↗
PubMed1976

[In vivo and in vitro investigations of the effect of decortilen (16-methylenprednisolone) on lecithin synthesis in the fetal lung (author's transl)].

Lecithin synthesis in fetal lungs of the rat over three-fold methylation and over choline and CDP-choline was quantitatively determined via the incorporation rate of marked metabolites. The ability of decortilen to influence both modes of synthesis was investigated. In vivo and in vitro, the glucocorticoid stimulates lecithin formation, which can be as high as 200%, only over choline and CDP-choline.

Animals↗
PubMed1976

[Experimental investigations in regard to the optimal stimulation of lecithin synthesis in the fetal lung via glucocorticoids (author's transl)].

On the basis of curves illustrating the effects of dosage on experimental animals, it was shown that glucocorticoids inhibit as well as stimulate lecithin synthesis in the fetal lung. Equivalent doses of corticoids produce comparable results. It was established that the concentration necessary to produce an optimal stimulation of lecithin synthesis was 0.5 to 2.0 mg/kg body weight.

Animals↗
PubMed1988

Ophthalmic observations in lecithin cholesterol acyltransferase deficiency.

Lecithin cholesterol acyltransferase is an enzyme that esterifies free cholesterol. A complete deficiency of this enzyme results in a diffusely cloudy cornea. This deficiency is thought to be transmitted as an autosomal recessive trait. We studied a family in which four members were homozygote recessive. In the homozygote recessive condition, a central corneal haze caused by deposition of numerous minute gray dots was consistently present. In the heterozygote condition, arcuslike changes were present in some of the patients studied. We found the corneal change in the recessive state to be sensitive and specific as a marker of this condition. Heterozygotes appear to have a higher incidence of arcuslike corneal changes.

Adolescent↗
PubMed1984

Decreased sodium influx and abnormal red cell membrane lipids in a patient with familial plasma lecithin: cholesterol acyltransferase deficiency.

Red cell membrane metabolism in familial lecithin:cholesterol acyltransferase (LCAT) deficiency was investigated. The family presented here is the third case discovered in Japan. An increase of free cholesterol was observed in the red cell membranes, concomitant with increased phosphatidyl choline. Osmotic fragility of the patient's red cells was diminished rather than increased. Red cell survival (51Cr T1/2) was shortened (15 days). Sodium influx was markedly decreased, although sodium efflux, both ouabain-sensitive and ouabain-insensitive, was normal. The activity of acetyl-cholinesterase as a marker of the outer leaflet of the red cell membranes was decreased, while the activity of glyceraldehyde-3-phosphate dehydrogenase as a marker of the inner leaflet was normal. No abnormalities of adenosine triphosphatases in red cell membranes were observed. These results suggest that the alteration of cholesterol metabolism in the plasma of LCAT deficiency increases the red cell membrane cholesterol and affects the functions of the red cell membranes, especially of the outer leaflet, which may result in decreased sodium influx.

Blood Transfusion↗
PubMed1979

Detection of erythrocyte membrane structural abnormalities in lecithin: cholesterol acyltransferase deficiency using a spin label approach.

The membrane fluidity of erythrocytes from patients with Lecithin: cholesterol acyltransferase (LCAT) deficiency was studied by means of electron spin resonance. The temperature dependence of the separation of the outer extrema of the spectra of 2-(3-carboxy-propyl)-4,4-dimethyl, 2-tridecyl-3-oxazolidinyloxyl spin probe was monitored for normal, presumed carrier and clinically affected subjects. The temperature profile of controls was significantly different from that of the presumed carriers and the clinically affected individuals. The results show that the compositional abnormalities previously noted in erythrocyte membranes from patients with LCAT deficiency are associated with alterations in the physiocochemical state of the membrane. An investigation of the spectral lineshapes below 10 degrees C allowed a distinction to be made at the membrane level between clinically affected subjects and clinically normal heterozygous carriers. Alterations in the temperature dependence of elec-ron spin resonance parameters may provide a sensitive index of red cell membrane alterations in pathological states of generalized membrane involvement.

Electron Spin Resonance Spectroscopy↗
PubMed1981

Spin label studies of erythrocytes with abnormal lipid composition: comparison of red cells in a hereditary hemolytic syndrome and lecithin: cholesterol acyltransferase deficiency.

Erythrocytes from patients with familial lecithin : cholesterol acyltransferase (LCAT) deficiency have been shown to exhibit an increase in membrane fluidity which is surprisingly small in view of the extensive alterations both in membrane lipid composition (namely, an elevation in cholesterol and phosphatidylcholine contents as well as a decrease in phosphatidylethanolamine) and in the functional properties of these cells. In the hope of deriving some information concerning the interrelationship between the structural and functional abnormalities, we have used the spin probe 5-doxyl stearic acid to investigate the temperature-dependent fluidity properties of red cells from two patients with a hereditary hemolytic syndrome (HHS) whose red cells are also characterized by qualitatively similar alterations in phosphatidylcholine and phosphatidylethanolamine but, unlike those in LCAT deficiency, have relatively normal levels of membrane cholesterol. A small increase in membrane fluidity of HHS erythrocytes equivalent to that previously observed in LCAT deficiency was found, indicating that membrane cholesterol level does not exert an important modulatory influence on membrane fluidity in these cells. It is concluded that while the distinct patterns of structural and functional erythrocyte alterations in these two disorders cannot be explained on the basis of differences in bulk membrane fluidity, the marginally increased fluidity may underlie the abnormalities in osmotic fragility and membrane p-nitrophenylphosphatase activity which are shared in common by both types of modified red cells.

Anemia, Hemolytic↗
PubMed1981

Familial lecithin-cholesterol acyltransferase: identification of heterozygotes with half-normal enzyme activity and mass.

Lecithin-cholesterol acyltransferase (LCAT) mass and activity was measured in Canadian kindred of Italian and Swedish descent with familial LCAT deficiency. Four subjects had LCAT mass of 5.21 +/- 0.87 micrograms/ml (mean +/- SD) and LCAT activity of 98.8 +/- 12.0 nmol/h/ml, well within their respective normal ranges. Five family members, including the parents, the maternal grandmother, and two of four siblings of the LCAT deficient subjects, had enzyme mass (2.85 +/- 0.32 micrograms/ml) and activity (50.8 +/- 6.3 nmol/h/ml) approximately one-half that of normal levels. These presumed heterozygotes had normal levels of apolipoproteins A-I, A-II, B and D. The two subjects with LCAT deficiency had no detectable LCAT mass (below 0.1 microgram/ml) or LCAT activity (below 0.76 nmol/h/ml), apolipoprotein A-I and D levels approximately 50% of normal, and apolipoproteins B and A-II levels only 30-35% of normal. LCAT deficiency in this family is determined by an autosomal recessive mode. Furthermore, LCAT levels and activity are determined by two autosomal codominant alleles, LCATn, the normal LCAT gene, and LCATd, the LCAT deficiency gene.

Female↗
PubMed1982

Familial lecithin-cholesterol acyltransferase deficiency in a Japanese family: evidence for functionally defective enzyme in homozygotes and obligate heterozygotes.

Lecithin-cholesterol acyltransferase (LCAT) mass and activity were measured in a Japanese family with familial LCAT deficiency. The two LCAT-deficient subjects had LCAT mass approximately 40-46% of normal (2.65 and 2.31 micrograms/ml respectively, as compared with normal levels of 5.76 +/- 0.95 microgram/ml in 19 Japanese subjects) and enzyme activity less than 10% of normal (9.1 and 8.3 nmol/h/ml respectively, as compared with normal levels of 100 nmol/h/ml). All obligate heterozygotes examined, including the father of the two LCAT-deficient subjects, and all five children of the deficient subjects had LCAT mass approximately 72-80% of the normal LCAT mass (4.12, 4.38, 4.45, 4.48, 4.49, 4.61 micrograms/ml, respectively) and LCAT activity approximately half normal (51.9, 52.4, 54.2, 56.6, and 57.2 nmol/h/ml). We conclude that the two LCAT-deficient subjects of this family have functionally defective enzyme. Furthermore, the data suggest that the plasma of the obligate heterozygotes contain both normal and functionally defective enzymes.

Adolescent↗
PubMed1988

Normalization of high density lipoprotein in fish eye disease plasma by purified normal human lecithin: cholesterol acyltransferase.

Plasma from a patient with fish eye disease has been enriched with autologous high density lipoproteins (HDL) and supplemented with highly purified normal human plasma lecithin:cholesterol acyltransferase (LCAT). Incubation of such plasma at 37 C in vitro resulted in normalization of its low HDL cholesteryl ester percentage, from 23% to 79%, associated with a two-fold increase in both the cholesteryl ester and triglyceride contents of the HDL fraction, as compared to incubation experiments with absent or heat-inactivated purified normal LCAT. The normalization of the HDL cholesteryl ester percentage induced by incubation with purified normal LCAT also was accompanied by an increase in the size of the original fish eye disease HDL particles, which had a mean mass of 115 kd, to HDL particle populations with mean particle masses ranging from 130-220 kd, depending on the concentration of purified LCAT in the incubate. Both HDL cholesterol esterification and particle enlargement were abolished completely by the LCAT inhibitor DTNB and by heat inactivation of the purified normal LCAT. The results give further evidence that fish eye disease is an alpha-LCAT deficiency.

Aged↗
PubMed2005

Cardiac surgery for a patient with familial lecithin: cholesterol acyltransferase deficiency.

A 62-year-old female with familial lecithin: cholesterol acyltransferase (LCAT) deficiency was subjected to cardiac surgery consisting of mitral valve repair, tricuspid valve annuloplasty, and left atrium plication, under cardiopulmonary bypass. Familial LCAT deficiency is a very rare disease with clinical features including corneal opacity, hemolytic anemia, and renal failure. Our patient manifests partial LCAT activity and no renal failure. Patients with LCAT deficiency have fragile red blood cells, renal dysfunction, and disturbed metabolism of platelet-activating factor. To date, no record of cardiac surgery on patients with LCAT deficiency has been reported. Thus, we present the result of this experience to share what we learned about this complicated and rare disease.

Cardiopulmonary Bypass↗