Mechanisms of ascorbic acid

Lowry JP, O Neill RD. Homogeneous mechanism of ascorbic acid interference in hydrogen peroxide detection at enzyme-modified electrodes. Analytical Chemistry 1992, 64, 453 156. 

The mechanism of this eflFect is not known. Hill and Starcher (49) postulated that reduction of copper from its divalent (cupric) state to its monovalent (cuprous) state accounted for the impaired absorption of copper in the presence of ascorbic acid they produced the same effect with another reducing agent, dimercaptopropanol (BAL). This explanation has been accepted by others (56), although the oxidation state of copper for maximum intestinal absorption has not been established. An intramucosal competition of ascorbic acid for sulfhydryl sites on metallo-thioneins was demonstrated (57). If this ligand has any regulatory role in copper uptake, this alternative mechanism of ascorbic acid-copper interaction could explain the mechanism. Experimental confirmation of an ascorbic-acid-induced inhibition of copper absorption in the human intestine has not been presented. 

There must also be a second mechanism of ascorbic acid transport through certain specialized cells, difierent from the diffusion of dehydro-ascorbic acid followed by intracellular reduction. There are no indications that dehydroascorbic acid is involved in the renal tubular absorption of ascorbic acid, and, contrary to earlier conclusions, it appears that the concentration of ascorbic acid into the aqueous humors of the eye occurs in the form of ascorbic acid itself. 

The traditional approach has been to accept that flavonoids retard the copper-catalysed oxidation of ascorbic acid by chelating with copper and possibly other trace elements. Harper, Morton and Rolfe have shown that the protective mechanism is possibly more complex than this they found that flavonoids exerted a strong protective action under conditions where EDTA (a potent inhibitor of copper-catalysed ascorbic aci oxidation) was ineffective [67]. As an alternative and possibly complementary mechanism, they suggested that the protective capacity is derived from the ability of flavonoids to act as free radical acceptors free radical formation is believed to be an important phase of ascorbic acid oxidation [67]. It should be noted, however, that the model system used for these studies was designed primarily to elucidate the mechanism of ascorbic acid protection by flavonoid in fruit juices at a low pH it would be improper, without qualification, to extrapolate them to physiological conditions of pH, temperature and concentration. 

Horio, F., and Yoshida, A., 1993, Regulatory mechanism of ascorbic acid biosynthesis stimulated by xenobiotics. Vitamins (Japan) 67 657-665. 

Ibric, L. L., Peterson, A. R., and Sevanian, A., 1991, Mechanisms of ascorbic acid-induced inhibition of chemical transformation in C3H/10T1/2 cells. Am. J. Clin. Nutr. 54 12368-12408. 

The oxidation mechanism of ascorbic acid has incited much research (Makaga and Maujean, 1994). It functions like an oxidation-reduction system. Its oxidized form is dehydroascorbic acid (Figure 9.2) ... 

Tissue, leukocyte, and plasma levels of ascorbic acid are quite variable and tend to fall in a "stress" situation (even myocardial infarction), with a corresponding fall in urinary excretion of ascorbic acid in the unsupplemented state.18 24 xhe amount of vitamin C within leukocytes on the 2nd or 3rd day after the onset of a cold is often at scorbutic levels,19 although the mechanisms of ascorbic acid uptake by leukocytes are not imparled by the stress of infection.23... 

Tetra Acetyl Glucosone Hydrate. A Novel Route to the Syntheses of Analogues of Ascorbic Acid and a Possible Mechanism for the Transformation of Hexoses into Kojic Acid, M. Stacey and L. M. Turton, J. Chem. Soc., (1946) 661 -664. 

Identical kinetics are found for the uranyl ion-catalysed aerobic oxidation of ascorbic acid and a similar mechanism has been put forward These results and others afford a sequence of catalytic activity for the aerobic oxidation of ascorbic acid ... 

A typical result for DPV In Fig. 4a shows the presence of two redox couples with peak potentials of 0.25 V and 0.19 V ( lOmV). Similar results have also been obtained with SWV. The relative Intensities of the two peaks vary from sample to sample but are always present with activated electrodes. The similarities between the potentials found for the surface species and for the oxidation of ascorbic acid suggest that an ec catalytic mechanism may be operative. The surface coverage of the o-qulnone Is estimated to be the order of 10 mol cm . It Is currently not possible to control the surface concentration of the o-qulnone-llke species or the oxygen content of the GCE surface. 

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. 

A chemical reaction subsequent to a fast (reversible) electrode reaction (Eq. 5.6.1, case b) can consume the product of the electrode reaction, whose concentration in solution thus decreases. This decreases the overpotential of the overall electrode process. This mechanism was proposed by R. Brdicka and D. H. M. Kern for the oxidation of ascorbic acid, converted by a fast electrode reaction at the mercury electrode to form dehydro-ascorbic acid. An equilibrium described by the Nernst equation is established at the electrode between the initial substance and this intermediate product. Dehydroascorbic acid is then deactivated by a fast chemical reaction with water to form diketogulonic acid, which is electroinactive. 

The conversion of L-xylosone into L-ascorbic acid has been reversed by treating the latter with pert-naphthindan-2,3,4-trione hydrate184 2,3-dioxo-L-zj/fo-hexonic acid is formed and is decarboxylated to L-xylosone. It was suggested that the destruction of ascorbic acid in vivo by this mechanism might explain the relatively high requirements for the vitamin in many species. 

Iron(III)-catalyzed autoxidation of ascorbic acid has received considerably less attention than the comparable reactions with copper species. Anaerobic studies confirmed that Fe(III) can easily oxidize ascorbic acid to dehydroascorbic acid. Xu and Jordan reported two-stage kinetics for this system in the presence of an excess of the metal ion, and suggested the fast formation of iron(III) ascorbate complexes which undergo reversible electron transfer steps (21). However, Bansch and coworkers did not find spectral evidence for the formation of ascorbate complexes in excess ascorbic acid (22). On the basis of a combined pH, temperature and pressure dependence study these authors confirmed that the oxidation by Fe(H20)g+ proceeds via an outer-sphere mechanism, while the reaction with Fe(H20)50H2+ is substitution-controlled and follows an inner-sphere electron transfer path. To some extent, these results may contradict with the model proposed by Taqui Khan and Martell (6), because the oxidation by the metal ion may take place before the ternary oxygen complex is actually formed in Eq. (17). 

The oxidative behaviour of glycolaldehyde towards hexacyanoferrate(III) in alkaline media has been investigated and a mechanism proposed, which involves an intermediate alkoxide ion. Reactions of tetranitromethane with the luminol and luminol-peroxide radical anions have been shown to contribute substantially to the tetranitromethane reduction in luminol oxidation with hexacyanoferrate(III) in aerated aqueous alkali solutions. The retarding effect of crown ethers on the oxidation of triethylamine by hexacyanoferrate(III) ion has been noted. The influence of ionic strength on the rate constant of oxidation of ascorbic acid by hexacyanofer-rate(III) in acidic media has been investigated. The oxidations of CH2=CHX (where X = CN, CONH2, and C02 ) by alkaline hexacyanoferrate(III) to diols have been studied. ... 

When several temperature-dependent rate constants have been determined or at least estimated, the adherence of the decay in the system to Arrhenius behavior can be easily determined. If a plot of these rate constants vs. reciprocal temperature (1/7) produces a linear correlation, the system is adhering to the well-studied Arrhenius kinetic model and some prediction of the rate of decay at any temperature can be made. As detailed in Figure 17, Carstensen s adaptation of data, originally described by Tardif (99), demonstrates the pseudo-first-order decay behavior of the decomposition of ascorbic acid in solid dosage forms at temperatures of 50° C, 60°C, and 70°C (100). Further analysis of the data confirmed that the system adhered closely to Arrhenius behavior as the plot of the rate constants with respect to reciprocal temperature (1/7) showed linearity (Fig. 18). Carsten-sen suggests that it is not always necessary to determine the mechanism of decay if some relevant property of the degradation can be explained as a function of time, and therefore logically quantified and rationally predicted. 

P. A. Garcia, R. Velasco, and F. Barba, Role of trace metal ions. Kinetic and mechanism of the copper(II)-catalyzed oxidation of ascorbic acid (vitamin C) from protected derivatives of D-glucitol, Synth. Commun., 21 (1991) 1153-1161. 

Studies on the antioxidant properties of anthocyanins on human low-density lipoprotein (LDL) and lecithin liposome systems in vitro showed that the inhibition of oxidation increased dose-dependently with antioxidant concentration. The oxidation was catalyzed by copper in the LDL system and the effects of the anthocyanins were explained by several antioxidant mechanisms including hydrogen donation, metal chelation and protein binding [33]. Anthocyanins also prevented the oxidation of ascorbic acid (vitamin C), through chelate formation with the metal ions, and finally by the formation of an ascorbic (copigment)-metal-anthocyanin complex [49]. 

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