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Lipid peroxidation isoprostane

One approach to determination of whole-body lipid peroxidation has been measurement of exhaled hydrocarbons by GLC, especially ethane. Hydrocarbon gases are, however, minor end-products of peroxidation and their formation depends on the decomposition of peroxide. Recent studies have demonstrated that isoprostane is a good biomarker of lipid peroxidation in the human body. Isoprostanes are specific products arising from the peroxidation of unsaturated fatty acid residues in lipids and detection of them and their metabolites in urine is a useful assay of whole-body lipid peroxidation. Isoprostanes can be accurately and sensitively measured by mass spec-trometric techniques. [Pg.1545]

A major drawback of this study was that we measured lipid peroxidation ex vivo, but not in vivo using the latest and most promising methods such as F2 isoprostanes (Roberts and Morrow, 2000). However, we are planning to do that soon, so hopefully future studies will bring us more detailed information about the effects of phloem on lipid peroxidation. In conclusion, our study showed that lignans are bioavailable from the wood matrix, that long-term consumption of phloem is safe and that ingestion of phloem can inhibit lipid peroxidation in humans. [Pg.293]

VANHARANTA M, VOUTILAINEN S, NURMI T, KAIKKONEN J, ROBERTS L J, MORROW J D, ADLERCREUTZ H, SALONEN J T (2002b) Association between low serum enterolactone and increased plasma F2-isoprostanes, a measure of lipid peroxidation, Atherosclerosis, 160,465-9. [Pg.297]

However, peroxidation can also occur in extracellular lipid transport proteins, such as low-density lipoprotein (LDL), that are protected from oxidation only by antioxidants present in the lipoprotein itself or the exttacellular environment of the artery wall. It appeats that these antioxidants are not always adequate to protect LDL from oxidation in vivo, and extensive lipid peroxidation can occur in the artery wall and contribute to the pathogenesis of atherosclerosis (Palinski et al., 1989 Ester-bauer et al., 1990, 1993 Yla-Herttuala et al., 1990 Salonen et al., 1992). Once initiation occurs the formation of the peroxyl radical results in a chain reaction, which, in effect, greatly amplifies the severity of the initial oxidative insult. In this situation it is likely that the peroxidation reaction can proceed unchecked resulting in the formation of toxic lipid decomposition products such as aldehydes and the F2 isoprostanes (Esterbauer et al., 1991 Morrow et al., 1990). In support of this hypothesis, cytotoxic aldehydes such as 4-... [Pg.24]

The determination of F2-isoprostanes, oxidation products of arachidonic acid, has been proposed as a more reliable index of oxidative stress in vivo, overcoming many of the methodological problems associated with other markers. The isoprostanes have emerged as a most effective method of quantifying the potential of antioxidants to inhibit lipid peroxidation. However, one drawback of this method is that quantification of F2-iP requires sophisticated techniques, in particular GC/MS and HPLC/MS... [Pg.277]

Thus, the formation of isoprostanes is rightly considered as a unique noninvasive method for the estimation of in vivo lipid peroxidation. However, the use of 8-Ao-PGF2a isoprostane (now known as iPF2a-III) as an index of nonenzymatic in vivo peroxidation has some limitations due to the possibility of its formation by COX-1- and COX-2-catalyzed... [Pg.791]

At present, antioxidants are extensively studied as supplements for the treatment diabetic patients. Several clinical trials have been carried out with vitamin E. In 1991, Ceriello et al. [136] showed that supplementation of vitamin E to insulin-requiring diabetic patients reduced protein glycosylation without changing plasma glucose, probably due to the inhibition of the Maillard reaction. Then, Paolisso et al. [137] found that vitamin E decreased glucose level and improved insulin action in noninsulin-dependent diabetic patients. Recently, Jain et al. [138] showed that vitamin E supplementation increased glutathione level and diminished lipid peroxidation and HbAi level in erythrocytes of type 1 diabetic children. Similarly, Skyrme-Jones et al. [139] demonstrated that vitamin E supplementation improved endothelial vasodilator function in type 1 diabetic children supposedly due to the suppression of LDL oxidation. Devaraj et al. [140] used the urinary F2-isoprostane test for the estimate of LDL oxidation in type 2 diabetics. They also found that LDL oxidation decreased after vitamin E supplementation to patients. [Pg.925]

Docosahexaenoic-acid-containing phospholipids are targets for lipid peroxidation. As a result of free-radical-catalyzed peroxidation, F4-isoprostanes are formed [75, 76]. F2-isoprostanes are also derived from free-radical-catalyzed peroxidation, although from AA instead [77]. [Pg.587]

Liu TZ, Stern A, Morrow JD (1998) The isoprostanes unique bioactive products of lipid peroxidation an overview. J Biomed Sci 5 415-420... [Pg.242]

Pratico D (1999) F(2)-isoprostanes sensitive and specific non-invasive indices of lipid peroxidation in vivo. Atherosclerosis 147 1-10... [Pg.244]


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See also in sourсe #XX -- [ Pg.333 ]




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