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Lipids protection from oxidation

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]

It is not known why the rat manunary gland is more responsive to CLA-mediated inhibition of lipid peroxidation than the liver, especially since CLA treated mouse liver microsomes exhibit inhibition of lipid peroxidation. Based on these observations it might be assumed that CLA affords different degrees of protection from oxidation in different tissues and sfpecies. In order to answer these questions, we are studying liver microsomes from rats and mice fed identical CLA-treated diets. [Pg.269]

Under physiological conditions, i.e., in neutral aqueous solution with a. significant p02, ferric ion (Fe ) is the predominant species and ferrous ion (Fe ) can only exist if protected from oxidation by specific coordination (Schneider 1988). Transient, enzymatic reduction of Fe " serves as a control point for the exchange of iron, for example in the mobilization of iron from ferritin stores and transport across lipid membranes. This is important in that most chelators presently in use or under investigation display sped-... [Pg.305]

Vitamin A is soluble in oils and fats. The vitamin is not easily destroyed by heat but is readily oxidized. Preparations must, therefore, be protected from oxidation and are prepared in an atmosphere of carbon dioxide or nitrogen. In the absence of air, vitamin A is unaltered at moderate temperatures. The creams and lotions must therefore be free of oxidases, and perfumes must be free of peroxides. The addition of antioxidants is useful to maintain stability. Pure vitamin E is effective as an antioxidant in lipid solutions of vitamin A. [Pg.366]

The Jing group investigated their poly(L-lysine)-6-poly(L-phenylalanine) vesicles for the development of synthetic blood, since PEG-lipid vesicles were previously used to encapsulate hemoglobin to protect it from oxidation and to increase circulation time. They extended this concept and demonstrated that functional hemoglobin could be encapsulated into their vesicles. The same polypeptide material was also used to complex DNA, which caused the vesicles to lose their... [Pg.130]

Dietary consumption of polyphenols is associated with a lower risk of degenerative diseases. In particular, protection of serum lipids from oxidation, which is a major step in the development of arteriosclerosis, has been demonstrated. More recently, new avenues have been explored in the capacity of polyphenols to interact with the expression of the human genetic potential. The understanding of the interaction between this heterogeneous class of compounds and cellular responses, due either to their ability to interplay in the cellular antioxidant network or directly to affect gene expression, has increased. [Pg.13]

Because the carotenoids favour hydrophobic domains they are generally localised in the membranes and lipoproteins of animal cells. In this location they can influence the oxidation of membrane lipids and prevent the passage of free radicals from one cellular compartment to another. Thus, DNA in the nucleus is protected from intracellularly generated ROS by (at least) the nuclear membrane and from extracellular ROS by a number of membranes. Should ROS reach the nucleus, base oxidation can occur. The base most susceptible to oxidation is guanine, although all other bases can also be affected. The cell has the ability to detect damaged bases, excise them. [Pg.110]

Esterbauer et cil. (1992) have studied the in vitro effects of copper on LDL oxidation and have shown that there are three distinct stages in this process. In the first part of the reaction, the rate of oxidation is low and this period is often referred to as the lag phase the lag phase is apparently dependent on the endogenous antioxidant content of the LDL, the lipid hydroperoxide content of the LDL particle and the fatty acid composition. In the second or propagation phase of the reaction, the rate of oxidation is much faster and independent of the initial antioxidant status of the LDL molecule. Ultimately, the termination reactions predominate and suppress the peroxidation process. The extensive studies of Esterbauer et al. have demonstrated the relative importance of the endogenous antioxidants within the LDL molecule in protecting it from oxidative modification. [Pg.47]

Flavonoids protect LDL from oxidation, delaying the onset of lipid peroxidation, however, the prevention of atherosclerosis by flavonoids occurs not only by the inhibition of LDL oxidation, but also by the increase of cellular resistance to harmful effects of the oxidized LDL (de Luis and Aller, 2008). The antioxidant activity of anthocyanidins, as well as their protective role against LDL oxidation, has been well demonstrated in different in vitro systems (Aviram and Fuhrman, 2002 Satue-Gracia and others 1997 Teissedre and others 1996). [Pg.160]

Vitamin (a-tocopherol) is an antioxidant. As a lipid-soluble compound, it is especially important for protecting other lipids from oxidative damage. [Pg.150]

Low HDL cholesterol (<35 mg/dL) is an independent risk factor for CHD. HDL appears to antagonize atherogenesis by at least two mechanisms. HDL can mobilize cholesterol from extrahepatic cells (such as arterial wall foam cells) and transport it to the liver for disposal (reverse cholesterol transport) HDL also has antioxidant properties. HDL contains the potent antioxidant enzyme paraoxonase, which may protect LDL lipids from oxidation. Thus, hypertriglyceridemia with... [Pg.273]


See other pages where Lipids protection from oxidation is mentioned: [Pg.42]    [Pg.136]    [Pg.193]    [Pg.861]    [Pg.829]    [Pg.202]    [Pg.620]    [Pg.830]    [Pg.351]    [Pg.551]    [Pg.510]    [Pg.262]    [Pg.48]    [Pg.327]    [Pg.172]    [Pg.135]    [Pg.531]    [Pg.112]    [Pg.1382]    [Pg.734]    [Pg.370]    [Pg.243]    [Pg.11]    [Pg.1295]    [Pg.309]    [Pg.23]    [Pg.90]    [Pg.103]    [Pg.131]    [Pg.179]    [Pg.445]    [Pg.833]    [Pg.852]    [Pg.852]    [Pg.99]    [Pg.354]    [Pg.80]    [Pg.217]    [Pg.627]    [Pg.779]   
See also in sourсe #XX -- [ Pg.861 ]

See also in sourсe #XX -- [ Pg.531 ]

See also in sourсe #XX -- [ Pg.531 ]




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Oxidized lipids

Protection from

Protective oxidation

Protective oxides

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