Synthesis of lecithin

The internal synthesis of lecithin in lecithin liposomes would be a signihcant step forwards. In parhcular, it would be very intereshng to see, given a certain excess of the enzymes, for how many generahons the cell self-reproduction could go on. It is clear, however, that after a certain number of generations, the system would undergo death by dilution. ... 

Both the a,/3-diglyceride and the phosphatidic acid may be used for the synthesis of phospholipids. The choline and ethanolamine required respectively for the synthesis of lecithins and cephalins must be available in an active form as their cytidine diphosphate derivatives. 

Sphingomyelin. Weiss and Kennedy (1956) have described the synthesis of lecithin from CDP-choline and a diglyceride. An analogous reaction was reported by Sribney and Kennedy (1958) to be involved in the biosynthesis of sphingomyelin. This reaction is formulated below ... 

Lecithin—This is an important constituent of bile which helps to keep cholesterol in solution. It is not generally considered to be an essential nutrient because it is thought that the body is able to synthesize the amounts it needs. However, some patients afflicted with gallstones have low levels of lecithin in their bile. Insufficient biliary lecithin may be due to dietary deficiencies of protein, vitamins, choline, and other nutrients which are involved in the synthesis of lecithin by the body. 

Lysolecithin, because of its cyto- and possibly myelinolytic effect, has been searched for and found in small quantities in normal white matter and MS plaques [135, 136]. It may represent an intermediary in the synthesis of lecithin [137]. It could be, however, a product of autolysis [138] since it accumulates in rat brain slices on incubation in vitro [139]. It was not, however, found in MS white matter in other investigations [134]. 

Enzymic hydrolysis of aminoethylphosphoric acid in the tissues is presumably followed by utilization of the inorganic phosphate for synthesis of lecithin and of demethylation of lecithin to form cephalin. The aminoethylphosphoric acid normally occurring in the body tissue may be a product of catabolism of cephalin. 

One of the most promising applications of enzyme-immobilized mesoporous materials is as microscopic reactors. Galameau et al. investigated the effect of mesoporous silica structures and their surface natures on the activity of immobilized lipases [199]. Too hydrophilic (pure silica) or too hydrophobic (butyl-grafted silica) supports are not appropriate for the development of high activity for lipases. An adequate hydrophobic/hydrophilic balance of the support, such as a supported-micelle, provides the best route to enhance lipase activity. They also encapsulated the lipases in sponge mesoporous silicates, a new procedure based on the addition of a mixture of lecithin and amines to a sol-gel synthesis to provide pore-size control. 

Fig. 2 Synthesis of facetted nanoparticles showing change in the color and nature of the sample with time and showing the phase separation observed in the isooctane/AOT (0.8 M)/Lecithin (0.4 M)/HAuCl4 (0.01 M) sample after 4 months...

The metabolism of HDL probably involves interaction with both hepatic and peripheral cells, as well as with other lipoproteins. HDL may remove cholesterol from tissues, the "scavenger hypothesis (11,12). The cholesterol may then be esterifed by the action of lecithin cholesterol acyl transferase. HDL may provide cholesterol to the liver for bile acid synthesis (13) and some HDL may be catabolized by the liver in the process. HDL has not been found to interfere with the binding of LDL in cultured human fibroblasts (6). However, in cultured human arterial cells, porcine or rat hepatocytes, and rat adrenal gland, there appears to be some competition of HDL with LDL binding sites, suggesting the presence of a "lipoprotein-binding" site (14). 

Figure 3.17 (Top) Transmission electron micrographs of mesoporous silica materials prepared by adding increasing amounts of lecithin to a typical MCM-41 synthesis solution. This biomolecule induces the formation of circular-shaped mesopores. (Bottom) A plausible scheme of the...

A few words about HDL these lipoproteins are synthesized largely by the liver. They act as ApoE, ApoC, and ApoA traffickers, but in addition, they also serve as a factory for the synthesis of cholesterol esters. HDL may absorb free cholesterol from various peripheral tissues, including arteries. Cholesterol is then converted to a large extent to fatty acyl esters by the action of the enzyme lecithin-cholesterol acyltransferase [LCAT see Equation 19.2)]. LCAT is activated by ApoA-I. Inactive LCAT is a plasma component. 

Commercially, tocopherol is available as a pure all-rac-a-tocopherol, mixed tocopherols having various contents of a-, p-, y-, or 8-tocopherols (diluted in vegetable oil) and synergistic mixtures containing tocopherols, ascorbyl palmitate or other antioxidants, and synergists such as lecithin, citric acid, and carriers. Extraction of tocopherols from natural sources and chemical synthesis of tocopherols are well described by Schuler (100). 

Liver health. As noted above, a biomarker of choline deficiency is elevated serum ALT levels, which is an indication of liver damage. One of the many functions of the liver is its role in fat metabolism. Without PC, the liver is unable to synthesize lipoproteins. Of particular importance in liver is the synthesis of very low-density lipoproteins (VLDL). With diminished VLDL production, the liver is not able to export lipid. This results in an accumulation of fat in the liver. Lipid accumulation in the liver leads to various stages of liver disease such as liver cell death, fibrosis, cirrhosis, and liver cancer (248-250). The role of choline in liver disease was underscored in the early 1990s when it was determined that patients on extended total parental nutrition (TPN) treatment developed fatty livers (251). At that time, TPN formulas did not include choline. Adding choline (in the form of lecithin) to TPN formulas reversed fatty buildup in these patients, and a... 

Lecithin plays an important role in the transport of fats and cholesterol from the liver to sites where they can be either used or stored. Since fats do not dissolve in water solutions like blood plasma, they are transported in spherical particles called lipoproteins. These particles can mix with water solutions because the water-friendly proteins, cholesterol and phospholipids are on the outside surface. The nonpolar fats associated with them make up the core, which is unexposed to water. Because lecithin is required for lipoprotein synthesis, a lecithin deficiency results in fats accumulating in the liver and leads to liver damage. Lecithin deficiency also leads to increased amounts of cholesterol in the blood and atherosclerosis, a disease in which narrowing of the arteries is caused primarily by the deposit of fats from the bloodstream. 

Cholesterol is formed in the liver (85%) and intestine (12%) - this constitutes 97% of the body s cholesterol synthesis of 3.2 mmol/day (= 1.25 g/day). Serum cholesterol is esterized to an extent of 70-80% with fatty acids (ca. 53% linolic acid, ca 23% oleic acid, ca 12% palmitic acid). The cholesterol pool (distributed in the liver, plasma and erythrocytes) is 5.16 mmol/day (= 2.0 g/day). Homocysteine stimulates the production of cholesterol in the liver cells as well as its subsequent secretion. Cholesterol may be removed from the pool by being channelled into the bile or, as VLDL and HDL particles, into the plasma. The key enzyme in the synthesis of cholesterol is hydroxy-methyl-glutaryl-CoA reductase (HGM-CoA reductase), which has a half-life of only 3 hours. Cholesterol is produced via the intermediate stages of mevalonate, squalene and lanosterol. Cholesterol esters are formed in the plasma by the linking of a lecithin fatty acid to free cholesterol (by means of LCAT) with the simultaneous release of lysolecithin. (s. figs. 3.8, 3.9) (s. tab. 3.8)... 

Choline (N,N,N-trimethyl-y6-hydroxyethylamine) is an important constituent of phospholipids (lecithin is phosphatidylcholine) and of acetylcholine. It can be completely synthesized from serine (Chapter 19), but only in the form of phosphatidylserine and then only when the dietary supply of amino acids is adequate. Betaine (N,N,N-trimethylglycine) readily replaces dietary choline for all species. Choline is conserved by a salvage pathway. In the lung, this salvage route is the principal route for the synthesis of the phosphatidylcholine needed as a surfactant (see Chapter 19). 

The liver is responsible for synthesis of cholesterol, high-density lipoproteins, and very-low-density lipoproteins. The enzymes lipoprotein lipase and lecithin-cholesterol acyltransferase also are synthesized in this organ. Increased serum triglyceride and FFA concentrations are encountered in patients with hepatic failure, primarily due to the increased lipolysis. The significant insulin resistance that can be seen in cirrhosis causes a shift to lipids as a fuel source. Whereas only 35% of total calories are derived from fat in normal patients after an overnight fast, this can increase to 75% in patients with cirrhosis. Incorporation of late evening snacks in patients with liver cirrhosis may correct abnormal substrate metabolism, increase carbohydrate, and decrease fat oxidation rates. ... 

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