Fatty acids cholesteryl esters

Hydrocarbons Triacylglycerols Mono-, diacylglycerols Free fatty acids Cholesteryl esters Cholesterol Phospholipids... 

The inert beta layers of the cell membrane complex are Upid-protein-type structures [78]. Sakamoto et al. [83] claim that fatty acids and wax esters are the main components of the internal lipids of human hair. Hilter-haus-Bong and Zahn [84] also find fatty acids, cholesteryl esters, and wax esters as main components however, they find polar lipids as major components. The fatty acids of this important component of human hair are predominately palmitic, stearic, and oleic acids. 

Figure 35.13 Cholesteryl ester. When cholesterol is esterifled with a fatty acid, cholesteryl ester is formed.

Specific chemical detection tests play an important role in identifying lipid components. From a practical standpoint, Kates (1986) has provided excellent guidelines for specific chemical identification tests. Specific chemical tests are very helpful in the determination of cholesterol, free fatty acids, cholesteryl esters, and several phospholipids. Experiment 6 employs specific chemical detection tests in TLC analysis. 

Cholesterol is the major sterol in the body and occurs mainly as the nonesterified free form, which is a fundamental component of cell membranes and the precursor for steroid hormones and bile acids. Cholesteryl esters present in the tissues and plasma are mainly formed by cholesterol esterification with long chain fatty acids these cholesterol esters act as a storage pool. Most of the requirements for cholesterol are met by endogenous synthesis, mainly in the liver, with the exogenous supplementation from the diet. 

Trade Names Containing C-1218D DREWPOL 10-10-0 Phosal 53 MCT Pro-tachem 35-A Servamlne KOO 330 Oleic acid aluminum saK. See Aluminum oleate Oleic acid amide. SeeOleamide Oleic acid ammonium saH. See Ammonium oleate Oleic acid calcium saH. See Calcium oleate Oleic acid cholesteryl ester. See Cholesteryl oleate Oleic acid, compound with N-octadec-9-enylpropane-1,3-diamine (2 1). See Fatty diamine dioleate... 

Cholesterol (Figure 14-17) is widely distributed in all cells of the body but particularly in nervous tissue. It is a major constituent of the plasma membrane and of plasma lipoproteins. It is often found as cholesteryl ester, where the hydroxyl group on position 3 is esteri-fied with a long-chain fatty acid. It occurs in animals but not in plants. 

Plasma lipids consist of triacylglycerols (16%), phospholipids (30%), cholesterol (14%), and cholesteryl esters (36%) and a much smaller fraction of unesteri-fied long-chain fatty acids (free fatty acids) (4%). This latter fraction, the free fatty acids (FFA), is metaboh-cally the most active of the plasma hpids. 

FIGURE 12.4 (A) Diagrammatic representation of the separation of major simple lipid classes on silica gel TLC — solvent system hexane diethylether formic acid (80 20 2) (CE = cholesteryl esters, WE = wax esters, HC = hydrocarbon, EEA = free fatty acids, TG = triacylglycerol, CHO = cholesterol, DG = diacylglycerol, PL = phospholipids and other complex lipids). (B) Diagrammatic representation of the separation of major phospholipids on silica gel TLC — solvent sytem chloroform methanol water (70 30 3) (PA = phosphatidic acid, PE = phosphatidylethanolamine, PS = phosphatidylserine, PC = phosphatidylcholine, SPM = sphingomyelin, LPC = Lysophosphatidylcholine). 

LOX-catalyzed oxidation of LDL has been studied in subsequent studies [26,27]. Belkner et al. [27] showed that LOX-catalyzed LDL oxidation was not restricted to the oxidation of lipids but also resulted in the cooxidative modification of apoproteins. It is known that LOX-catalyzed LDL oxidation is regio- and enantio-specific as opposed to free radical-mediated lipid peroxidation. In accord with this proposal Yamashita et al. [28] showed that LDL oxidation by 15-LOX from rabbit reticulocytes formed hydroperoxides of phosphatidylcholine and cholesteryl esters regio-, stereo-, and enantio-specifically. Sigari et al. [29] demonstrated that fibroblasts with overexpressed 15-LOX produced bioactive minimally modified LDL, which is probably responsible for LDL atherogenic effect in vivo. Ezaki et al. [30] found that the incubation of LDL with 15-LOX-overexpressed fibroblasts resulted in a sharp increase in the cholesteryl ester hydroperoxide level and a lesser increase in free fatty acid hydroperoxides. 

Belkner et al. [32] demonstrated that 15-LOX oxidized preferably LDL cholesterol esters. Even in the presence of free linoleic acid, cholesteryl linoleate continued to be a major LOX substrate. It was also found that the depletion of LDL from a-tocopherol has not prevented the LDL oxidation. This is of a special interest in connection with the role of a-tocopherol in LDL oxidation. As the majority of cholesteryl esters is normally buried in the core of a lipoprotein particle and cannot be directly oxidized by LOX, it has been suggested that LDL oxidation might be initiated by a-tocopheryl radical formed during the oxidation of a-tocopherol [33,34]. Correspondingly, it was concluded that the oxidation of LDL by soybean and recombinant human 15-LOXs may occur by two pathways (a) LDL-free fatty acids are oxidized enzymatically with the formation of a-tocopheryl radical, and (b) the a-tocopheryl-mediated oxidation of cholesteryl esters occurs via a nonenzymatic way. Pro and con proofs related to the prooxidant role of a-tocopherol were considered in Chapter 25 in connection with the study of nonenzymatic lipid oxidation and in Chapter 29 dedicated to antioxidants. It should be stressed that comparison of the possible effects of a-tocopherol and nitric oxide on LDL oxidation does not support importance of a-tocopherol prooxidant activity. It should be mentioned that the above data describing the activity of cholesteryl esters in LDL oxidation are in contradiction with some earlier results. Thus in 1988, Sparrow et al. [35] suggested that the 15-LOX-catalyzed oxidation of LDL is accelerated in the presence of phospholipase A2, i.e., the hydrolysis of cholesterol esters is an important step in LDL oxidation. 

Finally, dyslipidemia is a feature of FXR knockout mice levels of VLDL, LDL and HDL cholesterol and ApoB lipoproteins are increased concomitant with reduced clearance of HDL cholesteryl ester and elevated triglyceride and free fatty-acid levels. ... 

Cholesteryl esters are synthesized by combining free cholesterol with a fatty acid. 

C. Most plasma cholesterol is esterified to fatty acids and is thus highly water-insoluble. These cholesteryl esters circulate in complexes with the lipoproteins. 

HDL particles extract cholesterol from peripheral membranes and, after esterification of cholesterol to a fatty acid, the cholesteryl esters are delivered to the liver (to make bile salts) or steroidogenic tissues (precursor of steroids). 

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