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Ascorbic prooxidant

Ascorbic acid also forms soluble chelate complexes with iron (142—145). It seems ascorbic acid has no effect on high iron levels found in people with iron overload (146). It is well known, in fact, that ascorbic acid in the presence of iron can exhibit either prooxidant or antioxidant effects, depending on the concentration used (147). The combination of citric acid and ascorbic acid may enhance the iron load in aging populations. Iron overload may be the most important common etiologic factor in the development of heart disease, cancer, diabetes, osteoporosis, arthritis, and possibly other disorders. The synergistic combination of citric acid and ascorbic acid needs further study, particularly because the iron overload produced may be correctable (147). [Pg.22]

As mentioned earlier, ascorbate and ubihydroquinone regenerate a-tocopherol contained in a LDL particle and by this may enhance its antioxidant activity. Stocker and his coworkers [123] suggest that this role of ubihydroquinone is especially important. However, it is questionable because ubihydroquinone content in LDL is very small and only 50% to 60% of LDL particles contain a molecule of ubihydroquinone. Moreover, there is another apparently much more effective co-antioxidant of a-tocopherol in LDL particles, namely, nitric oxide [125], It has been already mentioned that nitric oxide exhibits both antioxidant and prooxidant effects depending on the 02 /NO ratio [42]. It is important that NO concentrates up to 25-fold in lipid membranes and LDL compartments due to the high lipid partition coefficient, charge neutrality, and small molecular radius [126,127]. Because of this, the value of 02 /N0 ratio should be very small, and the antioxidant effect of NO must exceed the prooxidant effect of peroxynitrite. As the rate constants for the recombination reaction of NO with peroxyl radicals are close to diffusion limit (about 109 1 mol 1 s 1 [125]), NO will inhibit both Reactions (7) and (8) and by that spare a-tocopherol in LDL oxidation. [Pg.793]

In contrast to numerous literature data, which indicate that protein oxidation, as a rule, precedes lipid peroxidation, Parinandi et al. [66] found that the modification of proteins in rat myocardial membranes exposed to prooxidants (ferrous ion/ascorbate, cupric ion/tert-butyl-hydroperoxide, linoleic acid hydroperoxide, and soybean lipoxygenase) accompanied lipid peroxidation initiated by these prooxidant systems. [Pg.829]

In vitro antioxidant and prooxidant properties of ascorbic acid have been clearly demonstrated. It is understandable that the competition between antioxidant and prooxidant activities of ascorbic acid depends on the rates of Reactions (11) and (12). [Pg.855]

Recently, Carr and Frei reviewed studies on the antioxidant and prooxidant effects of ascorbic acid [8]. These authors pointed out that a highly controversial work by Podmore and coworkers [71] who found that the prooxidant effect of ascorbic acid supplementation to healthy volunteers is much questionable. These authors demonstrated that of the 44 in vivo studies, 38 showed the antioxidant effect of ascorbic acid, 14 showed no change, and only six showed the enhancement of oxidative damage after ascorbate supplementation. It was concluded that ascorbic acid is an antioxidant in biological fluids, animals, and humans, both with and without iron supplementation. [Pg.856]

Therefore, depending on their structures, flavonoids may reduce the ascorbate radical or oxidize ascorbate, exhibiting antioxidant or prooxidant properties in the systems containing flavonoids and ascorbate together. [Pg.870]

In 1998, Schlotte et al. [259] showed that uric acid inhibited LDL oxidation. However, subsequent studies showed that in the case of copper-initiated LDL oxidation uric acid behaves itself as prooxidant [260,261]. It has been suggested that in this case uric acid enhances LDL oxidation by the reduction of cupric into cuprous ions and that the prooxidant effect of uric acid may be prevented by ascorbate. On the other hand, urate radicals formed during the interaction of uric acid with peroxyl radicals are able to react with other compounds, for example, flavonoids [262], and by that participate in the propagation of free radical damaging reactions. In addition to the inhibition of oxygen radical-mediated processes, uric acid is an effective scavenger of peroxynitrite [263]. [Pg.880]

Haase and Dunkley (1969B) reported that although high concentrations of ascorbic acid in model systems of potassium linoleate were prooxidant, a decrease in the rate of oxidation was observed. Haase and Dunkley (1969C) further noted that certain concentrations of ascorbic acid and copper inhibited the formation of conjugated dienes, but not the oxidation of ascorbic acid, and caused a rapid loss of part of the conjugated dienes already present in the system. They theorized that certain combination concentrations of ascorbic acid and copper inhibit oxidation by the formation of free radical inhibitors which terminate free- radical chain reactions, and that the inhibitors are complexes that include the free radicals. [Pg.250]

Phosphate, ascorbate, NaCl, nitrite, Maillard reaction products, and other antioxidants or prooxidants have been reported to influence development of WOF. Their roles have been reviewed (5), but newer evidence is now available and will be covered herein. [Pg.295]

Finally it should be noted that similar to vitamin C (ascorbate) (08PNA11105), resveratrol in pharmacological concentrations and in the presence of Cu-ions can act as a prooxidant leading to cytotoxicity and apoptosis induction (09JMC1963, 01MI1111). [Pg.206]

Superoxide radical anion, hydroxyl radical, and hydrogen peroxide are known as prooxidants, whereas substances that neutralize their effects are called antioxidants. Oxidative stress occurs when the prooxidant-antioxidant balance becomes too favorable to the prooxidants. The effects of prooxidants can be neutralized by their direct reaction with small-molecule antioxidants, including glutathione, ascorbate, and tocopherols. In addition, oxidizing radicals are scavenged from a living system by several enzymes, including peroxidase, superoxide dismutase, and catalase. Oxidative lesions on DNA may be repaired by DNA repair enzymes. [Pg.243]

Copper is present in foods as part of several copper-containing enzymes, including the polyphenolases. Copper is a very powerful prooxidant and catalyzes the oxidation of unsaturated fats and oils as well as ascorbic acid. The normal daily diet contains from 2 to 5 mg of copper, more than ample to cover the daily requirement of 0.6 to 2 mg. [Pg.134]

In vitro, ascorbate and Fe + ions are frequently used as a source of superoxide for such enzymes as indoleamine dioxygenase. Although ascorbate does have prooxidant and superoxide generating activity (Section 13.3.7), there is no evidence that it is the physiological source of this radical for superoxideutilizing enzymes. [Pg.369]

It seems likely that the prooxidant actions of ascorbate are of relatively little importance in vivo. Except in cases of iron overload, there are almost no transition metal ions in free solution. They are all bound to proteins, and because the renal transport system is readily saturated, plasma and tissue concentrations of ascorbate are unlikely to rise to a sufficient extent to lead to radical formation (Halliwell, 1996 Carr and Frei, 1999a). [Pg.371]

Several proteins that exist in food (e.g., lactoferrin, ferritin, transferritin, heme protein) possess strong binding sites for iron. Reducing agents (ascorbate, cysteine, superoxide anion) to low pH causes release of iron from proteins and accelerates lipid oxidation (34). Some amino acids and peptides found in muscle foods (e.g., carnosine) are capable of chelating metal ions and inhibit their prooxidant activity (35, 36). [Pg.482]

Metal Effects and Prooxidant Action. Ascorbic acid is prooxidant in some situations. Kanner et al. (28) showed that Cu increased the oxidation of linoleate using loss of 8-carotene as an indicator. However, when sufficient ascorbic acid was added to his system, copper catalysis was reversed. Furthermore, when Fe was added, the addition of ascorbic acid increased the prooxidant effect. Previous publications (29) have discussed the deactivation of copper catalysis by ascorbic acid, but in iron-catalyzed oxidation, Fe " initiates oxidation of lipid (2). Fe is formed from Fe by ascorbic acid. Many foods contain metals, and the... [Pg.545]

These studies support the observed prooxidant effect of ascorbic acid at high pH (milk) in the presence of copper but not in the presence of iron. [Pg.73]

In order to explain the effects observed by Nojeim and Clydesdale (1 3), I would like to propose a mechanism for the action of ascorbic acid in the presence of iron which might explain how it could act as both a reducing agent and a prooxidant as well as perhaps shedding some more light on its role in the chemistry and thus the bioavailability of iron. [Pg.73]


See other pages where Ascorbic prooxidant is mentioned: [Pg.779]    [Pg.855]    [Pg.855]    [Pg.856]    [Pg.267]    [Pg.780]    [Pg.856]    [Pg.856]    [Pg.857]    [Pg.442]    [Pg.574]    [Pg.65]    [Pg.142]    [Pg.145]    [Pg.146]    [Pg.147]    [Pg.153]    [Pg.1825]    [Pg.1825]    [Pg.713]    [Pg.73]    [Pg.60]   
See also in sourсe #XX -- [ Pg.217 ]




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