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Damage to lipids

Merry, P., Grootveld, M., Lunec, J. and Blake, D.R (1991). Oxidative damage to lipids within the inflamed human joint provides evidence of radical-mediated hypoxic-reperfusion injury. Am. J. Clin. Nutr. 53, 362S-369S. [Pg.20]

Vitamins (C and E), polyphenolic compounds, and carotenoids are the main groups of antioxidants present in fruits and vegetables. Vitamins are single molecules, but polyphenols and carotenoids are made up of hundreds of compounds with a wide range of structures and molecular masses. The intake of these antioxidants can lead to sustained reduction of the kind of oxidative damage to lipids, proteins, and DNA that is associated with the development of chronic diseases (Evans and Halliwell 2001). [Pg.223]

Vile, G. R, and Tyrrell, R. M. 1995. UVA radiation-induced oxidative damage to lipids and proteins in vitro and in human skin fibroblasts is dependent on iron and singlet oxygen. Free Rad. Biol. Med. 18 721-22. [Pg.49]

ROS can cause profound damage to lipids within cell membranes through lipid peroxidation. The mechanism involves free radical-mediated abstraction of a hydrogen atom from polyunsaturated fatty adds, such as linoleic acid (Scheme 3.11). A methylene group located between two double bonds in such a... [Pg.66]

The outcome of oxidative stress is a depletion of cellular GSH, NADPH, NADH, and ATP, and also damage to lipid membranes, structural and enzymatic proteins, and DNA. [Pg.69]

Figure 5.4 The levels of the autofluorescence pigment lipofuscin as a function of age. Lipo-fuscin accumulates within the retinal pigment epithelium as a result of oxidative damage to lipid membranes within the retina and is often regarded as a marker of the health of the retinal/RPE complex. (Data derived from Wing, G.L. et al., Invest. Ophthalmol. Vis. Sci., 17(7), 601-607, 1978.)... Figure 5.4 The levels of the autofluorescence pigment lipofuscin as a function of age. Lipo-fuscin accumulates within the retinal pigment epithelium as a result of oxidative damage to lipid membranes within the retina and is often regarded as a marker of the health of the retinal/RPE complex. (Data derived from Wing, G.L. et al., Invest. Ophthalmol. Vis. Sci., 17(7), 601-607, 1978.)...
Liu J, Wang X, Shigenaga MK, Yeo HC, Mori A, et al. 1996. Immobilization stress causes oxidative damage to lipid, protein, and DNA in the brain of rats. FASEB J 10 1532-1538. [Pg.307]

The many nonpolar C-C and C-H bonds of vitamin E make it fat soluble, and thus it dissolves in the nonpolar interior of the cell membrane, where it is thought to inhibit the oxidation of the unsaturated fatty acid residues in the phospholipids. Oxidative damage to lipids in cells via radical mechanisms is thought to play an important role in the aging process. For this reason, many anti-aging formulas with antioxidants like vitamin E are now popular consumer products. [Pg.556]

Aust A. E. and Lund L. G. (1990) The role of iron in asbestos-catalyzed damage to lipids and DNA. Biol. Oxidat. Syst. 2, 597-605. [Pg.4846]

Another proposed mechanism of neuronal death is oxidative stress due to the accumulation of free radicals. Normal and abnormal cellular metabolic processes involving molecular oxygen produce free radicals, which can cause oxidative damage to lipids, proteins and nucleic acids (Andersen, 2004). [Pg.575]

In the event that the LDL particle is exposed to high levels of toxic oxygen, the a-tocopherol within the particle may be overwhelmed, allowing damage to apo A. In the event that ascorbic levels are reduced or lowered in the immediate environment of the LDL particle, a-tocopherol may be similarly be overwhelmed. This situation may be more serious than it soxmds, as the a-tocopherol free radical (if given the time) may facilitate and catalyze damage to lipids at the core of the LDL particle. In this way, vitamin E may facilitate the transfer of free radicals from the aqueous phase at the smrface of the LDL particle to the fatty phase at its core (Upston et al, 1996 Thomas et ah, 1995 Bowry et ah, 1992). [Pg.637]

It is well established that Q is a component of the respiratory chain and plays a critical role in respiration and oxidative phosphorylation. It was thought that the presence of (X was confined exclusively to the inner mitochondrial membrane and its sole function was to serve as the redox component of the respiratory chain. However, this belief has been modified as it has been shown that Q is present in all cellular membranes examined. The major part of Q is present in the reduced form in human and animal tissues, and serves as an important antioxidant. In fact, it has been shown that QH2-IO, the reduced form of Q IO, efficiently scavenges free radicals and it is as effective as ct-tocopherol in preventing peroxidative damage to lipids, considered the best lipid-soluble antioxidant in humans. The antioxidant and prooxidant properties of mitochondrial ubiquinone have recently been reviewed. ... [Pg.414]


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See also in sourсe #XX -- [ Pg.499 ]

See also in sourсe #XX -- [ Pg.499 ]




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