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Radicals, ascorbic acid

Ascorbate is most likely required by hydroxylases to maintain iron or copper at the active enzyme site in the reduced form, since it is necessary for hydroxylation. The semidehydroascorbate radical is not very reactive (Bielski and Richter, 1975 Rose, 1989). It decays by disproportionation to ascorbate and dehydroascorbate (the latter subsequently degrades to oxalic acid and L-threonic acid), rather than acting as a reactive free radical. Reaction of ascorbic acid with (OH) is rapid and diffusion-dependent (K 7.2 x 10 -1.3 x lO o M- s- ) (Cabelli and Bielski, 1983). (O2) oxidizes ascorbic acid with a rate constant of 10 -10 M s (Bielski et al., 1985). Besides direct scavenging of radicals, ascorbic acid is known to have a number of physiological effects (Padh,... [Pg.446]

Synthetically useful organic reactions similar to ATRP, which are mediated by redox-active transition metal complexes, e.g., atom transfer radical addition or cyclization, can also be carried out successfully at low catalyst concentrations in the presence of both radical-based and non-radical (ascorbic acid) reducing agents. The continuous activator regeneration throughout the process via reduction has made these reactions more environmentally friendly than the traditionally used protocols. ... [Pg.340]

The most significant chemical characteristic of L-ascorbic acid (1) is its oxidation to dehydro-L-ascorbic acid (L-// fi (9-2,3-hexodiulosonic acid y-lactone) (3) (Fig. 1). Vitamin C is a redox system containing at least three substances L-ascorbic acid, monodehydro-L-ascorbic acid, and dehydro-L-ascorbic acid. Dehydro-L-ascorbic acid and the intermediate product of the oxidation, the monodehydro-L-ascorbic acid free radical (2), have antiscorbutic activity equal to L-ascorbic acid. [Pg.10]

L-Ascorbic acid (2) Monodehydro-L-ascorbic acid (free radical) HO... [Pg.10]

Antioxidant Activity. Ascorbic acid serves as an antioxidant to protect intraceUular and extraceUular components from free-radical damage. It... [Pg.21]

Ascorbic acid is a reasonably strong reducing agent. The biochemical and physiological functions of ascorbic acid most likely derive from its reducing properties—it functions as an electron carrier. Loss of one electron due to interactions with oxygen or metal ions leads to semidehydro-L-ascorbate, a reactive free radical (Figure 18.30) that can be reduced back to L-ascorbic acid by various enzymes in animals and plants. A characteristic reaction of ascorbic acid is its oxidation to dehydro-L-aseorbie add. Ascorbic acid and dehydroascor-bic acid form an effective redox system. [Pg.599]

Ascorbic acid—vitamin C—is an essential nutrient that the human body cannot manufacture from other compounds. It is needed for the formation of collagen, the protein that makes up connective tissue, and is essential to muscles, bones, cartilage, and blood vessels. It is a strong antioxidant, preventing damage from oxygen free radicals. [Pg.15]

The valency of the metal ion changes in every step so that a single atom of heavy metal (Me) may produce many free radicals. Metal chelating compounds, such as citric, tartaric or phosphoric acids, ascorbic acid, phytin or phosphatidic acids, combine with metals to form non-reactive compounds so that the oxidation reactions are inhibited and natural food antioxidants are saved. [Pg.300]

The most common natural antioxidants are tocopherols, ascorbic acid and P-carotene (more often synthetic nature-identical compounds than natural products). Their changes were studied in detail in model systems, fats and oils, but experimental evidence is mainly lacking on more complicated systems, such as natural foods and ready dishes. Still less is known on different antioxidants from spices and from essential oils. These data will probably be obtained gradually. Very little is known about synergism of antioxidants in food products other than edible fats and oils or their regeneration from the respective free radicals and quinones. In mixtures, some antioxidants are preferentially destroyed and others are saved. Some data have already been published, but these complex changes should be studied in more detail. [Pg.310]

N-Nitrosamine inhibitors Ascorbic acid and its derivatives, andDC-tocopherol have been widely studied as inhibitors of the N-nitrosation reactions in bacon (33,48-51). The effect of sodium ascorbate on NPYR formation is variable, complete inhibition is not achieved, and although results indicate lower levels of NPYR in ascorbate-containing bacon, there are examples of increases (52). Recently, it has been concluded (29) that the essential but probably not the only requirement for a potential anti-N-nitrosamine agent in bacon are its (a) ability to trap NO radicals, (b) lipophilicity, (c) non-steam volatility and (d) heat stability up to 174 C (maximum frying temperature). These appear important requirements since the precursors of NPYR have been associated with bacon adipose tissue (15). Consequently, ascorbyl paImitate has been found to be more effective than sodium ascorbate in reducing N-nitrosamine formation (33), while long chain acetals of ascorbic acid, when used at the 500 and lOOO mg/kg levels have been reported to be capable of reducing the formation of N-nitrosamines in the cooked-out fat by 92 and 97%, respectively (49). [Pg.169]

Kalyanaraman, B., Darley-Usmar, V.M., Wood, J., Joseph, J. and Parathasarathy, S. (1992). Synergistic interaction between the probucol phenoxyl radical and ascorbic acid in inhibiting the oxidation of LDL. J. Biol. Chem. 267, 6789—6795. [Pg.35]

Cabelli, D.E. and Bielski, B. (1983). Kinetics and mechanism for the oxidation of ascorbic acid (ascorbate by HO2/O2 radicals. A pulse radiolysis and stopped-flow photolysis study. J. Phys. Chem. 87, 1809. [Pg.49]

Fessenden, R.W. and Verma, N.C. (1978). A time-resolved electron spin resonance study of the oxidation of ascorbic acid by the hydroxyl radical. Biophys. J. 24, 93. [Pg.50]

The human lens is rich in ascorbate, which is required for normal collagen synthesis and acts as a water-soluble antioxidant, reacting rapidly with superoxide, hydroxyl and peroxyl radicals. However, ascorbic acid can undergo auto-oxidation and, at certain concentrations, can form hydroxyl radicals with hydrogen peroxide in the presence of light and riboflavin as described above (Delaye and Tardieu, 1983 Ueno et al., 1987). [Pg.131]

Nonaka, A., Manabe, T. and Tobe, T. (1991). Effect of a new synthetic ascorbic acid derivative as a free radical scavenger on the development of acute pancreatitis in mice. Gut 32, 528-532. [Pg.168]

A more recent study, which measured three established markers of free-radical activity in addition to serum ascorbic acid in two groups of elderly diabetic patients (with and without retinopathy), found no significant differences in any of the markers between patients and age-matched controls despite significant depletion of ascorbic acid in patients with diabetes, especially those with retinopathy (Sinclair et al., 1992). These rather paradoxical findings suggest the existence of a complex interrelationship between the levels of individual antioxidant molecules in cells and tissues. [Pg.186]

It should be remembered that some of the established antioxidants have other metabolic roles apart from free-radical scavenging. The finding of reduced antioxidant defences in diabetes, for example, may not be prima fascie evidence of increased oxidative stress, since alternative explanations may operate. For example, this may reflect a response to reduced free-radical activity as su ested by the results of a previous study (Collier et al., 1988). In the case of ascorbate, an alternative explanation has been proposed by Davis etal. (1983), who demonstrated competitive inhibition of ascorbate uptake by glucose into human lymphocytes. This view is supported by the similar molecular structure of glucose and ascorbic acid (see Fig. 12.4) and by a report of an inverse relationship between glycaemic control and ascorbate concentrations in experimental diabetes in rats. Other investigators, however, have not demonstrated this relationship (Som etal., 1981 Sinclair etal., 1991). [Pg.187]

Sinclair, A.J., Lunec, J., Girling, A.J. and Barnett, A.H. (1992). Modulators of free radical activity in diabetes mellitus role of ascorbic acid. In Free Radicals and Aging (eds. I. Emerit and B. Chance) pp. 342-352. BirkhauserVerlagBasel. [Pg.197]


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Acid radicals

Acidic radicals

Ascorbate radical

Ascorbic acid free radical form

Ascorbic acid free radical trapping

Ascorbic acid radiation-induced, free-radical

Ascorbic acid radical scavenger

Kinetics ascorbic acid free radical

Radicals, derived from ascorbic acid

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