Influence Of Lysophosphatidylcholine Research Articles

The influence of amylose-LPC complex formation on the susceptibility of wheat starch to amylase

This study was aimed to assess the role of lysophosphatidylcholine (LPC) in the development of slowly digestible starch (SDS). The influence of LPC, on the enzymatic degradation of diluted 9% wheat starch suspensions (w/w) was investigated, using an in vitro digestion method. Wheat starch suspensions containing 0.5–5% LPC (based on starch) were heated in a Rapid Visco Analyser (RVA) till 95°C and subjected to enzyme hydrolysis by porcine pancreatic α-amylase at 37°C for several digestion periods. In vitro digestion measurements demonstrated that complexing starch with 5% LPC leads to a 22% decrease in rate of reducing sugar compared to the reference while the samples containing 0.5% LPC showed an equal digestibility comparable to the control. A clear decrease in the formation of reducing sugars was observed in presence of 2–5% LPC, since the results after 15min digestion imply the formation of SDS due to the formation of amylose-LPC inclusion complexes. The DSC measurements proved the presence of amylose-LPC inclusion complexes even after 240min digestion demonstrating the low susceptibility of amylose-V complexes to amylase.

Influence of lysophosphatidylcholine on the gelation of diluted wheat starch suspensions

Starch is an omnipresent constituent which is used for its nutritional and structuring properties. Recently concerns have been raised since starch is a source of readily available glucose which is tightly correlated with diabetes type II and obesity. For this reason, the possibilities for modulating the digestibility of starch while preserving its functional properties were investigated; therefore the focus of this paper is on starch gelatinization and the effect of lysophosphatidylcholine (LPC) on the structuring properties of wheat starch. The effect of LPC on thermal properties and viscosity behavior of starch suspensions was studied using DSC and RVA, respectively. The influence on granular structure was observed by light microscopy. The RVA profile demonstrated no viscosity increase at high LPC concentrations which proves intact granular structure after gelatinization. LPC in intermediate concentrations resulted in a notable delay of pasting; however the peak and end viscosities were influenced as well. Lower LPC concentrations demonstrated a higher peak viscosity as compared with pure starch suspensions. DSC results imply that inclusion complexes of amylose–LPC might be formed during pasting time. Since the viscosity profiles are changed by LPC addition, swelling power and solubility of starch granules are influenced as well. LPC hinders swelling power and solubility of starch granules which are stimulated by heating.

Influence of lysophosphatidylcholine, phosphatidylcholine, and hen egg yolk on contractile effects of acetylcholine on smooth muscles of rat stomach

Experiments on smooth muscles of rat stomach showed that lysophosphatidylcholine in concentrations of 10(-8) and 10(-7) g/ml does not modulate the tonotropic effect of acetylcholine (10(-6) g/ml), in a concentration of 10(-6) g/ml potentiated this effect (similarly to phosphatidylcholine, 10(-6) g/ml), and reduced it in concentrations of 10(-5)-10(-4) g/ml (similarly to hen egg yolk in dilutions of 1:500, 1:100, and 1:500). These data indicate that lysophosphatidylcholine modifies signal transduction from the receptor to G protein.

Acute toxicity and depression of phagocytosis in vivo by liposomes: influence of lysophosphatidylcholine

Small unilamellar phospholipid vesicles (liposomes), intended as drug carriers, have recently been demonstrated to reversibly depress phagocytic activity in rats when injected in a single high dose (2g of lipid per kg body weight) as revealed by the carbon clearance test. Depression of the phagocytic function was found to vary widely depending on the lipid used [M. Brandl et al., Pharm. Pharmacol. Lett., 4 (1) 1-4, 1994]. This study has now been extended in two directions: Firstly, liposomes made of the same type of lipid but different batches of raw material were compared in terms of their influence on phagocytosis as well as for their contents of impurities. The test revealed great variability of RES suppression between different batches of hydrogenated soy PC, whereas the reproducibility of the carbon clearance test was satisfactory with liposomes made of a single batch of raw material. Thin layer chromatographic analyses of the used phosphatidylcholines (PCs) and limulus tests on lipopolysaccharides revealed lysophosphatidylcholine (lysoPC) as the only impurity which showed parallels with the observed differences in phagocytosis. Secondly by "spiking" phosphatidylcholine with increasing amounts of lysoPC the latter could be proven to enhance RES depression by liposomes in a dose-dependent manner. At the same time a strong and dose-limiting increase in acute toxicity of PC vesicles was observed with increasing contents of lysoPC. However, in cholesterol-containing vesicles lysoPC-spiking did not significantly alter their behaviour, for lysoPC contents of up to 10%. Only PC/cholesterol-vesicles containing lysoPC contents as high as 15% provoked enhanced RES depression and toxicity compared to lysoPC-free vesicles. LysoPC and cholesterol in liposomes are known to play a destabilizing and stabilizing role respectively within liposomal bilayers which might influence recognition and uptake of vesicles by macrophages and thus modulation of phagocytosis.

Acute toxicity and depression of phagocytosis in vivo by liposomes: Influence of lysophosphatidylcholine

Small unilamellar phospholipid vesicles (liposomes), intended as drug carriers, have recently been demonstrated to reversibly depress phagocytic activity in rats when injected in a single high dose (2g of lipid per kg body weight) as revealed by the carbon clearance test. Depression of the phagocytic function was found to vary widely depending on the lipid used [M. Brandl et al., Pharm. Pharmacol. Lett., 4 (1) 1–4, 1994]. This study has now been extended in two directions: Firstly, liposomes made of the same type of lipid but different batches of raw material were compared in terms of their influence on phagocytosis as well as for their contents of impurities. The test revealed great variability of RES suppression between different batches of hydrogenated soy PC, whereas the reproducibility of the carbon clearance test was satisfactory with liposomes made of a single batch of raw material. Thin layer chromatographic analyses of the used phosphatidylcholines (PCs) and limulus tests on lipopolysaccharides revealed lysophosphatidylcholine (lysoPC) as the only impurity which showed parallels with the observed differences in phagocytosis. Secondly by “spiking” phosphatidylcholine with increasing amounts of lysoPC the latter could be proven to enhance RES depression by liposomes in a dose-dependent manner. At the same time a strong and dose-limiting increase in acute toxicity of PC vesicles was observed with increasing contents of lysoPC. However, in cholesterol-containing vesicles lysoPC-spiking did not significantly alter their behaviour, for lysoPC contents of up to 10%. Only PC/cholesterol-vesicles containing lysoPC contents as high as 15% provoked enhanced RES depression and toxicity compared to lysoPC-free vesicles. LysoPC and cholesterol in liposomes are known to play a destabilizing and stabilizing role respectively within liposomal bilayers which might influence recognition and uptake of vesicles by macrophages and thus modulation of phagocytosis.

The effect of lysophosphatidylcholine on the activity of various mitochondrial enzymes

The influence of lysophosphatidylcholine (LPC) on H(+)-ATPase, cytochrome oxidase (COX), glycerolphosphate dehydrogenase (GPDH) and malate dehydrogenase (MDH) was followed. The activities of H(+)-ATPase and COX increased with increasing LPC concentration up to 0.5 mg/mg protein when maxima were achieved. This activatory effect is LPC-specific, because Lubrol-treated or frozen-thawed mitochondria showed lower activities of these enzymes. H(+)-ATPase was not influenced by higher concentration of LPC, while COX activity decreased with increasing amount of LPC. The activity of GPDH decreased at very low concentration of LPC and was not further modified at higher LPC concentration. In an attempt to find the concentration of LPC necessary for a complete permeabilization of inner mitochondrial membrane we followed the influence of lysolipid on the release of MDH activity from the mitochondrial matrix. The full activity of this enzyme was obtained with a concentration 0.75 mg LPC/mg protein indicating that mitochondria were completely broken. Our data indicate that LPC significantly affects activity of enzymes connected with mitochondrial membrane and can be useful for evaluation of the importance of phospholipid microenvironment for the enzyme function.

Influence of lysophosphatidylcholine on the C-apolipoprotein content of rat and human triglyceride-rich lipoproteins during triglyceride hydrolysis.

Remnants produced from rat chylomicrons in hepatectomized rats or from human chylomicrons by incubation in postheparin plasma contained much less C-apolipoproteins, but more lysophosphatidylcholine than the parent chylomicrons. A phospholipid-triglyceride emulsion absorbed C-apolipoproteins during incubation in serum, yet not in postheparin plasma, which led to lipid-hydrolysis and increased in lysophosphatidylcholine. The fraction d = 1.006-1.019 g/ml of human serum comprised more lysophosphatidylcholine and less C-apolipoproteins than the fraction d less than 1.006 g/ml. Injection of heparin induced hydrolysis with an increase in lysophosphatidylcholine and loss of C-apolipoproteins in both fractions. These inverse changes of lysophosphatidylcholine and C-apolipoproteins during lipid-hydrolysis suggest a causal relationship, which is strongly supported by the induction of loss of C-apolipoproteins from rat chylomicrons and human triglyceride-rich lipoproteins by addition of lysophosphatidylcholine in vitro. Apolipoprotein C-II was more affected than C-III. These results may elucidate a mechanism for the regulation of the termination of the triglyceride hydrolysis and the final hepatic uptake of remnants.

Lysophosphatidylcholine and taurodeoxycholate increase stomach permeability to different-sized molecules.

The influence of lysophosphatidylcholine (LPC), taurocholate (TC), and taurodeoxycholate (TDC) on gastric mucosal permeability was studied in a rat experimental model, with different-sized polyethylene glycols (PEGs) in the 722-1206-dalton range as permeability markers. Gastric mucosal morphology was also studied by transmission electron microscopy. We found that 2.5 mM and 5 mM LPC and TDC, but not TC, caused an increase in the passage of PEGs across the gastric mucosa. LPC altered the permeability significantly more than did TDC. Morphologically damaged intercellular microvillous structures could be seen after LPC treatment, whereas no obvious changes could be seen after TC or TDC treatment. These findings indicate that LPC and TDC may damage the gastric mucosa and enable permeation of molecules in the 722-1206-dalton range. Molecules within this range could potentially be toxic or antigenic, and this therefore represents an aspect of interest in the pathology of enterogastric reflux. Furthermore, the results indicate that dihydroxy secondary bile acids (TDC) have a more pronounced effect on gastric mucosal permeability than trihydroxy primary bile acids (TC).

Lysophosphatidylcholine potentiates the increase in mucosal permeability after small-intestinal ischaemia.

The influence of lysophosphatidylcholine (lysoPC), taurodeoxycholate (TDC), and taurochenodeoxycholate (TCDC) on the permeability properties of the ischaemic small-intestinal mucosa was investigated. We first studied the effect of ischaemia alone, then of lysoPC, TDC, or TCDC alone, and finally of ischaemia together with lysoPC, TDC, or TCDC on the permeability to sodium fluorescein in a ligated loop of the distal ileum in the rat. Longer periods of ischaemia alone (10 min or more) caused increased permeability, as did high concentrations (10 mM) of any of the agents. Low concentrations (1 mM) of lysoPC alone did not alter the gut permeability, but it significantly potentiated the increased permeability caused by 30 min of ischaemia. In contrast, 1 mM TDC or TCDC did not influence the permeability after 30 min of ischaemia. These findings imply that the ischaemic small intestine may be damaged by small amounts of lysoPC, with increased absorption of potentially pathogenic compounds as a possible consequence. They also point to the possibility that endogenously formed lysoPC may play a role in the mucosal damage and the increased permeability that occurs after small-intestinal ischaemia.

Cation permeability and mechanical properties of the erythrocyte membrane under the influence of lysophosphatidylcholine (LPC) in isotonic and hypotonic media.

The osmotic behaviour of erythrocytes under the influence of lysophosphatidylcholine (LPC) was investigated at temperatures of +4 degrees C and 20 degrees C by allowing them either to swell rapidly in hypotonic media in the presence of LPC or to swell gradually at first and then interact with LPC. Prelytic potassium release, the degree of hemolysis and the cell volume under various osmotic conditions were measured, together with the 'returning volumes', i.e. the volumes in an isotonic solution to which the cells returned from that in the hypotonic solution. LPC had a hemolyzing effect on erythrocytes in an isotonic medium and in slightly hypotonic media under all the osmotic conditions investigated, and the degree of hemolysis increased with increasing concentrations of LPC or decreasing temperatures, being greater during gradual than during rapid swelling. LPC also produced a prelytic leakage of potassium connected with the decrease in cell volume in an isotonic medium and in 'returning volumes' in all the media and under all the osmotic conditions investigated. The semipermeability of the membrane was preserved in all these cases, however, for osmotic swelling of the erythrocytes was observed, although to a lesser extent than without LPC. During rapid swelling both the curves for the prelytic potassium leakage and the degree of hemolysis were shifted towards more dilute solutions. Since the critical hemolytic volume was not increased, the shift in potassium leakage and hemolysis caused by LPC may be due to increased rigidity in the cell membrane. The curves for both potassium leakage and hemolysis shifted towards more concentrated solutions during gradual swelling, perhaps due to increased membrane fragmentation.

Influence of lysophosphatidylcholine on calcium exchange and membrane integrity in rabbit myocardium : M.A. Tones, P.A. Poole-Wilson. Cardiothoracic Institute, 2 Beaumont Street, London W1N 2DX, England

Influence of lysophosphatidylcholine on calcium exchange and membrane integrity in rabbit myocardium : M.A. Tones, P.A. Poole-Wilson. Cardiothoracic Institute, 2 Beaumont Street, London W1N 2DX, England

Influence of lysophosphatidylcholine on calcium exchange and membrane integrity in rabbit myocardium: M.A. Tones, P.A. Poole-Wilson. Cardiothoracic Institute, 2 Beaumont Street, London W1N 2DX, England

Influence of lysophosphatidylcholine on calcium exchange and membrane integrity in rabbit myocardium: M.A. Tones, P.A. Poole-Wilson. Cardiothoracic Institute, 2 Beaumont Street, London W1N 2DX, England

Influence of lysophosphatidylcholine on the metabolism of plasma lipoproteins

Both low density lipoproteins and cellular membranes are known to have a high affinity for lysophosphatidylcholine. In this study lysophosphatidylcholine influenced the retention of lipoproteins by arterial tissue in vitro and the rate of disappearance of low density lipoproteins from the blood in vivo. Pieces of aorta from rabbits or rhesus monkeys were successively incubated for 90 min each in 2 or 3 solutions. After the last incubation the intima plus inner media was dissected from the remainder of the aorta for analysis. The second incubation always contained lipoproteins labeled with [ 3H]leucine. When lysophosphatidylcholine was included in the first but not in the second incubation fluid, the retention of low, very low, or high density lipoproteins by the intima plus inner media increased. A subsequent incubation of the piece of artery in a fluid with trypsin or lysophosphatidylcholine caused a release of some of the lipoproteins. Lysophosphatidylcholine was bound simultaneously by plasma low density lipoproteins and vascular tissue in vitro and appeared to promote the association of the latter two components. When lysophosphatidylcholine equal to 2–10 times the usual total intravascular content was injected intravenously into control squirrel monkeys or rabbits, it was rapidly cleared from the blood. On the other hand, injected lysophosphatidylcholine persisted in the blood of hyperlipoproteinemic rabbits and was associated with the low density lipoproteins. In control animals, the injection of lysophosphatidylcholine was associated with an increase in the rate of removal of 125I-labelled low density lipoprotein from plasma and of its appearance in liver.