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Cholesteryl linoleate

Detection of cholesteryl linoleate hydroperoxides and phosphatidylcholine hydroperoxides 63... [Pg.219]

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. [Pg.810]

Figure 11.15 The reaction catalysed by lecithin cholesterol acyltransferase (LCAT). LinoLeate is transferred from a phospholipid in the blood to cholesterol to form cholesteryl linoleate, catalysed by LCAT. The cholesterol ester forms the core of HDL, which transfers cholesterol to the liver. Discoidal HDL (i.e. HDL3) is secreted by the liver and collects cholesterol from the peripheral tissues, especially endothellial cells (see Figure 22.10). Cholesterol is then esterified with lin-oleic acid and HDL changes its structure (HDL2) to a more stable form as shown in the lower part of the figure. R is linoleate. Figure 11.15 The reaction catalysed by lecithin cholesterol acyltransferase (LCAT). LinoLeate is transferred from a phospholipid in the blood to cholesterol to form cholesteryl linoleate, catalysed by LCAT. The cholesterol ester forms the core of HDL, which transfers cholesterol to the liver. Discoidal HDL (i.e. HDL3) is secreted by the liver and collects cholesterol from the peripheral tissues, especially endothellial cells (see Figure 22.10). Cholesterol is then esterified with lin-oleic acid and HDL changes its structure (HDL2) to a more stable form as shown in the lower part of the figure. R is linoleate.
At present the number of steroid 13C NMR studies on molecules of biological interest is very small. The spectra of cholesteryl linoleate alone and in aqueous codispersions of egg phosphatidylcholine have been reported. (37) Line width considerations are used to draw conclusions of steroid organization and molecular motion. These results have been compared with the changes in the spectra of human serum... [Pg.210]

ApoE mice Human femoral arteries Atherosclerosis MSI Mouse and human Phosphatidylcholine Cholesteryl linoleate Cholesterol oleate Human triacylglycerol (29)... [Pg.287]

The antiatherosclerotic effect of proanthocyanidin-rich grape seed extracts was examined in cholesterol-fed rabbits. The proanthocyanidin-rich extracts [0.1% and 1% in diets (w/w)] did not change the serum lipid profile, but reduced the level of the cholesteryl ester hydroperoxides (ChE-OOH) induced by 2,2/-azo-bis(2-amidinopropane-dihydrochloride (AAPH), the aortic malonaldehyde (MDA) content and severe atherosclerosis. The immuno-histochemical analysis revealed a decrease in the number of the oxidized LDL-positive macrophage-derived foam cells on the atherosclerotic lesions of the aorta in the rabbits fed the proanthocyanidin-rich extract. When the proanthocyanidin-rich extract was administered orally to the rats, proantho-cyanidin was detected in the plasma. In an in vitro experiment using human plasma, the addition of the proanthocyanidin-rich extract to the plasma inhibited the oxidation of cholesteryl linoleate in the LDL, but not in the LDL isolated after the plasma and the extract were incubated in advance. From these results, proanthocyanidins of the major polyphenols in red wine might trap ROSs in the plasma and interstitial fluid of the arterial wall, and consequently display antiatherosclerotic activity by inhibiting the oxidation of the LDL [92]. [Pg.36]

Figure 4. Normal phase high-pressure liquid chromatography of cholesterol esters isolated from atherosclerotic lesions of human aorta (I), free cholesterol (II), oxygenated cholesterol esters (III), cholesteryl arachidonate (IV), cholesteryl linoleate (V), cholesteryl oleate and cholesteryl palmitate. Figure 4. Normal phase high-pressure liquid chromatography of cholesterol esters isolated from atherosclerotic lesions of human aorta (I), free cholesterol (II), oxygenated cholesterol esters (III), cholesteryl arachidonate (IV), cholesteryl linoleate (V), cholesteryl oleate and cholesteryl palmitate.
W.A.Harland, l.D.Gilbert and C.Brooks, Lipids of human atheroma. Vlll. Oxidized derivatives of cholesteryl linoleate, Biochim.Biophys. Acta 316 (1973) 378-385. [Pg.230]

I]LDL [ H]Cholesteryl linoleate-labeled LDL Suppression of HMG-CoA reductase in 6 h Activation of cholesteryl ester formation in 6 h Suppression of LDL receptor activity in 48 h... [Pg.55]

Fig. 7. Oxidation of LDL phospholipids in the generation of minimally modified LDL. Seeding molecules like HPETE, HPODE, and cholesteryl linoleate hydroperoxide (CE-OOH) are proposed to trigger the oxidation of l-palmitoyl-2-arachidonoyl phosphatidylcholine in LDL, leading to the generation of three oxidized phosphatidylcholine species that confer atherogenic activity to minimally modified LDL. 12-LO, 12-lipoxygenase. Adapted from Ref. [28]. Reproduced with permission from the publisher. Fig. 7. Oxidation of LDL phospholipids in the generation of minimally modified LDL. Seeding molecules like HPETE, HPODE, and cholesteryl linoleate hydroperoxide (CE-OOH) are proposed to trigger the oxidation of l-palmitoyl-2-arachidonoyl phosphatidylcholine in LDL, leading to the generation of three oxidized phosphatidylcholine species that confer atherogenic activity to minimally modified LDL. 12-LO, 12-lipoxygenase. Adapted from Ref. [28]. Reproduced with permission from the publisher.
During a study, there has been evaluated the effect of supplementation with a low dose of co-3, obtained by olive oil, on the oxidative modification of low density lipoprotein (LDL) in a group of healthy volunteers, for 16 weeks. Oxidative modification of LDL was assessed measuring the concentrations of free cholesterol, cholesteryl esters and cholesteryl linoleate hydroperoxide in LDL, following copper-induced lipid peroxidation for 0, 2, 3 and 4 h. LDL eicosapentaenoic acid and docosahexaenoic acid compositions were significantly lower in the group treated with )-3 olive oil than the group treated with w-3 fish oil. [Pg.894]

The levels of palmitic acid, palmitoleic acid, stearic acid and oleic acid increased in both groups, after 4 h of copper-oxidation. While concentrations of cholesteryl oleate, cholesteryl linoleate, cholesteryl arachidonate and cholesteryl docosahexanoate were reduced, following copper stimulated oxidation, in both groups [85]. [Pg.894]

A round-bottomed flask was charged with 300 mg cholesteryl linoleate (0.462 mmol) and was diluted to 0.20 M with 0.876 mL 1,4-cyclohexadiene (9.26 mmol) and 1.43 mL dry benzene. DTBN (2 mg) was added to the solution, and the sealed flask was heated to 37°C under an oxygen atmosphere. After 24 h, TLC indicated the formation of peroxidic products. Butylated hydroxytoluene (BHT, 2 mg) was added to the reaction. Analytical HPLC (tandem silicon columns, 0.5% 2-propanol in hexanes, X = 234 nm) indicated the formation of four major components in the mixture 2, /r = 15.0 min 3, Jr = 17.5 min 4, fR = 20.1 min and 5, fR = 20.5 min. Semipreparative HPLC (0.66% 2-propanol in hexane) was used to separate the components. Compounds 4 and 5 were isolated as a mixture. [Pg.1441]

Angiotensin-11 type 1 receptor Cholesteryl linoleate Conjngated linoleic acid Carbonate radical Cyclooxygenase... [Pg.112]

Sevanian et al. (1994) applied GLC and LC/TS/MS for the analysis of plasma cholesterol-7-hydroperoxides and 7-ketocholesterol. Analysis of human and rabbit plasma identified the commonly occurring oxidation products, yet dramatic increases in 7-ketocholesterol and cholesterol-5p, 6P-epoxide were observed. The study failed to reveal the presence of choles-terol-7-hydroperoxides, which were either too unstable for isolation, metabolized or further decomposed. The principal ions of cholesterol oxides monitored by LC/TS/MS were m/z 438 (cholestane triol) m/z 401 (cholesterol-7-hydroperoxide) m/z 401 (7-ketocholesterol) m/z 367 (7a-hydroxycholesterol) m/z 399 (cholesta-3,5-dien-7-one) and m/z 385 (choles-terol-5a,6a-epoxide). The major ions were supported by minor ions consistent with the steroid structure. Kamido et al. (1992a, b) synthesized the cholesteryl 5-oxovaleroyl and 9-oxononanoyl esters as stable secondary oxidation products of cholesteryl arachidonate and linoleate, respectively. These compounds were identified as the 3,5-dinitrophenylhydrazone (DNPH) derivatives by reversed-phase LC/NICI/MS. These standards were used to identify cholesteryl and 7-ketocholesteryl 5-oxovaleroyl and 9-oxononanoyl esters as major components of the cholesteryl ester core aldehydes generated by copper-catalysed peroxidation of low-density lipoprotein (LDL). In addition to 9-oxoalkanoate (major product), minor amounts of the 8, 9, 10, 11 and 12 oxo-alkanoates were also identified among the peroxidation products of cholesteryl linoleate. Peroxidation of cholesteryl arachidonate yielded the 4, 6, 7, 8, 9 and 10 oxo-alkanoates of cholesterol as minor products. The oxysterols resulting from the peroxidation of the steroid ring were mainly 7-keto, 7a-hydroxy and 7P-... [Pg.193]

Both low-density lipoproteins (LDL) and high-density lipoproteins (HDL) consist of a core of triacylglycer-ols and cholesterol esters surrounded by a single phospholipid layer. Draw the structural formula of cholesteryl linoleate, one of the cholesterol esters found in this core. [Pg.670]

Figure 6.18. Coordination (Ag+) ion spray-mass spectrometry (CIS-MS) of oxidized cholesteryl linoleate showing heterolytic cleavage of silver adducts of cholesteryl linoleate hydroperoxides. Adapted from Havrilla et al (2000). Figure 6.18. Coordination (Ag+) ion spray-mass spectrometry (CIS-MS) of oxidized cholesteryl linoleate showing heterolytic cleavage of silver adducts of cholesteryl linoleate hydroperoxides. Adapted from Havrilla et al (2000).
FIGURE 4. Foam cell formation The effect of ascorbic acid and copper concentration. The culture of murine peritoneal macrophages with artificial lipoproteins composed of cholesteryl linoleate and bovine serum albumin (BSA) leads to foam cell formation which can be monitored by measuring the intracellular accumulation of the fluorescent lipopigment, ceroid. The effect of ascorbic acid (0-3 mM) and Cu (II) concentration (O-I xM) is shown. Reprinted with permission (Hunt et ai, 1992a). [Pg.378]


See other pages where Cholesteryl linoleate is mentioned: [Pg.163]    [Pg.29]    [Pg.782]    [Pg.782]    [Pg.785]    [Pg.236]    [Pg.693]    [Pg.693]    [Pg.30]    [Pg.783]    [Pg.783]    [Pg.786]    [Pg.184]    [Pg.1095]    [Pg.221]    [Pg.756]    [Pg.199]    [Pg.103]    [Pg.194]    [Pg.416]    [Pg.247]    [Pg.21]   
See also in sourсe #XX -- [ Pg.9 , Pg.456 , Pg.461 , Pg.464 , Pg.467 ]

See also in sourсe #XX -- [ Pg.9 , Pg.456 , Pg.461 , Pg.464 , Pg.467 ]

See also in sourсe #XX -- [ Pg.103 ]

See also in sourсe #XX -- [ Pg.194 ]




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Cholesteryl

Cholesteryl linoleate, hydroperoxide

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