Lipid peroxidation mechanisms

Esterbauer, H., Zollner, H. and Schaur, KJ. (1990). Aldehydes formed by lipid peroxidation mechanisms of formation, occurrence and determination. In Lipid Oxidation (ed. C. Vigo-Pelfrey) pp. 239-283. CRC Press, Boca Raton, FL. [Pg.244]

Oxidation to CO of biodiesel results in the formation of hydroperoxides. The formation of a hydroperoxide follows a well-known peroxidation chain mechanism. Oxidative lipid modifications occur through lipid peroxidation mechanisms in which free radicals and reactive oxygen species abstract a methylene hydrogen atom from polyunsaturated fatty acids, producing a carbon-centered lipid radical. Spontaneous rearrangement of the 1,4-pentadiene yields a conjugated diene, which reacts with molecular oxygen to form a lipid peroxyl radical. [Pg.74]

Niki, E., Yoshida, Y., Saito, Y., and Noguchi, N. Lipid peroxidation Mechanisms, inhibition, and biological effects. Biochem. Biophys. Res. Commun. 338, 668-676, 2005. [Pg.411]

Kappus, H. (1985) Lipid peroxidation mechanisms, analysis, enzymology and biological relevance. In H. Sies (Ed.), Oxidative Stress, Academic Press, New York, pp. 273-310. [Pg.493]

Peroxide oxidation processes in human organism are one of based phenomena that is responsible for homeostasis. For this reason development and investigation of interaction mechanism between different biomacromolecules and lipids peroxide are important for forming complete picture of functioning of human being as biological system. [Pg.54]

Halliwell B, Chirico S Lipid peroxidation its mechanism, measurement, and significance. Am J Clin Nutr 1993 57(5 Suppl) 715S. [Pg.497]

Cojocel C, Beuter W, Muller W, et al. 1989. Lipid peroxidation A possible mechanism of trichloroethylene-induced nephrotoxicity. Toxicology 55 131-141. [Pg.258]

The basic mechanisms of lipid peroxidation are well understood and described in the literature in many excellent reviews (e.g. Girotti, 1985 Gardner, 1989 Buettner, 1993). Here, apart from essential background information, we will restrict our discussion in this short overview to recent advances in our understanding of lipid peroxidation, emphasizing those aspects relevant to coronary heart disease. Some of the biological implications of these reactions will be discussed by others in this volume. [Pg.24]

In this section, the general principles of lipid peroxidation reactions, which are well established, are discussed first and specific mechanisms, which may be relevant in vivo, are considered later. [Pg.24]

In the previous section, we have described some of the mechanisms that may lead to the fijrmation of lipid hydroperoxides or peroxyl radicals in lipids. If the peroxyl radical is formed, then this will lead to propagation if no chain-breaking antioxidants are present (Scheme 2.1). However, in many biological situations chain-breaking antioxidants are present, for example, in LDL, and these will terminate the peroxyl radical and are consumed in the process. This will concomitandy increase the size of the peroxide pool in the membrane or lipoprotein. Such peroxides may be metabolized by the glutathione peroxidases in a cellular environment but are probably more stable in the plasma comjxutment. In the next section, the promotion of lipid peroxidation if the lipid peroxides encounter a transition metal will be considered. [Pg.27]

O Brien, P.J. (1969). Intracellular mechanisms for the decomposition of a lipid hydroperoxide I. Decomposition of a lipid peroxide by metals ions, haem compounds and nucleophils. Can. J. Biochem. 47, 485-492. [Pg.51]

Although atherosclerosis and rheumatoid arthritis (RA) are distinct disease states, both disorders are chronic inflammatory conditions and may have common mechanisms of disease perpetuation. At sites of inflammation, such as the arterial intima undergoing atherogen-esis or the rheumatoid joint, oxygen radicals, in the presence of transition-metal ions, may initiate the peroxidation of low-density lipoprotein (LDL) to produce oxidatively modified LDL (ox-LDL). Ox-LDL has several pro-inflammatory properties and may contribute to the formation of arterial lesions (Steinberg et /., 1989). Increased levels of lipid peroxidation products have been detected in inflammatory synovial fluid (Rowley et /., 1984 Winyard et al., 1987a Merry et al., 1991 Selley et al., 1992 detailed below), but the potential pro-inflammatory role of ox-LDL in the rheumatoid joint has not been considered. We hypothesize that the oxidation of LDL within the inflamed rheumatoid joint plays a pro-inflammatory role just as ox-LDL has the identical capacity within the arterial intima in atherosclerosis. [Pg.98]

Mechanisms of lipid peroxidation that have been implicated in atherosclerosis may be pertinent to RA. Cellular lipoxygenase enzymes may promote LDL modification by inserting hydroperoxide groups into unsaturated fetty-acid side chains of the LDL complex (Yla-Herttuala etal., 1990). 15-Lipoxygenase has been implicated as an initiator of LDL oxidation (Cathcart etal., 1991) whilst 5-lipoxygenase does not appear to be involved (Jessup et al., 1991). Products of activated lipoxygenase enzymes within inflammatory synovial fluid surest that this pathway could be activated in RA (Costello etal., 1992). [Pg.106]

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