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PubMed1986

Passage of molecules through the wall of the gastrointestinal tract. Influence of lysolecithin on rat ileal permeability to different-sized molecules.

We have studied the influence of lysolecithin on mucosal permeability to different-sized molecules in the distal part of the ileum. Using a rat experimental model, we determined the intestinal permeability to ethylene glycol (62 dalton), different-sized polyethylene glycols (634- to 1206-dalton PEGs), and dextran 3000, in the absence and presence of lysolecithin. We also examined the morphology of the ileal mucosa and determined the activity of brush border enzymes after deposition of lysolecithin in the gut lumen. We found that lysolecithin did not affect the absorption of ethylene glycol and had no influence on the activities of the enzymes. In contrast, lysolecithin enhanced the desquamation of enterocytes at the villous tips and increased the permeability to 634- to 1206-dalton PEGs and dextran 3000. These findings indicate that lysolecithin may facilitate the uptake of larger, potentially antigenic and toxic molecules in the distal ileum, although the underlying epithelial desquamation might have little or no influence on the absorption of small compounds.

Animals↗
PubMed1976

Duodenogastric reflux of lysolecithin in the pathogenesis of experimental porcine stress ulceration.

The role of duodenogastric reflux of lysolecithin, a normal constituent of duodenal juice, in the pathogenesis of gastric stress ulcerations was investigated with a swine shock-ulcer model. Twenty-seven piglets, weighing 8 to 12 kilograms, were used. In an intact animal, the average concentration of intragastric lysolecithin before shock was 138 mug per milliliter (median, N = 6). At the end of the shock period, the average concentration of lysolecithin was 540 mug per milliliter and the over-all amount in the gastric juice was 14.3 mg. (median, N = 6). Following hemorrhagic shock (3 hours duration; mean arterial pressure, 40 mm. Hg), all six control animals with normal gastroduodenal continuity got gastric ulcerations. Interruption of duodenogastric reflux by duodenal exclusion and gastrojejunostomy completely abolished the development of these ulcerations in six test animals. When the interrupted duodenogastric reflux was replaced artificially by intragastric instillation of lysolecithin (500 mug per milliliter; 25 ml.), all six animals developed lesions. Intragastric lysolecithin without shock had no effect. The results provide further support to the concept that regurgitation of duodenal juice into the stomach is an essential factor in the pathogenesis of gastric stress ulceration. The results also suggest that, in this respect, one of the active components in duodenal juice is lysolecithin.

Animals↗
PubMed1976

Formation and inhibition of lysolecithin in human gallbladder bile.

Homogenized human gallbladder epithelium was incubated at 37 degrees C with 14C-lecithin in diluted gallbladder bile. During the incubation, lecithin was transformed to lysolecithin. The reaction rate was higher at pH 4.5 than at pH 7.0. No degradation of lecithin occurred if the reaction mixture did not contain the homogenate. Lysolecithin was mixed with red blood cells in (a) diluted human gallbladder bile and (b) 0.15 M saline. The surface activity in the different systems was then assessed from the amount of hemoglobin recovered in the red cell pellet after centrifugation. In human bile, 500 mug lysolecithin/ml did not affect the amount of hemoglobin recovered whereas in saline, concentrations exceeding 25-30 mug/ml affected the red blood cells such that no hemoglobin was pelleted by the centrifugation. Lysolecithin was further studied for effect upon lecithin-3H-cholesterol-dicetylphosphate liposomes containing 14C-glucose. The surface activity of lysolecithin was assessed from the distribution of 3H- and 14C-activity after centrifugation. Although 500 mug lysolecithin/ml increased the non-sedimented 14C-activity, 5000 mug lysolecithin/ml was necessary to decrease significantly the amount of sedimented 3H-activity. The results are interpreted such that phospholipase A activity from the gallbladder epithelium, if released into the gallbladder bile, may generate lysolecithin from lecithin. However, the surface activity and, thus, the inflammatory mediating activity of lysolecithin is inhibited by components in the gallbladder bile, possibly lecithin.

Bile↗
PubMed1976

The biochemical prerequisites for preventing pathogenic lysolecithin activity in the human gallbladder.

Human gallbladder epithelium was disintegrated to complete loss of microscopic structure and incubated at 37 degree C together with unlabelled lysolecithin and 14C-lysolecithin. During each incubation lysolecithin was degraded and stoichiometrically equivalent amounts of free fatty acids formed. The maximum rate of degradation was obtained at pH 7.0 and at 200 muM lysolecithin. With increasing amounts of gallbladder epithelial cell constituents the reaction became faster. After heating the epithelial components at 70 degrees C for 10 min the reaction was inhibited. The results suggest the presence of a heat labile lysophospholipase (phospholipase B) activity in the human gallbladder epithelium. This activity may operate to protect the gallbladder epithelium against potentially pathogenic lysolecithin activity. Its presence in the gallbladder epithelium meets the prerequisites for a local anti-inflammatory mechanism and lends further support to the hypothesis of lysolecithin as a mediator of cholecystitis.

Cholecystitis↗
PubMed1995

Rapid inhibition of mRNA synthesis during preimplantation embryo development: vital permeabilization by lysolecithin potentiates the action of alpha-amanitin.

Lysolecithin was used to permeabilize embryonic cells to impermeant compounds without compromising embryo viability. Within 2 min of exposure to 0.05% lysolecithin, mouse morulae became permeable to inositol 1,4,5-trisphosphate, leading to the release of calcium from intracellular stores. Although these morulae remained permeable for at least 2 h, they developed normally to the blastocyst stage during subsequent culture in vitro. Lysolecithin permeabilization was then used to potentiate the internalization of alpha-amanitin. Pretreatment with lysolecithin for 2 min markedly accelerated the onset of transcriptional inhibition from 3 h to 10 min after alpha-amanitin addition. The rapid inhibition by alpha-amanitin of mRNA synthesis in lysolecithin-treated embryos provided a precise method for delineating developmentally important transcriptional periods. Using this protocol, we found that mRNAs required for embryonic cavitation were synthesized between 87 and 91 h post-hCG, shortly before blastocoel formation commenced.

Amanitins↗
PubMed1982

Degeneration of non-myelinated axons in the rat sciatic nerve following lysolecithin injection.

Lysolecithin has been used in many studies to induce demyelination in peripheral nerves. In the present investigation lysolecithin (lysophosphatidyl choline) was injected into rat sciatic nerves at a dose of 2-3 microns of a 10 mg/ml solution in order to study the effects of this lipid on cellular elements other than myelin within the nerve. Twenty-four hours after injection, there was splitting of myelin, lysis of Schwann cells, and complete loss of non-myelinated axons and their Schwann cells at the site of injection. Numerous swollen non-myelinated axons containing accumulated organelles were seen just proximal to the site of injection at 48 h. Loss of non-myelinated axons from the distal part of the nerve was also noted at 3 days after injection but 7 days regenerating non-myelinated axons had re-appeared in the distal part of the nerve. Although demyelination, followed by remyelination was prominent feature in the injected segment of the nerve, no damage to myelinated axons was detected. These results suggest that the presence of the myelin sheath protects the large myelinated axons against the action of lysolecithin, but with lysis of Schwann cells, the non-myelinated axons are exposed to the action of lysolecithin. Apart from selective damage to non-myelinated fibres with subsequent degeneration, it is also possible that lysolecithin interferes with axoplasmic flow in non-myelinated axons.

Animals↗
PubMed1987

The kinetic mechanism of acyl-CoA:lysolecithin acyltransferase from rabbit lung.

Acyl-CoA:lysolecithin acyltransferase is a key enzyme in the deacylation-reacylation pathway of biosynthesis of molecular species of lecithin. However, the mechanism of the reaction has been little studied. In this paper, the kinetic mechanism of acyl-CoA:lysolecithin acyltransferase, partially purified from rabbit lung, is studied. The double-reciprocal plots of initial velocity vs substrate concentration gave two sets of parallel lines which fitted to a ping-pong equation with the following parameters: Km (palmitoyl-CoA) = 8.5 +/- 2 microM, Km (lysolecithin) = 61 +/- 16 microM, and V = 18 +/- 4 nmol/min/mg protein. Inhibition studies by substrates, alternate substrates, and products supported the ping-pong mechanism, although some nonclassical behavior was observed. Palmitoyl-CoA did not inhibit even at concentrations of 100 Km. In contrast, lysolecithin was a dead-end inhibitor with a dissociation constant of Ki = 930 +/- 40 microM. Alternate substrates and CoA showed alternate pathways for the reaction due to the formation of ternary complexes. Dipalmitoylphosphatidylcholine inhibition pointed to an isomerization of the free enzyme prior to the start of the reaction. From these results, an iso-ping-pong kinetic mechanism for lysolecithin acyltransferase is proposed. The kinetic steps of the reaction are correlated with previous chemical studies of the enzyme.

1-Acylglycerophosphocholine O-Acyltransferase↗
PubMed1992

Lysolecithin actions on vascular smooth muscle cells.

Oxidation of low density lipoprotein increases its atherogenic potential. During oxidation there is an extensive conversion of lecithin to lysolecithin. In rat aortic smooth muscle cells, 2-25 micrograms/ml lysolecithin elevated cytosolic calcium concentration up to 560%. Lysolecithin (10-20 micrograms/ml) increased [3H]thymidine incorporation from 15 cpm/mg cell protein (controls) up to 189 cpm/mg cell protein. Lysolecithin (10 micrograms/ml) potentiated the PDGF-induced (50 ng/ml) [3H]thymidine incorporation up to 6.3 times. The results indicate that lysolecithin could induce mechanisms, by which oxidized low density lipoproteins could promote cell growth and thus contribute to atherosclerosis.

Animals↗
PubMedDate not supplied

Plasma concentrations of lysolecithin and other phospholipids in the healthy population and in men suffering from atherosclerotic diseases.

The concentrations of individual phospholipids and of cholesterol have been determined in plasma samples taken from 77 apparently healthy individuals, and from 76 male patients presenting with atherosclerotic diseases. Significant differences in the relative and absolute concentrations of lysolecithin were found between different populations. In healthy individuals the plasma levels of lysolecithin were lower in women than in men and lower in the younger age groups studied. The relative and absolute concentrations of plasma lysolecithin were lower in men suffering from chronic ischaemic heart disease and peripheral arterial disease when compared with age-matched healthy male subjects. The lowest levels of plasma lysolecthin were, however, associated with patients suffering from acute myocardial infarction or acute myocardial ischaemia studied within 48 hr of the onset of chest pain. In a further study, significantly decreased relative concentrations of lysolecithin were found in blood platelets and erythrocytes as well as in plasma of patients suffering from chronic ischaemic heart disease. The results are discussed in terms of a possible thrombo-protective role for plasma lysolecithin in man.

Acute Disease↗
PubMed1986

Lysolecithin-induced Ca2+ uptake by pigeon red cells.

Lysolecithin (LPC) induced a rapid but transitory increase in 45Ca2+ influx, and an abrupt 45Ca2+ net uptake by pigeon red cells. The effect on uptake was seen with doses of added lysolecithin calculated to be 2.1-8.4% of the cytoplasmic membrane phospholipid, well within the reported physiological range of 1-9%. Lysolecithin effects were not due to prelytic membrane changes nor action as a platelet activating factor agonist. Changes in the amino acids in the medium mimicking human homocysteinuria, an atherosclerosis risk factor, increased the lysolecithin effect. The findings are consistent with a role for lysolecithin in atherosclerosis.

Amino Acid Metabolism, Inborn Errors↗
PubMed1984

Activation of an erythrocyte NAD:arginine ADP-ribosyltransferase by lysolecithin and nonionic and zwitterionic detergents.

The activity of an NAD:arginine ADP-ribosyltransferase was stimulated 4-6-fold by lysolecithin; lysolecithins containing long-chain fatty acids such as stearoyl (C18) and palmitoyl (C16) were more effective than those with shorter chains: C14 greater than C12 greater than C10 congruent to C8. The analogue lacking a fatty acid at C-1, alpha-glycerophosphocholine, was inactive as were choline, lysophosphatidic acid, lysophosphatidylserine, lysophosphatidylglycerol, lysophosphatidylethanolamine, lecithin, phosphatidic acid, phosphatidylserine, and phosphatidylethanolamine. Activation of the transferase was, however, also observed with certain nonionic (e.g., Triton X-100) and zwitterionic [3-[ ( cholamidopropyl ) dimethylammonio ]-1-propanesulfonate] detergents. The transferase was shown previously to be stimulated by chaotropic salts or histones; in the presence of maximally effective concentrations of lysolecithin, salt, and histone, the activity was similar to that observed in the presence of histone or salt alone. Maximal activation by lysolecithin and detergents was less than that observed with either salt or histone. It appears that activation by lysolecithin shows significant differences from that observed previously with histones or salt and can be mimicked by certain nonionic and zwitterionic detergents.

ADP Ribose Transferases↗
PubMed2000

Effects of phospholipase A2, free fatty acids and 2-lysolecithin on the crystallization of cholesterol in gallbladder bile.

BACKGROUND: Phospholipase A2 (PLA2) and its enzymatic products free fatty acids (FFAs) and 2-lysolecithin are physiological constituents of bile. Their role in the crystallization of cholesterol in gallbladder bile of patients with cholesterol gallstones is still controversial. DESIGN: To clarify this issue we evaluated the activity of PLA2 and the concentration and pattern of FFAs in the gallbladder bile of cholesterol stone patients. We furthermore added PLA2, FFAs and 2-lysolecithin to isotropic gallbladder bile, determined the crystal observation time (COT) and counted the cholesterol crystals in a crystal growth assay for up to 21 days. RESULTS: A PLA2 activity of 1.8 +/- 1.2 U L(-1) and total FFA concentrations of 1.32 +/- 0.71 mmol L(-1) were determined. After incubation of bile for 24 h at 37 degrees C total FFAs increased to 2.72 +/- 1.29 mmol L(-1) (P<0.005). Biliary saturated and unsaturated FFAs were found in equal proportions before and after incubation, pointing to an additional presence of lipases other than PLA2. A COTof 1 day was observed in all gallbladder biles and increased to 1.7 +/- 0.5 days after addition of 5 U L(-1) of PLA2 (P<0.01). An even higher COT of 2.5 +/- 0.8 days was seen after addition of 5 mmol L(-1) of a 'biliary' mixture of FFAs (P<0.005) but the COT remained unchanged after addition of 5 mmol L(-1) of 2-lysolecithin. However, in the crystal growth assay in gallbladder bile addition of 5 U L(-1) of PLA2, of 5 mmol L(-1) of 'biliary' FFAs and of 5 mmol L(-1) of 2-lysolecithin decreased significantly the number of cholesterol crystals formed during follow-up. CONCLUSION: An elevated activity of PLA2 in gallbladder bile may counteract the formation of cholesterol crystals through increased formation of FFAs and 2-lysolecithin. However, regarding the comparatively low activity of PLA2 in gallbladder bile PLA2 seems to be of only minor pathophysiological importance in the formation of cholesterol gallstones.

Adult↗
PubMed1982

Bile acid and lysolecithin concentrations in the stomach in patients with duodenal ulcer before operation and after treatment by highly selective vagotomy, partial gastrectomy, or truncal vagotomy and drainage.

Duodenogastric reflux of bile acids and lysolecithin in the course of a standard test meal was measured in normal people and in patients with duodenal ulcer before operation and more than one year after highly selective vagotomy, Polya partial gastrectomy, truncal vagotomy and pyloroplasty, and truncal vagotomy and gastrojejunostomy. Before operation, duodenal ulcer patients had significantly higher fasting, post-prandial, and peak bile acid concentrations in the stomach than had normal subjects. After Polya partial gastrectomy, fasting, post-prandial, and peak concentrations of bile acids and lysolecithin were significantly higher than in preoperative duodenal ulcer patients. After highly selective vagotomy, in contrast, bile acid concentrations in the stomach were significantly lower than in preoperative duodenal ulcer patients and post-prandial and peak lysolecithin concentrations were less than half (NS) those recorded in preoperative duodenal ulcer patients. After highly selective vagotomy, bile acid concentrations were also significantly lower than bile acid concentrations after Polya partial gastrectomy, truncal vagotomy and pyloroplasty, and truncal vagotomy and gastrojejunostomy; and post-prandial and peak lysolecithin concentrations were significantly lower than after Polya partial gastrectomy and truncal vagotomy and gastrojejunostomy. Thus, when used in the treatment of patients with duodenal ulcer, highly selective vagotomy keeps ;bile' out of the stomach, probably through its effect on gastric smooth muscle, combined with the preservation of an intact antropyloroduodenal segment. In contrast, Polya partial gastrectomy, truncal vagotomy and gastrojejunostomy, and truncal vagotomy and pyloroplasty all lead to a significant increase in reflux of bile acids and lysolecithin into the stomach. The clinical importance of these findings is that both gastritis and, in the long term, gastric carcinoma may prove to be less common after highly selective vagotomy than after partial gastrectomy or vagotomy with a drainage procedure.

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↗
PubMed1979

Liposomes in immunology: impairment of the adjuvant effect of liposomes by incorporation of the adjuvant lysolecithin and the role of macrophages.

The immune response against HSA (human serum albumin) was studied in rabbits after intravenous injection of various HSA preparations. When HSA was injected one day after, together with or coupled to lysolecithin, a late response was found in twelve out of thirteen rabbits, whereas a minority of the rabbits responded when lysolecithin was omitted. These results confirm the adjuvant activity of lysolecithin. A rapid response starting on day 6 was found in rabbits injected with HSA entrapped in liposomes which had been composed of lecithin, phosphatidic acid and cholesterol (PPC liposomes). The response against liposome entrapped HSA was delayed for about one day when the phospholipid adjuvant lysolecithin was incorporated in the liposomes (LPPC liposomes). Results lend support to the hypothesis that the adjuvant activity of lysolecithin and its opposite inhibition of the adjuvant activity of liposomes are mediated by the same mechanism, i.e. inhibition of enzymatic digestion in lysosomes of macrophages.

Adjuvants, Immunologic↗
PubMed1984

The flow behavior of lysolecithin-induced echinocytes.

Lysolecithin is formed by enzymatic processes in the blood plasma both in vivo and in vitro. Erythrocyte suspensions which are treated with lysolecithin, have a higher viscosity than normal erythrocytes. At high shear rates this may be attributed to a reduced deformability of these cells. At shear rates below 10 s-1, however, these erythrocytes maintain their resting shape (which is that of a spiculated sphere) and their viscosity is 8 times higher than that of aldehyde-hardened erythrocytes. It is therefore concluded that the reduced deformability of lysolecithin-treated erythrocytes is not the cause of their high viscosity at low flow velocities. The results of this paper suggest that lysolecithin-treated red cells have an increased functional volume due to the immobilization of fluid between their spicules. Furthermore the lysolecithin-treated erythrocytes, despite their sphered shape can attach to each other when the suspending medium contains long-chain molecules. Both the increased functional volume and the attachment of the cells can explain the high viscosity values at the lower shear rates.

Adolescent↗
PubMed1992

[The effect of lysolecithin on rat liver microsome monooxygenase activity after induction by xenobiotics of the methylcholanthrene type].

Effects of exogenous gamma-myristoyl- and gamma-palmitoyllysolecithins on physico-chemical characteristics of rat liver microsomes, such as hydrophobicity and viscosity, as well as on oxidative NADPH-dependent O-deethylation of 7-ethoxycoumarin (7-EC), O-demethylation of p-nitroanisole (p-NA) and hydroxylation of 3.4-benz(a)pyrene (BP) induced by the mechylcholanthrene xenobiotics methylcholanthrene (MCh), beta-naphthoflavone (NF) and Sovol (SV) have been investigated. The specific inducible form of P-450c showed different affinity for the substrates. Lysolecithin decreased the hydrophobicity but only slightly increased membrane viscosity, whereas the monooxygenase substrates neutralized these effects. Lysolecithin (2-20 micrograms/mg of microsomal protein) inhibited the activity of deethylase 7-EC (maximally by 11%) in NF- and SV-induced microsomes, this inhibiting effect being more pronounced than that in MCh-induced microsomes. At higher concentrations lysolecithin inhibited the rate of 7-EC deethylation in MCh-induced microsomes more strongly; the maximal inhibition (23%) was observed at the protein concentration of 60 micrograms/mg. In case of NF- and SV-induced microsomes the inhibition was 18%. The inhibiting effect of lysolecithin on 7-EC dealkylation was expressed in a lesser degree than that on p-NA O-demethylation in induced (but not intact) microsomes. A significant positive correlation has been found between the changes in hydrophobicity and inhibition rates in the presence of lysolecithin, however only for 7-EC deethylation.

Animals↗
PubMedDate not supplied

Lysolecithin induced membrane alterations in thymocytes. Effects of lysophosphatides possessing adjuvant and immuno-suppressive activities on cell agglutination by concanavalin A.

The effects of lysolecithin and of 2 synthetic ether-desoxy lysolecithin analogs, containing alkyl residues of 16 or 12 carbon atoms, on the agglutination kinetics of calf and rabbit thymocytes by concanavalin A (Con A) were investigated. Unlike the natural lysolecithin, these synthetic analogs are resistant to metabolism by membrane associated enzymes. It was found that pretreatment of thymocytes with lysolecithin or with the C16-analog leads to slightly increased agglutination rates. The C12-analog, in contrast, significantly inhibits thymocyte agglutination by Con A. Moreover, a comparison of these results with lysophosphatide effects on the agglutinability of erythrocytes of various species revealed that the inhibitory effect of the short-chain phosphatide is rather specific for thymocytes. The finding that long- and short-chain lysophosphatides, which have previously been shown to react as adjuvants or immunosuppressants, respectively, induce adserve alterations in thymocyte membranes indicates that these substances may affect the immune response by changing the membrane properties of immune competent cells. Concerning the nature of these membrane alterations it was shown that lysolecithin did not affect the number of Con A receptors per cell nor the affinity of lectin binding. It is therefore concluded that the lysophosphatide induced alterations of Con A agglutinability can not be caused by an uncovering or covering of lectin-receptors.

Agglutination↗