Monodehydroascorbic acid

For example, when 02 is formed in the hydrophilic stage, vitamin C (18, L-ascorbic acid present in hydrophilic stage) assists the hydrogen atoms to form dehydroascorbic acid (19) via monodehydroascorbic acid, and hydrogen peroxide (eq. 1.9). 

The oxidation of ascorbic acid in certain reactions has given evidence of an intermediate with the properties of a free radical which could be formed by one-electron oxidation. Thus, the rate-limiting step of ascorbic acid oxidation by Fe + and H2O2 was this one-electron oxidation (G12). Such a radical has now been identified in hydrogen peroxide-ascorbic acid solutions at pH 4.8 by electron paramagnetic resonance spectroscopy. The free radical, commonly referred to as monodehydroascorbic acid, decayed in about 15 minutes at this acid pH. It was also formed during the enzymatic oxidation of ascorbic acid by peroxidase (Yl). The existence of the monodehydroascorbic acid radical makes possible very... 

Other effects of ascorbic acid are probably also dependent upon the monodehydroascorbic free radical. One is the depolymerization of hyaluronic acid, first shown by Robertson et al. (R14). This is particularly likely, since subsequent studies have shown that the depolymerization was not prevented by catalase, as should have occurred if peroxide were the active component. There is no reason to believe that this hyaluroni-dase-like action is physiological. There is every reason to believe, however, that the monodehydroascorbic acid radical is formed in vivo. It is unlikely that all of the reactions in the body of such a reactive molecule are catalyzed by enzymes. 

Staudinger s interpretation of this involves the central problem of such hydroxylation reactions the generation of free radicals from O2 as the possible hydroxylating agents (K4). The hypothesis is that the reaction of TPNH with O2 in Ae mitochondrial 11-P-hydroxylase generates such free radicals, and so does the oxidation of ascorbic acid by the DPNH-oxidase-cytochrome be system (Eq. 15). The monodehydroascorbic acid formed in the latter system is already well documented. 

Commoner (1958) noted a signal after AA oxidation, belonging to monodehydroascorbic acid (MDHA). This signal and the one obtained in chlorophyll photoreduction were stucturally similar but MDHA had a greater life time than the radical of chlorophyll. Bubnov et al. (1960) and others (Krasnovsky and Umrikhina, 1958 Krasnovsky, 1960 Krasnovsky et al., 1980) have also shown this signal However, the signal disappeared when the light was turned off and did not reappear, without the reductant. 

The name vitamin C refers not only to L-ascorbic acid, but also to the whole reversible redox system that includes the one-electron oxidation product of L-ascorbic acid, known as L-ascorbyl radical (or L-monodehydroascorbic acid or semidehydroascorbic acid), and the two-electron oxidation product of L-ascorbic acid known as L-dehydroascorbic acid (Figure 5.26). Ascorbic acid and ascorbyl radical mainly occur as anions in solutions at physiological pH. 

As shown in Figure 13.3, oxidation of ascorbic acid, for example, by the reduction of superoxide to hydrogen peroxide or Fe + to Fe +, and similar reduction of other transition metal ions, proceeds by a one-electron process, forming the monodehydroascorbate radical. The radical rapidly disproportionates into ascorbate and dehydroascorbate. Most tissues also have both nicotinamide adenine dinucleotide phosphate (NADPH) and glutathione-dependent monodehydroascorbate reductases, which reduce the radical back to ascorbate. Ascorbate is thus an effective quencher of singlet oxygen and other radicals. 

The ready oxidation of ascorbic acid will catalyze chemical changes in a number of other substances. Thus, unsaturated fatty acids in lecithins and tissues are catalytically oxidized in the presence of ascorbic acid to a substance producing color with thiobarbiturate (B21). The product of the ascorbic acid-catalyzed oxidation is malonaldehyde, which can also inhibit L-gulonolactone oxidase, the enzyme forming ascorbic acid (Cl). It has been suggested that this enzyme inhibition may occur in vivo in animals deficient in vitamin E, a compound believed to have antioxidant actions which would prevent the ascorbic acid-catalyzed lipid oxidation from giving rise to malonaldehyde. It is quite probable that the active intermediate in the formation of malonaldehyde is the monodehydroascorbate radical which initiates the lipid oxidation. 

Fig. I. The xamhophyll cycle and its effects on light-harvesting and energy dissipation within the photosynthetic apparatus. The enzyme violaxanthin de-epoxidase (VDE) catalyzes the sequential conversion of violaxanthin to zeaxanthin via antheraxanthin using ascorbic acid (AA) as a reductant and generating monodehydroascorbate (MDHA). The epoxidation of zeaxanthin to violaxanthin in the reverse reaction sequence is catalyzed by the enzyme zeaxanthin epoxidase (ZE).

Harwood Jr., H. J., Greene, Y. J., and Stacpoole, P. W., 1986, Inhibition of human leukocyte 3-hydroxy-3-methylglutaryl coenzyme A reductase activity by ascorbic acid An effect mediated by the free radical monodehydroascorbate, J. Biol. Chem. 261 7127-7135. 

Oxidoreductases (such as ascorbate oxidase, ascorbate peroxidase, monodehydroascorbate reductase, dehydroascorbate reductase, superoxide dismutase and ascorbate cytochrome-fo reductase) that act in the metabolism of vitamin C in animals and plants can be considered to be antivitamins C. Other oxidoreductases, such as enzymes known trivially as polyphenoloxidases and some others, may indirectly cause loss of ascorbic acid. 

As shown in Figure 1, oxidation of ascorbic acid proceeds by a one-electron process, forming mono-dehydroascorbate, which disproportionates to ascorbate and dehydroascorbate. Most tissues also contain monodehydroascorbate reductase (EC 1.6.5.4), a flavoprotein that reduces the radical back to ascorbate. Dehydroascorbate is reduced to ascorbate by dehydroascorbate reductase (EC 1.8.5.1), a glutathione-dependent enzyme little is oxidized to diketogulonic acid in human beings. 

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