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Vitamin oxidation, radical formation

There are numerous synthetic and natural compounds called antioxidants which regulate or block oxidative reactions by quenching free radicals or by preventing free-radical formation. Vitamins A, C, and E and the mineral selenium are common antioxidants occurring naturally in foods (104,105). A broad range of flavonoid or phenoHc compounds have been found to be functional antioxidants in numerous test systems (106—108). The antioxidant properties of tea flavonoids have been characterized using models of chemical and biological oxidation reactions. [Pg.373]

Ellis et al. [72] recently studied the effects of short- and long-term vitamin C therapy in the patients with chronic heart failure (CHF). It was found that oxygen radical production and TBAR product formation were higher in patients with CHF than in control subjects. Both short-term (intravenous) and long-term (oral) vitamin C therapy exhibited favorable effects on the parameters of oxidative stress in patients the treatments decreased oxygen radical formation and the level of lipid peroxidation and improved flow-mediated dilation in brachial artery. However, there was no correlation between changes in endothelial function and oxidative stress. [Pg.856]

Cystic fibrosis is the most common lethal autosomal-recessive disease, in which oxidative stress takes place at the airway surface [274]. This disease is characterized by chronic infection and inflammation. Enhanced free radical formation in cystic fibrosis has been shown as early as 1989 [275] and was confirmed in many following studies (see references in Ref. [274]). Contemporary studies also confirm the importance of oxidative stress in the development of cystic fibrosis. Ciabattoni et al. [276] demonstrated the enhanced in vivo lipid peroxidation and platelet activation in this disease. These authors found that urinary excretion of the products of nonenzymatic lipid peroxidation PGF2 and TXB2 was significantly higher in cystic fibrotic patients than in control subjects. It is of importance that vitamin E supplementation resulted in the reduction of the levels of these products of peroxidation. Exhaled ethane, a noninvasive marker of oxidative stress, has also been shown to increase in cystic fibrosis patients [277]. [Pg.934]

As acute strenuous exercise and chronic exercise training increase the requirement for various antioxidants, it is conceivable that dietary supplementation of specific antioxidants would be beneficial. Older subjects may be more susceptible to oxidative stress and may benefit from the antioxidant protection provided by vitamin E. During severe oxidative stress such as strenuous exercise, the enzymatic and nonenzymatic antioxidant systems of skeletal muscle are not able to cope with the massive free-radical formation, which results in an increase in lipid peroxidation. Vitamin E decreases exercise-induced lipid peroxidation. The exercise may increase superoxide anion generation in the heart, and the increase in the activity of superoxide dismutase (SOD) in skeletal muscle may be... [Pg.86]

Lipid oxidation in muscle foods is one of the major deteriorative reactions causing losses in quality during processing and storage. The oxidation of unsaturated fatty acids leads to formation of free radicals and hydroperoxide. These intermediary compounds are unstable and cause the oxidation of pigments, flavors, and vitamins. Oxidized unsaturated lipids bind to protein and form insoluble lipid-protein complexes. This accounts for toughened texture and poor flavor of frozen seafoods (Khayat and Schwell, 1983). [Pg.288]

FIGURE 16 (Top) A family of rearrangement reactions that depend upon free radical formation involving an enzyme-bound form of the vitamin B12 coenzyme S -deoxyadenosylcobalamin (Fig. 7). The rearrangement of (R) methylmalonyl-CoA to succinyl-CoA (the opposite of the reaction shown here) is one of the two essential vitamin Bi2-dependent reactions in the human body, and plays an important role in fatty acid oxidation, as is indicated in Fig. 12. [Pg.215]

There is increased formation of 8-hydroxyguanine (a marker of oxidative radical damage) in DNA during (short-term) vitamin C depletion, and the rate of removal of 8-hydroxyguanine from DNA by excision repair, and hence its urinary excretion, is affected by vitamin C status. This suggests that measurement of urinary excretion of 8-hydroxyguanine may provide a biomarker of optimum status, as a basis for estimating requirements. [Pg.52]

Vitamin E can also act as an antioxidant (qv) in animals and humans alone or in combination with vitamin C (qv). Both are good free-radical scavengers with the vitamin C acting to preserve the levels of vitamin E (35). Vitamin E in turn can preserve the levels of vitamin A in animals (13). It has been shown that vitamin E reduces the incidence of cardiovascular disease (36—39). This most likely results from the antioxidant property of the vitamin which inhibits the oxidation of low density Hpoproteins (LDLs) (40—42). The formation of the oxidized LDLs is considered important in decreasing the incidence of cardiovascular disease (43). [Pg.147]

The third primary intermediate in the oxidation chemistry of a-tocopherol, and the central species in this chapter, is the orr/zo-quinone methide 3. In contrast to the other two primary intermediates 2 and 4, it can be formed by quite different ways (Fig. 6.4), which already might be taken as an indication of the importance of this intermediate in vitamin E chemistry. o-QM 3 is formed, as mentioned above, from chromanoxylium cation 4 by proton loss at C-5a, or by a further single-electron oxidation step from radical 2 with concomitant proton loss from C-5a. Its most prominent and most frequently employed formation way is the direct generation from a-tocopherol by two-electron oxidation in inert media. Although in aqueous or protic media, initial... [Pg.166]


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See also in sourсe #XX -- [ Pg.51 ]




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Formate radicals

Oxidation radical

Oxidation vitamin

Oxide Radicals

Radical formation

Radicals vitamin

Vitamin formation

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