Interaction between lecithins and cholesterol at the air-water and oil-water interfaces

Spread mixed monolayers at the air—water of cholesterol and phospholipids (dipalmitoyl lecithin and stearoyl-oleoyl lecithin) were investigated using the Goodrich method. It was found that a weak interaction occurred between cholesterol and dipalmitoyl lecithin, on the contrary a large interaction was observed for the system cholesterol, stearoyl-oleoyl lecithin. Recently a theory was developed concerning the ideal behaviour of mixed adsorbed films. Since at the oil—water interface mixed adsorbed monolayers of cholesterol and the above mentioned phospholipids show an ideal behaviour, the conclusion was drawn that the interaction at the air—water interface is mainly due to Van der Waals—London attraction forces

Permeability changes of erythrocytes and liposomes by 5-(n-alk(en)yl) resorcinols from rye

5-(n-Alk(en)yl) resorcinols can induce potassium release from liposomes and erythrocytes. The results suggest that 5-(n-pentyl)resorcinol can induce a specific permeability to protons as well as to potassium and other small molecules. The highest permeability changes were found in the presence of 5-(n-pentadecyl)resorcinol and alkenyl resorcinols. Orcin and resorcin were without effect. The size of permeant as investigated by turbidity measurements indicated that Ca2+ and Mg2+ cannot pass through the alkyl resorcinol-modified membrane but can pass through the alkenyl resorcinol-modified membrane. It was observed that alkenyl resorcinol at a concentration of 15 μM induced not only potassium release but also lysis of erythrocytes

The interaction energies of cholesterol and lecithin in spread mixed monolayers at the air-water interface

1. 1. The interaction between dilauroyl lecithin, diundecyloyl lecithin, didecanoyl lecithin and dinonanoyl lecithin with cholesterol was investigated using the Goodrich method. No interaction with cholesterol was found for dinonanoyl lecithin, while with didecanoyl lecithin small effects could be detected only at high surface pressure. Strong condensation effects occurred with diundecyloyl lecithin and dilauroyl lecithin. The pressure-area curves of these lecithins are given. 2. 2. Assuming a regular surface mixture, a theory was derived which allows one to describe the collapse pressure of a mixed monolayer with miscible components. 3. 3. The interaction between distearoyl lecithin, dipalmitoyl lecithin, dimyristoyl lecithin, dilauroyl lecithin, diundecyloyl lecithin, didecanoyl lecithin, dinonanoyl lecithin, oleoyl-stearoyl lecithin, dioleoyl lecithin and dilinoleoyl lecithin with cholesterol was investigated by measuring the collapse pressure of the mixed monolayers. An interaction parameter and interaction energies were calculated. 4. 4. According to this method distearoyl lecithin, dipalmitoyl lecithin, dinonanoyl lecithin and dilinoleoyl lecithin showed no interaction with cholesterol; while dimyristoyl lecithin, dilauroyl lecithin, diundecyloyl lecithin, oleoyl-stearoyl lecithin and dioleoyl lecithin interacted markedly with cholesterol. A small effect was observed for didecanoyl lecithin.The most pronounced effect was observed for dilauroyl lecithin and oleoyl-stearoyl lecithin. 5. 5. The results obtained using the Goodrich and collapse pressure methods are in good agreement

Interactions of hemin, antimalarial drugs and hemin-antimalarial complexes with phospholipid monolayers

Hemin, antimalarial drugs and complexes formed between them, have demonstrable effects on biological membranes. Using the phospholipid monolayer model, we show that hemin intercalates into the membrane and increases its surface pressure, depending on the lipid composition and the initial surface pressure: negative surface charges and particularly looser compaction of the phospholipids reduce the effect of hemin. With increasing surface pressure hemin tends to intercalate as a monomer, and the half-saturation concentration of its effect increases exponentially. The antimalarial monovalent drugs quinine and mefloquine, but not chloroquine, also penetrate into the membrane and expand it. All three drugs markedly increase the effect of hemin, but chloroquine reduces the effect in monolayers composed of unsaturated phospholipids. The drugs' effect is mostly due to an increase in the maximal surface pressure and suggests a complexation of hemin and drug within the membrane phase. Preformed hemin-drug complexes decrease the half-saturation concentration of the effect and suggest that the complexes adsorb to the membrane, releasing the hemin through an apolar continuum into the phospholipid phase. The implications of the results to the membrane toxicity mechanism proposed for the molecular mode of action of antimalarial drugs are discussed

The interaction energies of cholesterol and lecithin in spread mixed monolayers at the air-water interface

1. 1. The interaction between dilauroyl lecithin, diundecyloyl lecithin, didecanoyl lecithin and dinonanoyl lecithin with cholesterol was investigated using the Goodrich method. No interaction with cholesterol was found for dinonanoyl lecithin, while with didecanoyl lecithin small effects could be detected only at high surface pressure. Strong condensation effects occurred with diundecyloyl lecithin and dilauroyl lecithin. The pressure-area curves of these lecithins are given. 2. 2. Assuming a regular surface mixture, a theory was derived which allows one to describe the collapse pressure of a mixed monolayer with miscible components. 3. 3. The interaction between distearoyl lecithin, dipalmitoyl lecithin, dimyristoyl lecithin, dilauroyl lecithin, diundecyloyl lecithin, didecanoyl lecithin, dinonanoyl lecithin, oleoyl-stearoyl lecithin, dioleoyl lecithin and dilinoleoyl lecithin with cholesterol was investigated by measuring the collapse pressure of the mixed monolayers. An interaction parameter and interaction energies were calculated. 4. 4. According to this method distearoyl lecithin, dipalmitoyl lecithin, dinonanoyl lecithin and dilinoleoyl lecithin showed no interaction with cholesterol; while dimyristoyl lecithin, dilauroyl lecithin, diundecyloyl lecithin, oleoyl-stearoyl lecithin and dioleoyl lecithin interacted markedly with cholesterol. A small effect was observed for didecanoyl lecithin.The most pronounced effect was observed for dilauroyl lecithin and oleoyl-stearoyl lecithin. 5. 5. The results obtained using the Goodrich and collapse pressure methods are in good agreement

Penetration of lipid monolayers by psychoactive drugs

The ability of a number of psychoactive drugs to penetrate lipid monolayers of varying composition was examined, and the following observation were made: (1) The increase in surface pressure of a monomolecular film appeared to depend on the chemical nature of the lipid as well as on the initial film pressure. (2) Several psychoactive compounds showed a significant interaction with anionic lipid films at initial surface pressure above 18 dynes/cm. (3) The results support the view that coulombic attractions between cationic drugs and negatively changed lipids are involved. (4) Significant differences in the magnitude of the effect of different drugs on films of gangliosides are demonstrated

Interaction of plasma apolipoproteins with lipid monolayers

The monolayer technique has been used to study the interaction of lipids with plasma apolipoproteins. Apolipoprotein C-II and C-III from human very low density lipoproteins, apolipoprotein A-I from human high density lipoproteins and arginine-rich protein from swine very low density lipoproteins were studied. The injection of each apoprotein underneath a monolayer of egg phosphatidyl[14C]choline at 20 mN/m caused an increase in surface pressure to approximately 30 mN/m. With apolipoprotein C-II and apolipoprotein C-III there was a decrease in surface radioactivity indicating that the apoproteins were removing phospholipid from the interface; the removal of phospholipid was specific for apolipoprotein C-II and apolipoprotein C-III. Although there was a removal of phospholipid from the monolayer, the surface pressure remained constant and was due to the accumulation of apoprotein at the interface. The rate of surface radioactivity decrease was a function of protein concentration, required lipid in a fluid state and, of the lipids tested, was specific for phosphatidylcholine. Cholesterol and phosphatidylinositol were not removed from the interface. The addition of 33 mol% cholesterol to the phosphatidylcholine monolayer did not affect the removal of phospholipid by apolipoprotein C-III. The addition of phospholipid liposomes to the subphase greatly facilitated the apolipoprotein C-II-mediated removal of phospholipid from the interface

Lipoprotein lipase-catalyzed hydrolysis of tri[14C]oleoylglycerol in a phospholipid interface : A monolayer study

The lipoprotein lipase-catalyzed hydrolysis of triacylglycerol was determined in a lipid monolayer containing egg phosphatidylcholine and tri[14C]oleoylglycerol. In the presence of purified bovine milk lipoprotein lipase and fatty acid-free albumin, the rate of hydrolysis of tri[14C]oleoylglycerol, as determined by the decrease in surface activity, was dependent upon enzyme concentration and was enhanced by the addition of apolipoprotein C-II, the activator protein for the enzyme. Increasing the triacylglycerol content of the phospholipid monolayer from 1 to 6 mol% (relative to phospholipid) enhanced the rate of catalysis in the presence and absence of apolipoprotein C-II. However, at low substrate concentrations (less than 4 mol% tri[14C]oleoylglycerol), the activation factor for apolipoprotein C-II was greater than at high (4–6 mol%) triacylglycerol concentrations. The addition of sphingomyelin to the phosphatidylcholine monolayer decreased lipoprotein lipase activity. Based on these monolayer studies, we conclude that lipoprotein lipase catalyzes the hydrolysis of triacylglycerol at a phospholipid interface and that the rate of catalysis is dependent on the lipid composition of the monolayer

Interaction of plasma apolipoproteins with lipid monolayers

The monolayer technique has been used to study the interaction of lipids with plasma apolipoproteins. Apolipoprotein C-II and C-III from human very low density lipoproteins, apolipoprotein A-I from human high density lipoproteins and arginine-rich protein from swine very low density lipoproteins were studied. The injection of each apoprotein underneath a monolayer of egg phosphatidyl[14C]choline at 20 mN/m caused an increase in surface pressure to approximately 30 mN/m. With apolipoprotein C-II and apolipoprotein C-III there was a decrease in surface radioactivity indicating that the apoproteins were removing phospholipid from the interface; the removal of phospholipid was specific for apolipoprotein C-II and apolipoprotein C-III. Although there was a removal of phospholipid from the monolayer, the surface pressure remained constant and was due to the accumulation of apoprotein at the interface. The rate of surface radioactivity decrease was a function of protein concentration, required lipid in a fluid state and, of the lipids tested, was specific for phosphatidylcholine. Cholesterol and phosphatidylinositol were not removed from the interface. The addition of 33 mol% cholesterol to the phosphatidylcholine monolayer did not affect the removal of phospholipid by apolipoprotein C-III. The addition of phospholipid liposomes to the subphase greatly facilitated the apolipoprotein C-II-mediated removal of phospholipid from the interface