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PubMed1975

The interaction of apoA-I from human high density lipoprotein with lysolecithin.

The binding of apoA-I to lysolecithin has been studied by fluorescence and circular dichroism. The influence of the conformation of apoA-I on its interaction with lysolecithin has also been evaluated. ApoA-I is bound to lysolecithin with an association greater than 10(7) whether apoA-I is native or highly unfolded in 1.8 M guanidinium hydrochloride. The association of apoA-I with lysolecithin results in an increase in secondary structure. A 25-residue fragment of apoA-I binds to lysolecithin equally strongly as the native molecule.

Apoproteins↗

PubMed1984

The role of bile salts in cysteamine-induced duodenal ulcer in the rat and the ulceroprotective property of lysolecithin.

UNLABELLED: Cysteamine induces duodenal ulcers in rats, but bile diversion inhibits ulcer formation. Since lysolecithin inhibits stress ulceration in rats, it is assessed now whether lysolecithin inhibits cysteamine-induced ulcers, too. Male rats were operated: division of the duodenum distally to the pylorus, duodenojejunostomy. Roux-en-Y duodenojejunostomy. 4 groups comprising 10 animals. Drinking solution for group 1, 3 and 4: Na taurocholate and glycocholic acid (5 mmol/l). For group 2 addition of 0.2 mmol/l lysolecithin. Cysteamine-HCl (10%) twice subcutaneously on the 19th day in group 1, 3 and 4, isotonic NaCl in group 2. In group four 1 ml lysolecithin per gastric tube 1 h before cysteamine. RESULTS: Group 1: 8 animals with 16 ulcers, group 2: 7 with 10 ulcers, group 3: no ulcers, group 4: 3 with 5 ulcers (p less than 0.05/p less than 0.02). CONCLUSION: Lysolecithin, a substance produced during fat digestion, exerted an ulceroprotective property (lyso-protection) under experimental conditions, as shown here for the first time, to the author's knowledge. The enhancement of cysteamine-induced duodenal ulcer development by bile salts is again documented.

Animals↗

PubMed1978

Effects of lysolecithin on isolated gastric mucosa.

The effects of lysolecithin, a normal constituent of duodenal juice, on gastric mucosa were measured under isolated conditions. In a relatively low concentration (0.5 mg/ml), lysolecithin, added to the luminal side, caused liberation of organic acids without altering the spontaneous rate of mineral (i.e., HCl) acid secretion by fundic mucosa. The low concentration of lysolecithin also did not appear to affect other active ion transport processes or permeability of either fundic or antral mucosa. However, at a higher concentration (1 mg/ml) lysolecithin inhibited spontaneous mineral acid secretion by fundus, altered active transport of other ions, and increased mucosal permeability of both fundic and antral mucosa. The results suggest that intraluminal lysolecithin in concentrations found in vivo may contribute to gastric mucosal damage.

Animals↗

PubMed1980

[Lysolecithin and stress ulcers in rats].

The effect of lysolecithin on gastric mucosa in rats has been investigated using a new operative model. Ten rats underwent sham-laparotomy. In 4 other groups, each of 10 animals, the rats underwent pyloro-jejunostomy and Roux-en-Y anastomosis. 9 of 10 rats operated upon in this way, and given a solution of lysolecithin to drink before administration of restraint stress, produced stress ulcers. However, only 3 of 10 animals given Ringer-solution produced minor mucosal defects. Lysolecithin not combined with stress had no noteworthy deleterious effect on gastric mucosa either in sham-operated rats or in those with our operation model. Thus, lysolecithin combined with stress in our model performed an important function in the pathogenesis of stress lesions. Lysolecithin is produced in considerable quantities during fat metabolism in the intestine, and may be regurgitated together with duodenal contents into the stomach.

Animals↗

PubMed1987

The role of lysolecithin in the relaxation of vascular smooth muscle.

The effect of lysolecithin (lysophosphatidylcholine) on the relaxation of rabbit aortic strip closely resembled that produced by acetylcholine (ACh) which releases the endothelium-derived relaxing factor (EDRF). Relaxation induced by lysolecithin depended on the presence of endothelium and was inhibited by hemoglobin and methylene blue. It appeared to be mediated by the second messenger, c-GMP. Lysolecithin induced relaxation was slower but more persistent than that resulting from the endothelium-derived relaxing factor (EDRF) produced by acetylcholine (ACh). Like lysolecithin, Triton X-100, a non-ionic detergent, also preferentially relaxed aortic strips with intact endothelium. The results demonstrate the importance of phospholipids derived from cell membranes in vascular smooth muscle relaxation. Endothelium-derived relaxing factors appear as a group of heterogeneous substances.

Animals↗

PubMed1984

Induced mucosal penetration and transfer to portal blood of luminal horseradish peroxidase after exposure of mucosa of guinea pig small intestine to ethanol and lysolecithin.

The effect of luminal 150 mmol saline, 0.05-0.2% (w/v) lysolecithin, and 5-20% (v/v) ethanol was studied on the mucosal morphology of the proximal small intestine in conscious guinea pigs as well as on the mucosal penetration and transfer to portal venous blood of luminal horseradish peroxidase (HRP). No ultrastructural evidence of mucosal damage was identified in any of the lysolecithin-perfused animals compared with saline controls. Ten and 20% ethanol (v/v) resulted in the appearance of fluid-filled spaces between enterocytes and in cytoplasmic lipid deposits and an increased number of autophagic vesicles within the cells themselves. Tight junctions remained intact. These changes after luminal 5% ethanol (v/v) were much less conspicuous. In the presence of saline, luminal HRP was largely confined to the brush border. Both lysolecithin and ethanol (5% v/v) rapidly induced mucosal penetration of HRP which was seen in cytoplasmic vesicles within enterocytes, between enterocytes, and in the lamina propria. Peak portal venous blood levels of HRP studied in multiple samples over 3 hr were one log unit greater than saline controls. Absorption of HRP was proportional to the luminal concentration of lysolecithin in the range tested. These studies show that mucosal penetration and absorption of functional exogenous macromolecules may be induced, in the absence of morphological evidence of mucosal damage, by luminal constituents which may perturb the structure of enterocyte membranes.

Animals↗

PubMed1978

The effect of lysolecithin on contractile force of isolated gastric smooth muscle.

Mechanical activity of smooth muscle preparations was recorded in circular strips of antrum, corpus, and fundus from guinea-pig stomach. Whereas acetylcholine stimulated both rhythmic and tonic (shift of the base line) activity of the tested muscles, lysolecithin induced tonic contractions, but had no influence on the rhythmic activity. Lysolecithin was ineffective in the absence of external calcium. The tonic activations of corpus and fundus preparations induced by lysolecithin were suppressed by sodium nitroprusside. D 600 (methoxy-verapamil) did not counteract the lysolecithin effect.

Animals↗

PubMedDate not supplied

Normothermic ischaemic cardiac arrest of the isolated perfused rat heart: effects of trifluoperazine and lysolecithin on mechanical and metabolic recovery.

To evaluate the hypothesis that maintenance of the integrity of myocardial membrane systems and prevention of Ca2+ influx into the cell are significant in the survival of ischaemic tissue, the effect of trifluoperazine and lysolecithin, were tested on the recovery of globally ischaemic rat hearts. Trifluoperazine increases membrane stabilization, inhibits calmodulin and binds to other Ca2+-dependent proteins. Lysolecithin, on the other hand, has a detergent action on myocardial cell membranes and facilitates Ca2+ ingress in ischaemic tissue. With trifluoperazine (2.45 microM), added before induction of ischaemia or during reperfusion only, hearts subjected to 40 min normothermic ischaemic cardiac arrest recovered mechanically. Untreated hearts failed after 20 min of ischaemia. The drug had no effect on tissue high energy phosphate levels or mitochondrial oxidative phosphorylation. Conversely, lysolecithin (2.5-10 microM) caused all hearts to fail after being subjected to 15 min ischaemia. Mechanical failure during reperfusion of such hearts was associated with a significant reduction in tissue ATP and CrP levels. Trifluoperazine counteracted the harmful effects of lysolecithin to a limited extent.

Adenosine Diphosphate↗

PubMed1976

Molecular aggregation of the slow reacting hemolytic lysolecithin analog 1-octadecyl-2-benzyl-glycero-3-phosphorylcholine in aqueous solution.

An attempt has been made to relate the retarded adsoprtion to red cells of the slow reacting hemolytic phosphatide Rac. 1-octadecyl-2-benzyl-glycero-3-phosphorylcholine (benzyl-lysolecithin) to its aggregation status in aqueous solution. Light scattering measurements indicate a critical micelle concentration at 37 degrees of less than 2 X 10(-6) M. The micellar weight as determined by angle dependent light scattering is 6 X 10(7) with about 97 000 molecules per micells. The aggregates, which according to electron-microscopic observations are more similar to lecithin-liposomes than to usual lysolecithin-micelles, undergo a phase transition at 14 degrees from a tightly packed liquid-crystalline state to the more loose structure of a gel phase with increased mobility of the aliphatic chains. The enthalpy of transition is 4.2 kcal/mole. These changes of the micellar structure are reflected in the binding kinetics of benzyl-lysolecithin to red cells in that the binding rate is rather constant below, but strongly increasing above the transition temperature. It is concluded that the unusual micellar structure is responsible for the retarded adsorption of this lysolecithin analog to red cells and that the rate of adsorption is probably determined by the rate of escape of single lysophosphatide molecules from the micelles.

Binding Sites↗

PubMed1988

Excision repair of UV damage in human fibroblasts reversibly permeabilized by lysolecithin.

We have examined nucleotide excision repair synthesis in confluent human diploid fibroblasts permeabilized with lysolecithin. Following a UV dose of 12 J/m2, maximal incorporation of [alpha 35S]dNTPs occurred at a lysolecithin concentration (approximately 80 micrograms/ml) where slightly more than 90% of the cells were initially permeable to trypan blue. However, autoradiography of cells, permeabilized at this lysolecithin concentration, demonstrated that only about 20% of the total cell population incorporated significant levels of 35S into DNA. This result presumably reflected the fact that approximately 20% of the total cell population remained permeable for much longer periods of time (up to 2 h) than the remaining cell population (less than 20 min). The incorporation of dNTPs by UV-irradiated, permeabilized cells appeared to be bona fide excision repair synthesis since: (1) Incorporation was completely absent in unirradiated, permeabilized cells and in irradiated, permeabilized repair-deficient cells. (2) Nucleotides incorporated in the presence of BrdUTP were associated with normal density DNA. (3) The apparent Km for all 4 dNTPs was 50-100 nM, in agreement with past reports on human fibroblasts irreversibly permeabilized by cell lysis. (4) DNA associated with the newly incorporated dNTPs underwent ligation and rearrangements in chromatin structure analogous to what is observed in intact human cells. Repair incorporation of dNTPs was rapid and linear during the first 2 h after UV irradiation and permeabilization. After this time, incorporation ceased or continued at a much slower rate. Cell viability experiments and autoradiography demonstrated that the cells permeabilized to [3H]dNTPs were capable of carrying out DNA replication and cell division. Thus, confluent human diploid fibroblasts can be reversibly permeabilized to labeled dNTPs by lysolecithin for the study of excision repair following physiologic doses of UV radiation. However, under these conditions, only a fraction of the cells remain permeable for an extended period of time.

Cell Membrane Permeability↗

PubMed1992

High-density lipoprotein antagonizes the inhibitory effects of oxidized low-density lipoprotein and lysolecithin on soluble guanylyl cyclase.

Oxidatively modified LDL (LDLox) reduces the response of soluble guanylyl cyclase to nitrovasodilators. We now demonstrate that this desensitization can be antagonized by HDL. Similar to its protective effect against LDLox, HDL also inhibited the lysolecithin-induced desensitization of soluble guanylyl cyclase. Since the lysolecithin content of LDLox correlated with the amount of lysolecithin necessary to diminish stimulation of soluble guanylyl cyclase, our data support the hypothesis that lysolecithin may be responsible for the inhibitory effect of LDLox on smooth muscle relaxation and provide evidence that the antagonistic effect of HDL against desensitization of soluble guanylyl cyclase by atherogenic compounds could be responsible for the protective role of HDL in atherosclerosis.

Animals↗

PubMed1995

Enhancement of Agkistrodon piscivorus piscivorus venom phospholipase A2 activity toward phosphatidylcholine vesicles by lysolecithin and palmitic acid: studies with fluorescent probes of membrane structure.

The activity of phospholipase A2 from snake venom to hydrolyze bilayers of phosphatidylcholines is greatly enhanced by the presence of the hydrolysis products, lysolecithin and fatty acid, in the bilayer. The fluorescence of several probes of membrane structure was used to monitor changes in bilayer physical properties during vesicle hydrolysis. These changes were compared to emission spectra and fluorescence polarization results occurring upon direct addition of lysolecithin and/or fatty acid to the bilayer. The excimer to monomer ratio of 1,3-bis(1-pyrene)propane was insensitive to vesicle hydrolysis, suggesting that changes in the order of the phospholipid chains were not relevant to the effect of the hydrolysis products on phospholipase activity. The fluorescence of 6-propionyl-2-(dimethylamino)-naphthalene (Prodan) suggested that the polarity of the bilayer in the region of the phospholipid head groups increases as the hydrolysis products accumulate in the bilayer. The fluorescence of 6-dodecanoyl-2-(dimethylamino)naphthalene (Laurdan) confirmed that such effects were restricted to the bilayer surface. Furthermore, the lysolecithin appeared to be the product most responsible for these changes. These results suggested that lysolecithin increases the activity of phospholipase A2 during vesicle hydrolysis by disrupting the bilayer surface, making the phospholipid molecules more accessible to the enzyme active site.

2-Naphthylamine↗

PubMed1980

Effect of lysolecithin on the binding of 1-anilino-8-naphthalene sulfonate to apoHDL, apoA-I or apoA-II from human serum high density lipoprotein.

The binding of 1-anilino-8-naphthalene sulfonate to human serum high density apolipoprotein and to apoA-I and apoA-II which are major protein components of high density apolipoprotein was measured by a fluorometric method. The maximum number of 1-anilino-8-naphthalene sulfonate bound to high density apolipoprotein was about 950 mumol per g of protein, and those to apoA-I and apoA-II were 27 and 13 mol per mol of protein (there values correspond to 964 for apoA-I and 765 for apoA-II in mumol per g of protein), respectively. After preincubation of apolipoprotein with lysolecithin (less than 10 microM), the binding affinities for the dye increased twice or more with all the proteins, but the maximum binding numbers changed little. With apoA-I, two mol of the dye were bound with high affinity and lysolecithin did not compete with the dye for the binding sites. The fluorescence intensity of tryptophanyl residues of apoA-I was changed by incubation with lysolecithin at concentrations lower than the critical micellar concentration. These results indicate that the binding of lysolecithin molecules to apoA-I or other proteins makes the protein conformation more suitable for the binding of hydrophobic ligands.

Anilino Naphthalenesulfonates↗

PubMed1976

The lecithin: cholesterol acyltransferase reaction, lysolecithin and red cell ageing in blood stored under normal transfusion service conditions.

The lecithin:cholesterol acyltransferase (LCAT) activity and lysolecithin content of human blood stored under standard blood transfusion service conditions at 4 degrees C for 6 weeks has been investigated. Cooling the blood to 4 degrees C rapidly inactivates the LCAT reaction, but the enzyme is not denatured during storage under these conditions. Citrate in the anticoagulant did not activate the LCAT reaction in freshly-taken whole blood. The total phospholipid and total lysolecithin content of whole blood decreased during storage at 4 degrees C for 6 weeks. The lysolecithin content of fresh red cells (2.0-3.0 mumol lysolecithin x 10(-11) per cell) showed no significant change during the storage period.

Acyltransferases↗

PubMed1983

Is lysolecithin an in vivo constituent of chromaffin granules?

It was recently claimed that lysolecithin (lysophosphatidylcholine) in chromaffin granules is a post-mortem artefact. We have, therefore, determined catecholamine/lysolecithin ratios in adrenal tissues and isolated chromaffin granules. In rat adrenals and bovine medulla the ratios in both tissues and granules were similar. This indicates that even in rapidly frozen rat adrenal glands, sufficient lysolecithin is present in the total tissue to account for its presence in isolated organelles. Owing to the high cortex/medulla ratios such studies cannot be performed with guinea pig or rabbit adrenals. However, isolated chromaffin granules from guinea pig, in contrast to a previous study, do contain lysolecithin. We conclude that lysolecithin is an in vivo constituent of chromaffin granules of all species so far investigated.

Adrenal Medulla↗

PubMed1973

Significance of plasma lysolecithin in patients with multiple sclerosis: a longitudinal study.

Five patients with multiple sclerosis and four normal subjects have been followed for over two years. Plasma phospholipid levels and phospholipid fatty acid composition have been assayed periodically. The increased amount of plasma lysolecithin already described by us has been confirmed in this longitudinal study. A significant increase in saturated fatty acids of lysolecithin has also been demonstrated. In contrast, the lecithin concentration and fatty acid composition do not show any significant variations. The lysolecithin saturated/unsaturated fatty acid ratio was different in the same patients at different times, but no correlation was established between these variations and the clinical symptoms measured using the Kurtzke scale. The possible significance of saturated fatty acid increase in lysolecithin in the pathogenetic mechanisms of multiple sclerosis is discussed.

Acute Disease↗

PubMed1977

Increase in activity of partially purified alkaline phosphatase after treatment with Mg2+, Zn2+ and lysolecithin.

When lysolecithin predispersed in 0.15 mol/l KCl was sonicated with partially purified alkaline phosphatase, the enzyme activity was increased. Lysolecithin moderately modified the kinetic parameters by increasing the apparent Vmax and decreasing the apparent Km. The pH profile of the enzyme was shifted slightly from a peak at pH 9.5 for the soluble enzyme to a plateau between pH 9.5 and 10.2 for the lysolecithin enzyme mixture. In addition, lysolecithin enhanced the thermostability and resistance of the soluble enzyme preparation to chemical denaturants.

Alkaline Phosphatase↗

PubMed1975

Lysolecithin-mediated inflammatory reaction in rabbit gallbladder. Permeability increase and enzyme liberation.

Aseptic inflammation in the gallbladder wall was studied in vitro using rabbit gallbladders. Wall permeability changes, measured as changes in the transmural passage of radioactively labelled hippuran and biligraphin as well as enzyme (acid phosphatase) release from wall to lumen were registered as parameters permitting quantitative assessment of an inflammatory process. Lysolecithin, a surface-active substance of possible significance in the pathogenesis of acute cholecystitis was chosen as inflammation-inducing agent. When 6-20 mg/ml lysolecithin was instilled into the gallbladders, dose-dependent increases in permeability and enzyme release occurred. No effects as compared with controls were seen when 2 mg/ml was instilled. Lysolecithin-treated gallbladders showed morphological signs of inflammation as opposed to untreated. The data reported are consistent with earlier observations that lysolecithin may cause inflammatory lesions to the gallbladder wall. The experimental model used may prove useful in examining the effects of aggressive and protective agents upon the gallbladder mucous membrane.

Acid Phosphatase↗