Phosphatidylcholine surface activity

Phospholipids are amphiphilic compoimds with high surface activity. They can significantly influence the physical properties of emulsions and foams used in the food industry. Rodriguez Patino et al. (2007) investigated structural, morphological, and surface rheology of dipalmitoylpho-sphatidylcholine (DPPC) and dioleoyl phosphatidylcholine (DOPC) monolayers at air-water interface. DPPC monolayers showed structural polymorphisms at the air-water interface as a function of surface pressure and the pH of the aqueous phase (Fig. 6.18). DOPC monolayers showed a... 

We found these conditions by introducing surface-active materials to a solution of a specially prepared catalytic complex containing molybdenum and stabilized by magnesium ions [22]. The structure of the complex which was isolated from the solution in its oxidized form is presented on Figure 5 [23]. When it is reduced to the Mo state the complex becomes an active catalyst of dinitrogen reduction to hydrazine and ammonia by sodium amalgam. Phospholipid (phosphatidylcholine)... 

Type II pneumocytes isolated from the lungs of rnide rats by treatment with elastase, discontinuous density centrifugation, and adherence in primary culture, after P-adrenergic stimulation (10/iM l-epinephrine, L-isoprenaline, OL-terbutaline, respectively) released significantly increased quantities of [ Cldisaturated phosphatidylcholine, the major component of surface-active material (Dobbs and Mason 1979). 

Surfactant is a lipid-protein complex that is synthesized and released hy alveolar type II epithelial cells. This complex surface-active compound contains both hydrophobic and hydrophilic regions to allow the molecule to spontaneously adsorb to and form monolayers along the air-liquid interface. The role of surfactant in pulmonary fluid mechanics depends on its natural ability to disrupt intermolecular forces by interfering with the attractive forces between water molecules at the interfacial surface—thus lowering the surface tension. While this surfactant mixture is largely comprised of lipids (90%), the surfactant proteins (10%) are required for normal function (Hall et al. 1992 Yu and Possmayer 1993). Finally, the molecule dipalmitoyl phosphatidylcholine (DPPC) makes up 80% of the phospholipid and is largely responsible for the ultra-low surface tensions necessary for respiratory function (<5 dyn/cm) (Klaus et al. 1961 Hawco et al. 1981 Tchoreloff et al. 1991). 

The peculiar electrochemical behaviour of electrode surfaces coated with a layer of phosphatidylcholine (PC) adds a new dimension to the practical applications of this type of sensor as it enables development of electrochemical processes within a lipid layer. Redox-active amphiphiles readily... 

LCAT catalyzes the transfer of a preferentially unesterified fatty acid from the sn-2 position of phosphatidylcholine to the 3/i-hydroxy group of cholesterol, and thereby produces lysophosphatidylcholine and a cholesteryl ester [50]. Depending on the mutation in the LCAT gene, homozygous or compound heterozygous patients present with one of two clinical phenotypes, classical LCAT deficiency or fish-eye disease [58, 85]. Classical LCAT deficiency is caused by a broad spectrum of missense and non-sense mutations that interfere with the synthesis or secretion or affect the catalytic activity of LCAT [10]. Fish-eye disease is caused by a limited number of missense point mutations that alter the surface polarity, and thereby interfere with the binding of the enzyme to apoA-I containing lipoproteins [77]). 

Arachidonic acid is not present in significant amounts in tissues as the free acid but is stored as a fatty acid at the sn-2 position of phospholipids. Prostaglandin biosynthesis is initiated by the interaction of a stimulus with the cell surface. Depending on the cell type, the stimulus can take the form of a hormone, such as angiotensin II or antidiuretic hormone, or a protease such as thrombin (involved in blood clotting), or both hormone and protease. These agents bind to a specific receptor that activates a phospholipase A2 that specifically releases the arachidonic acid from a phospholipid such as phosphatidylcholine. The release of arachidonic acid by phospholipase A2 is believed to be the rate-limiting step for the biosynthesis of eicosanoids. 

Unlike fatty acids, cholesterol is not degraded to yield energy. Instead excess cholesterol is removed from tissues by HDL for delivery to the liver from which it is excreted in the form of bile salts into the intestine. The transfer of cholesterol from extrahepatic tissues to the liver is called reverse cholesterol transport. When HDL is secreted into the plasma from the liver, it has a discoidal shape and is almost devoid of cholesteryl ester. These newly formed HDL particles are good acceptors for cholesterol in the plasma membranes of cells and are converted into spherical particles by the accumulation of cholesteryl ester. The cholesteryl ester is derived from a reaction between cholesterol and phosphatidylcholine on the surface of the HDL particle catalyzed by lecithimcholesterol acyltransferase (LCAT) (fig. 20.17). LCAT is associated with FIDL in plasma and is activated by apoprotein A-I, a component of HDL (see table 20.3). Associated with the LCAT-HDL complex is cholesteryl ester transfer protein, which catalyzes the transfer of cholesteryl esters from HDL to VLDL or LDL. In the steady state, cholesteryl esters that are synthesized by LCAT are transferred to LDL and VLDL and are catabolized as noted earlier. The HDL particles themselves turn over, but how they are degraded is not firmly established. 

During the surge in interest in the phosphatidylinositol derivatives, Takai et al. (1979) noted that an unsaturated diacylglycerol diminished the Ca2+ and phospholipid concentration required for complete activation of a Ca2+-activated, phospholipid-dependent protein kinase (now known as protein kinase C). In this latter system, phosphatidylserine was most active (as the required phospholipid), with phosphatidylethanolamine and phosphatidyl inositol much less effective and phosphatidylcholine without any activity. Probably the enzyme was activated by an amphipathic molecule bearing a net negative charge, and any available cellular phospholipid mixture with the requisite surface change served this purpose. 

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