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Lipoproteins PUFA oxidation

About half of all fatty acids are PUFAs. The major PUFA is linoleic acid (18 3) that is about 7 times more frequent than arachidonic (20 4) or doc-osahexaenoic acids (22 6) (J9). Many of the products that have been measured are largely from arachidonic acid that represents a minor constituent of the lipoproteins. Each oxidation product listed in Table 1 is considered in the following text, and apparent normal reference ranges for some of them are listed in Table 2 along with the source from which the information was derived. [Pg.10]

The long-term influence of omega-3 fatty acid supplements is not known, and, for this reason, the American Heart Association has not recommended that supplements be taken (Krauss et al., 19%). There is a very real concern that dietary PUFAs of all types may enhance the accumulation of lipid oxidation products in lipoprotein particles, thus allowing the attack of lipid oxidation products on the protein component of the LDL, the enhanced uptake of the damaged LDL by macrophages in the artery wall, and increased atherosclerosis (Allard et al., 1997 Felton et al., 1994). (Monoimsaturated fatty acids are thought not to be involved in the oxidation scenario leading to atherosclerosis.)... [Pg.643]

Oxidation of polyunsaturated fatty acids (PUFA) in lipoproteins may be mediated by reactive species such as radicals, transition metals, other electrophiles, and by enzymes. Once initiated, oxidation of lipids may proceed by a chain reaction, illustrated in Fig. 4 (R5). In step I, an oxidant captures an electron from a PUFA to produce a lipid radical. In step 2, after rearrangement, the conjugated diene radical reacts rapidly with singlet oxygen to produce a lipid peroxide radical, which is the kinetically preferred reaction (step 3) (B5). The chain can be terminated if the lipid radical reacts with an antioxidant to produce a stable peroxide (step 4). Otherwise, the peroxyl radical can react with another polyunsaturated fatty acid as shown in step 5 to perpetuate a chain reaction. The chain reaction requires production of lipid peroxides, giving it the name peroxidation. Fatty acids oxidized in the core are largely triglycerides and cholesterol esters, while toward the outer layer fatty acids in phospholipids are oxidized. [Pg.8]

For these reasons, and because they can be measured in urine and plasma, PGF are generally considered to offer a noninvasive, sensitive, specific direct method for measuring lipid peroxidation in vivo (Y1). The main drawback is that the methods are very complicated, tedious, and not usually available in clinical laboratories. Like other lipid oxidation products, PGF can be generated ex vivo. For this reason, fluids should be preserved with butylated hydroxy toluene (BHT) and EDTA to prevent further oxidation and measured immediately or stored at —70°C (M8). An ELISA has been developed for urine for 8-Iso-PGF2a that is commercially available (02), but the method is tedious since it requires a column separation prior to ELISA (Bl). Also, since PGF are mainly indicators of arachidonic acid oxidation, they do not reflect oxidation of the major PUFA comprising lipoproteins. [Pg.11]

HODEs are primarily Cl8 oxidation products of linoleic acid (J9). These have not been as widely studied as isoprostanes, but like isoprostanes, these are specific products of nonenzymatic lipid peroxidation that are associated with arteriosclerotic disease and are found in arteriosclerotic plaques (J9, W2). Likewise, they are measured by specific GC/MS techniques that are generally not available in clinical laboratories (JIO). They have the advantage that they are products of the major PUFA in lipoproteins—linoleic acid— but they have generally been measured only in lipoproteins extracted from plasma. [Pg.11]

Amino acid residues are potential targets of free radical oxidation and nitration. Carbonyl derivatives of proteins may be formed by the interaction of protein amino acid side chains, mainly cysteine, histidine, and lysine residues with reactive aldehydes, such as HNE and ONE generated by peroxidation of PUFAs (polyunsaturated fatty acids). Amino acid and peptide biomarkers of oxidative stress are typically focused on specific proteins related to disease pathology. For instance, the oxidation of histidine and methionine are typically discussed in (3-amyloid plaque formation and HNE-derived histidine adducts are the main focus of modifications on low-density lipoprotein (LDL) (An-nangudi et al., 2008). However, there are several specific examples of general biomarkers of oxidative stress that include endogenous histidine containing dipeptides such as carnosine and anserine as well as the very stable o,o -dityrosine. These will be discussed below. [Pg.659]

SDG directly lowers serum cholesterol. Because lignans modulate the enzymes 7-hydroxylase and acyl CoA cholesterol transferase, they may be able to decrease serum cholesterol, as both of these enzymes are involved in cholesterol metabolism. Lignans may also lower oxidative stress. Enterodiol, enterolactone, and SDG act as antioxidants by inhibiting the peroxidation of PUFA in vitro at levels that may be achievable in vivo. Inhibiting peroxidation of PUFA may decrease oxidation of low-density lipoprotein, a key player in atherogenesis. Finally, SDG has been reported to act as an antagonist of platelet-activating factor (PAF) [58]. [Pg.66]


See other pages where Lipoproteins PUFA oxidation is mentioned: [Pg.764]    [Pg.446]    [Pg.134]    [Pg.474]    [Pg.641]    [Pg.409]    [Pg.552]    [Pg.623]    [Pg.632]    [Pg.636]    [Pg.1450]    [Pg.3179]    [Pg.242]    [Pg.330]    [Pg.25]    [Pg.157]    [Pg.21]    [Pg.253]    [Pg.302]    [Pg.253]    [Pg.21]    [Pg.165]    [Pg.188]    [Pg.189]   
See also in sourсe #XX -- [ Pg.8 , Pg.9 ]




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