Lysolecithin, formation

Bile salts apparently play a certain role in the development of acute pancreatitis. The flux of bile and bile acids into the pancreatic ducts activates phospholipase A, which may cause via lysolecithin formation autodigestion of pancreatic tissue. Bile acids may also act directly on pancreatic cells as toxic agents by producing coagulation necrosis (cf. 231). 

Lysolecithins act by dissolving cholesterol and cause massive losses of the sterol from membranes (19). Lysolecithins have been shown to cause the formation of openings 300-400 A in diameter in erythrocyte plasma membranes (20). Unlike saponins, lysolecithin membrane openings are permanent. 

The stimulatory effect of nonionic detergents on the sialyltransferase reactions may reflect an interaction of the hydrophobic environments of the active sites with the detergents, possibly by the insertion of the latter into the lipid bilayer surrounding the enzymes or by the formation of detergent-enzyme complexes, thus inducing more active enzyme conformations (51,52,53). The effect of nonionic detergents may be similar to the previously reported effects of phosphatidyl ethanolamine (34), CDP-choline and lysolecithin (54,55), phospho-diglycerol and cardiolipid (56). 

LCAT has three catalytic functions it acts as an acyltransferase (G9), a phospholipase (A25, P14), and a lysolecithin acyltransferase (S60). In this review only the acyltransferase action of LCAT will be discussed in any detail. The enzyme transfers the acyl group from the number two position of lecithin to the 3-hydroxyl group of cholesterol, resulting in the formation of cholesteryl ester and lysolecithin. 

Ohtsuru et al. (25) have recently investigated the behavior of phosphatidylcholine in a model system that simulated soy milk. They used spin-labelled phosphatidylcholine (PC ) synthesized from egg lysolecithin and 12-nitroxide stearic acid anhydride. The ESR spectrum of a mixture of PC (250 yg) and native soy protein (20 mg) homogenized in water by sonication resembled that observed for PC alone before sonication. However, when PC (250 yg) was sonicated in the presence of heat-denatured soy protein (20 mg), splitting of the ESR signal occurred. On this basis, they postulated the existence of two phases PC making up a fluid lamella phase and PC immobilized probably due to the hydrophobic interaction with the denatured protein. In a study of a soy-milk model, Ohtsuru et al. (25) reported that a ternary protein-oil-PC complex occurred when the three materials were subjected to sonication under the proper condition. Based on data from the ESR study, a schematic model has been proposed for the reversible formation-deformation of the ternary complex in soy milk (Figure 2). 

The mechanism of Ca2+ binding is not clear yet. However, increase in repulsive double layer forces between neutral diacylphosphatidylcholine bilayer in aqueous media in the presence of divalent ions has been identified by other methods as well [293-296]. These systems differ from the foam- film model by virtue of their interface ordered lipid phase/water in place of the air/water interface of foam films. Nevertheless, the CaCb concentration where the transition from NBF to silver films is observed in experiments with foam films is very close to the concentrations where increase in the distance between the bilayers was found [293,294,296]. Results with microscopic films are also in good agreement with the established increase in the free energy of formation of macroscopic films stabilised with lysolecithin in the presence of CaCl2 [287]. 

Sequential removal of the fatty acids by phospholipase action results in the formation of lysolecithin (glycerophosphorylcholine), then hydrolysis to release choline. Acetylcholine is synthesized in neurons using acetyl CoA. 

The digestion of triacylglycerols in adult nonruminant mammals has been described as initiated in the mouth by hngual lipase released in the sahva at the base of the tongue (52). Up to 6% of the fatty acids are hydrolyzed and initiate emulsion formation in the stomach. The digesta (called chyme at this location) is released from the stomach slowly into the duodenum to ensure complete mixing with the bile salts and emulsification. Lipolysis occurs by association of pancreatic lipase and co-lipase at the surface of the bile salt-stabihzed emulsion. Amphipathic molecules (fatty acids, sn-2 monoacylglycerols, and lysolecithins) are produced and associate with the bile salts to form water-soluble micelles from which absorption occurs. 

The triacylglycerols are incorporated into a heterogeneous population of spherical lipoprotein particles known as chylomicrons (diameter, 75-600 nm) that contain about 89% triacylglycerol, 8% phospholipid, 2% cholesterol, and 1 % protein. Phospholipids of the chylomicron arise by de novo synthesis (Chapter 19) or from reacylation of absorbed lysolecithin. Cholesterol is supplied by de novo synthesis (Chapter 19) or is absorbed. The protein apolipoprotein B-48 (apo B-48) forms a characteristic protein complement of chylomicrons and is synthesized in the enterocyte. Synthesis of apo B-48 is an obligatory step in chylomicron formation. Absence of apo B-48 synthesis, as in the rare hereditary disease abetalipoproteinemia,... 

This reaction is responsible for formation of most of the cholesteryl ester in plasma. The preferred substrate is phosphatidylcholine, which contains an unsaturated fatty acid residue on the 2-carbon of the glycerol moiety. HDL and LDL are the major sources of the phosphatidylcholine and cholesterol. Apo A-I, which is a part of HDL, is a powerful activator of LCAT. Apo C-I has also been implicated as an activator of this enzyme however, activation may depend on the nature of the phospholipid substrate. LCAT is synthesized in the liver. The plasma level of LCAT is higher in males than in females. The enzyme converts excess free cholesterol to cholesteryl ester with the simultaneous conversion of lecithin to lysolecithin. The products are subsequently removed from circulation. Thus, LCAT plays a significant role in the removal of cholesterol and lecithin from the circulation, similar to the role of lipoprotein lipase in the removal of triacylglycerol contained in chylomicrons and VLDL. Since LCAT regulates the levels of free cholesterol, cholesteryl esters, and phosphatidylcholine in plasma, it may play an important role in maintaining normal membrane structure and fluidity in peripheral tissue cells. 

Feldberg, W. Kellaway, C. H. (1938). Liberation of histamine and formation of lysolecithin-like substances by cobra venom. J. Physiol. 94,187-226. 

Laureth Laureth-9 phosphate Laurie acid Laurylpyridinium chloride Lysolecithin Magnesium dodecylbenzene sulfonate 4-(1-Methylethyl) cyclohexadiene-1-ethanol formate Myristalkonium chloride 2-Naphthalenesulfonic acid Naphthenic acid Nonoxynol-14 Nonoxynol-16 Nonoxynol-17 Nonoxynol-18 Nonoxynol-23 Nonoxynol-25 Nonoxynol-55 Nonoxynol-75 Nonoxynol-150 Nonoxynol-10 carboxylic acid Nonoxynol-3 phosphate Octadecene nitrile Octadecenyl succinic anhydride Octoxynol-4 Octoxynol-7... 

LCAT catalyzes the transfer reaction of unsaturated fatty acids in position II of lecithin (PC) to free cholesterol (FC), giving rise to the formation of CE and lysolecithin. LCAT does not act on artificial Upid emulsions containing PC and FC without any apoUpoprotein, but there exist some cofactors which catalyze the above reaction [1]. 

When P < 1/3, individual molecules are conically shaped, as shown in Figure 10. This results in the formation of spherical micelles in solution. As the volume of the hydrophobic tail is increased, P increases. For 1/3 < P < 1/2, nonspherical (cylindrical) micelles are formed. As P increases further, bilayer structures are formed. At P > 1, inverted structures are formed. This packing parameter can be used to rationalize why sodium dodecyl sulfate (SDS) forms spherical micelles in solution, while lysolecithin forms wormlike micelles. 

M. Rodbell, and L. D. Turner Enzymatic formation of monopalmitoleyl- and mono-palmitoyllecithin (lysolecithins). J. biol. Chem. 206, 431—41 (1954). 

Lecithinase A forms lysolecithin, a powerful hemolytic agent. The lysis of red blood cells resulting from the bite of a rattlesnake (Crotalus sp.) is due to the formation of lysolecithin by this enz3une. This enzyme is apparently the only one so far obtained in crystalhne form. ... 

Figure 6. Because the solubility of cholesterol in aqueous systems is low, its absorption depends on the formation of detergent structures (mixed micelles) in the small intestine. Initially, when dietary fat enters the stomach and passes into the small intestine, it takes the form of relatively large lipid droplets (shown in grey). Bile acids (shown in black) reduce the surface tension in the hpid droplets, leading to the formation of smaller structures (mixed micelles). Mixed micelles consist of an outer sheU of bile acids, monoacylglycerols, phospholipids and lysolecithin, and an inner core of digestion products of fats such as fatty acids, monoacylglycerols, cholesterol (of which 90% infreeform), andfat-soluble micronutrients.

Reichert, A., Ringsdorf, H. and Wagenknecht, A. (1992) Spontaneous domain formation of phospholipase A2 at interfaces fluorescence microscopy of the interaction of phospholipase A2 with mixed monolayers of lecithin, lysolecithin and fatty acid, Biochim. Biophys. Acta, submitted. 

It has been shown that bile acid conjugates have a protective effect against proteolytic inactivation of pancreatic cholesterol esterase (Vahouny ei al., 1965, 1967). Complete protection against inactivation was provided by 3a,12a-dihydroxy and 3o ,7a,12a-trihydroxycholanate. The protective effect seems to be due to the formation of a specific bile salt enzyme complex. Phospholipase A, another pancreatic enzyme, is activated by bile acid conjugates (Magee et al., 1962). This enzyme removes a fatty acid moiety from lecithin, giving lysolecithin. This hydrolysis of lecithin is of importance for the intestinal absorption of this phosphatide (Nilsson and Bergstrom, 1967 Nilsson, 1968). 

---