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Cholesterol lipid oxidation

Tart cherries Cirmamic acid derivatives, anthocyanins and flavonols dominate Raw and cooked beef patties Reduces secondary lipid oxidation and cholesterol oxidation products up to 90% Britt et al., 1998... [Pg.335]

In the laboratory, apples have been found to have very strong antioxidant activity, inhibit cancer cell proliferation, decrease lipid oxidation, and lower cholesterol (Boyer... [Pg.22]

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]

Lebovics, V.K. Farkas, J. Andrassy, E. Meszaros, L. Lugasi, A. Gaal, O. Reduction of Cholesterol and Lipid Oxidation in Radiation Decontaminated Mechanically Deboned Turkey Meat, Poster presented at the 48th ICoMST, Rome, 25-30 August 2002. [Pg.808]

Fats, see also Fatty acids Lipid Oxidation Lipids cholesterol... [Pg.760]

Shellfish, cholesterol content, 461 Silver, protein staining, 171-172,180,182, 199, 202, 204-205 Simple lipids, extraction of, 432 Single-substrate reaction, 333 Site-specific lipid oxidation of emulsions, 627... [Pg.766]

The effects of wine and its polyphenol constituents on early indicators of coronary heart disease such as elevated levels of plasma lipids, platelets and serum antioxidant activity were discussed in a review by Cooper et al. (2004). This review also addressed whether the polyphenols or alcohol are responsible for the beneficial effects of wine on cardio-vascular health. The authors conclude that red wine polyphenols have little effect on plasma lipid concentrations, but that wine consumption reduces the susceptibility of low-density lipoprotein (LDL) cholesterol to oxidation and increase serum antioxidant capacity. These effects, however, do depend on the amount of wine that is consumed and the period of supplementation. It was suggested that specific polyphenols appear to have endothelium-dependent vaso-relaxing abilities. Red wine phenolics also have an inhibitory effect on platelet aggregation. Evidence suggests that alcohol has a positive synergistic effect with wine polyphenols on some atherosclerosis risk factors. Thus, evidence that wine drinking is beneficial for cardiac health appears positive. [Pg.240]

Ahn, D.U., Nam, K.C., Du, M., Jo, C. 2001. Effect of irradiation and packaging conditions after cooking on the formation of cholesterol and lipid oxidation products in meats during storage. Meat Sci. 57, 413-418. [Pg.667]

Abstract. Content of cholesterol in various tissues of experimental animals (blood plasma, thoracal department of aorta, liver microsomes) was increased during atherogenesis depending on the level of aorta impairment. In atherogenesis content of both primary and secondary products of lipid peroxidation was also increased in microsomal membranes of rabbit and mini-pig liver tissue the increase in the rate of microsomal lipid oxidation was accompanied by a decrease in the activity of membrane-bound microsomal 7a-hydroxylase of cholesterol. [Pg.230]

Low-density lipoproteins contain numerous other lipid oxidation products apart from aldehydes that can participate in pathological events leading to atherosclerosis, or to modulation of gene expression. Indeed, oxidized derivatives of the major components of LDL, i.e., cholesterol and cholesterol esters, are of interest in this respect because they are consistendy foimd in human atherosclerotic lesions. [Pg.65]

It has now been recognized that oxidation of human LDL cholesterol by free radicals arising from lipid oxidation products maybe involved in the pathogenesis of atherosclerosis, and transition metal... [Pg.226]

Other oxidation products include epoxides that can arise from hydroperoxide rearranganent [25-27], but are also formed by enzymic processes [28,29], Products of lipid oxidation may be quantified after formation from simple lipids, for example, oxidation of cholesterol or PUFA. These lipids may be components of more complex lipids like cholesteryl esters [30] or PUFA-containing phospholipids [31]. An analysis of the oxidized products can be performed on the intact lipid or after the individual Upid components are separated by hydrolysis. [Pg.139]

Several oxysterol classes present in oxLDL appear to be cytotoxic toward fibroblasts, ECs, and vascular smooth muscle cells, especially 7-hydroperoxycholes-terol (7-OOH-chol), 7P- and 7a-hydroxycholesterol (7-OH-chol), 7-ketocholesterol (7-keto-chol), and cholesterol epoxides (epoxy-chol). 7p-OOH-chol, a precursor of hydroxyl- and keto-oxysterols, was reported to be the most toxic. During LDL oxidation 7P-OOH-chol was produced in three to five times higher quantities than 7a-OOH-chol, other oxysterols and even hydroxy-nonenal, which is one of the most abundant lipid oxidation products. Cytotoxicity of oxysterols was connected to increased cellular oxidative stress. Some studies suggest that oxysterols are even involved in oxidative stress induction. Animal models indicate that dietary oxysterols can significantly decrease glutathione levels and increase expression of glutathione peroxidase and superoxide dismutase. In apolipoprotein-deficient mice, the NADPH-oxidase activity was induced by 7-keto-chol, 7p-OH-chol, and Sp,6P-epoxy-chol. The increased activity of NADPH oxidase yields more superoxide anions that amplify oxidative stress. [Pg.164]

Holleboom AG, Daniil G, Fu X et al. Lipid oxidation in carriers of lecithin cholesterol acyltransferase gene mutations. Arteriosclemsis, Thrombosis, and Vascular Biology 2012 32 3066-3075. [Pg.306]

Cholesterol oxidation products are undoubtedly among the lipid oxidation products that most likely contribute to the development of atherosclerotic lesions in human large- and medium-sized arteries. They are known collectively as oxysterols, and their importance stems not only from the quantitative impact of cholesterol and its esters on the lipid-metabolism-dependent effects on atherosclerosis, but also from the various significant biochemical properties exhibited by this class of compounds. [Pg.309]

Egg PC/cholesterol /9-Carotene state 1527 cm-" resonance band 1400-1600 111527/I14401 reaches minimum at cholesterol/ lipid ratio of 0.9 indicating oxidation of carotene Verma and Wallach (1977)... [Pg.403]


See other pages where Cholesterol lipid oxidation is mentioned: [Pg.334]    [Pg.43]    [Pg.168]    [Pg.123]    [Pg.128]    [Pg.219]    [Pg.131]    [Pg.253]    [Pg.88]    [Pg.644]    [Pg.123]    [Pg.128]    [Pg.409]    [Pg.262]    [Pg.37]    [Pg.4]    [Pg.7]    [Pg.586]    [Pg.557]    [Pg.574]    [Pg.2743]    [Pg.95]    [Pg.85]    [Pg.5]    [Pg.453]    [Pg.137]    [Pg.9]    [Pg.11]    [Pg.14]    [Pg.242]    [Pg.243]    [Pg.315]    [Pg.323]   


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