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PubMedDate not supplied

[Effect of alcohol intoxication on ascorbic and dehydroascorbic acid levels in rat tissue. and human blood].

It is found that acute ethanol intoxication is accompanied by a decrease in the ascorbic acid content in the brain, liver and kidneys. The content of dehydroascorbic acid in kidneys in this case increases and in the brain tends to decrease. The chronic alcohol intoxication of rats has an opposite (as compared to the acute intoxication) effect on changes in the content of ascorbic and dehydroascorbic acids in the studied organs. People with chronic alcohol intoxication have the lower content of ascorbic acid in blood plasma and the higher content in erythrocytes, the content of dehydroascorbic acid being increased.

Alcoholic Intoxication↗
PubMed1988

Effect of monosaccharide on dehydroascorbic acid uptake by placental membrane vesicles.

Dehydroascorbic acid (DHA), the oxidized form of vitamin C, is transported across the microvillous surface of the human placental syncytiotrophoblast by the D-glucose transporter. The existence of this mechanism suggests that maternal hyperglycemia may influence placental transfer of vitamin C. Therefore, we examined the effect of monosaccharides, equilibrated across the membrane, on the uptake of 0.5 mmol/L DHA by placental membrane vesicles. Relative to uptake in the absence of monosaccharide, the rate of DHA uptake was enhanced by up to 90% in the presence of 3-O-methyl-D-glucose equilibrated across the membrane. Comparable results were obtained with D-glucose and D-galactose. An inward-directed monosaccharide concentration gradient inhibited DHA uptake. However, with elevated equilibrium concentrations of monosaccharide, the magnitude of such uptake inhibition was reduced. Relative to DHA uptake at normal blood glucose concentrations (5 mmol/L), the results suggest that moderate maternal hyperglycemia does not alter, but that severe hypo- or hyperglycemia decreases, placental uptake of DHA from the maternal circulation.

3-O-Methylglucose↗
PubMedDate not supplied

[Determining the level of dehydroascorbic acid in food products].

Ascorbic acid stability was studied under conditions of dehydroascorbic acid assay. The minimum amounts of cysteine and volumes of reagents utilized were specified. Based on the data of 2,6-dibromoindophenol stability the method of indophenol-xylol extraction was proved to be unsatisfactory for the assay of dehydroascorbic acid.

Ascorbic Acid↗
PubMed1996

Reduction of extracellular dehydroascorbic acid by K562 cells.

K562 erythroleukaemic cells produced ascorbate when incubated with dehydroascorbic acid. The reduction depended on the number of cells and on the concentration of dehydroascorbic acid. The observed rate consists of a high affinity (apparent Km 7 mu M, Vmax 3 center dot 25 pmol min-1 (10(6) cells)-1 and a low affinity component, which was non-saturable up to 1 mM of DHA (rate increase of 0 center dot 1 pmol min-1 (10(6) cells)-1 (1 mu M of DHA-1). The rate was dependent on temperature and was stimulated by glucose and inhibited by phloretin, N-ethylmaleimide, parachloro-mercuribenzoate and the noyltrifluoroacetone. Although uptake of DHA proceeded at a higher rate than its extracellular reduction, the generation of extracellular ascorbate from DHA cannot be accounted for by intracellular reduction and the release of ascorbate, since the latter was not linear with time and had an initial rate of approximately 3 pmol min-1 (10(6) cells-1). At a concentration of DHA of 100 mu M this is 25 per cent of the observed reduction.

Ascorbic Acid↗
PubMed1986

Effect of ascorbic, isoascorbic and dehydroascorbic acids on the growth and survival of Campylobacter jejuni.

Ascorbic acid (AsA), added to nutrient broth at a concentration of 5 mmol/l, was bactericidal towards Campylobacter jejuni grown at 42 degrees C in a micro-aerobic atmosphere. Specific enzymes, radical scavengers, metal chelators and reducing agents were tested as possible antagonists to the cytotoxicity of AsA. The addition of catalase or of the metal chelators ceruloplasmin or Desferal did not prevent the cytotoxic effect of AsA. The addition of the hydroxyl radical scavengers mannitol, formate, histidine or DMSO also failed to counteract the toxicity of AsA. On the other hand, thiourea or cysteamine and the reducing agents cysteine or dithionite significantly increased the recovery of C. jejuni in the presence of AsA. Although the possibility of the involvement of hydroxyl radicals in AsA cytotoxicity cannot be ruled out, it appears that the toxic effect of AsA is due mostly to the formation of products of oxidation of AsA and particularly to dehydroascorbic acid (DHA). Dehydroascorbic acid was also bactericidal to C. jejuni at a concentration of 5 mmol/l. Of all the compounds tested, only cysteamine was effective in preventing (partially) the toxic effect of DHA. The growth of C. jejuni was not inhibited by the addition of 5 mmol/l of isoascorbic acid or sodium isoascorbate.

Ascorbic Acid↗
PubMed1991

Assay for both ascorbic and dehydroascorbic acid in dairy foods by high-performance liquid chromatography using precolumn derivatization with methoxy- and ethoxy-1,2-phenylenediamine.

A procedure for the simultaneous determination of both ascorbic and dehydroascorbic acid in dairy foods by high-performance liquid chromatography using precolumn derivatization with 4-methoxy- and 4-ethoxy-1,2-phenylenediamine is presented. The derivatives are isolated by solid-phase extraction and analysed by fluorescence detection on a resin-type reversed-phase column at pH 9. Retention times are 2 and 3.2 min for the derivatives of ascorbic and dehydroascorbic acid, respectively. Relative standard deviations of the within- and between-assay tests are 7.1 and 5.5%, respectively, for ascorbic and 11 and 9%, respectively, dehydroascorbic acid. The limits of detection are 50 and 70 fmol per 5-microl injection for ascorbic and dehydroascorbic acid, respectively.

Animals↗
PubMed1985

Effect of ascorbic and dehydroascorbic acid on glyoxalase enzyme system.

The authors studied the effect of ascorbic and dehydroascorbic acid on glyoxalase enzyme system, in order to establish if these substances influence cell proliferation by interfering with glyoxalase activity. The results demonstrate that both ascorbic and dehydroascorbic acid do not alter glyoxalase activity in vitro, even if employed at high doses.

Animals↗
PubMed1989

Ascorbic and dehydroascorbic acids status in rats fed diets varying in vitamin E levels.

Vitamin E, ascorbic and dehydroascorbic acids were determined in plasma and selected tissues of rats fed for 2-3 months different diets varying in vitamin E content. The diets contained as low as 5 IU for group LE, a normal amount of 50 IU for group NE and as high as 250 IU of vitamin E for group HE. Small increases in total vitamin C were observed only in liver, kidney, spleen and plasma with increased dietary levels of vitamin E, however, this was not followed by a substantial increment in the ascorbate/dehydroascorbate ratio. These differences were only observed between diets LE and HE; there was no correlation between vitamin E and vitamin C levels in the tissue. These data suggest that the interactions that readily take place in vitro between these two vitamins do not occur in vivo, probably due to the complexity of natural membranes.

Administration, Oral↗
PubMed1982

Inhibiting effect of dehydroascorbic acid on cell division in ascites tumors in mice.

The transplantable murine ascites tumors, P388 leukemia and Ehrlich carcinoma, demonstrated complete inhibition of mitotic activity after treatment with dehydroascorbic acid in mice. Citric acid at the same pH value (2.4), however, showed no diminution of mitoses. Microscopic examination of the stained ascites exudate taken from the mice treated with 10 mg dehydroascorbic acid revealed few tumor cells and a pronounced increase in white blood cells, whereas the ascites tumor exposed to citric acid appeared normal.

Animals↗
PubMed1993

Mammalian facilitative hexose transporters mediate the transport of dehydroascorbic acid.

Although vitamin C is critical to human physiology, it is not clear how it is taken up into cells. The kinetics of cell and tissue accumulation of ascorbic acid in vitro indicate that the process is mediated by specific transporters at the cell membrane. Some experimental observations have linked the transport of ascorbic acid with hexose transport systems in mammalian cells, although no clear information is available regarding the specific role(s) of these transporters, if any, in this process. Here we use the Xenopus laevis oocyte expression system to show that the mammalian facilitative hexose transporters are efficient transporters of the oxidized form of vitamin C (dehydroascorbic acid). Two transport pathways, one with low affinity and one with high affinity for dehydroascorbic acid, were found in oocytes expressing the mammalian transporters, and these oocytes accumulated vitamin C against a concentration gradient when supplied with dehydroascorbic acid. We obtained similar results in experiments using normal human neutrophils. These observations indicate that mammalian facilitative hexose transporters are a physiologically significant pathway for the uptake and accumulation of vitamin C by cells, and suggest a mechanism for the accumulation of ascorbic acid against a concentration gradient.

Animals↗
PubMed1996

Genistein is a natural inhibitor of hexose and dehydroascorbic acid transport through the glucose transporter, GLUT1.

Genistein is a dietary-derived plant product that inhibits the activity of protein-tyrosine kinases. We show here that it is a potent inhibitor of the mammalian facilitative hexose transporter GLUT1. In human HL-60 cells, which express GLUT1, genistein inhibited the transport of dehydroascorbic acid, deoxyglucose, and methylglucose in a dose-dependent manner. Transport was not affected by daidzein, an inactive genistein analog that does not inhibit protein-tyrosine kinase activity, or by the general protein kinase inhibitor staurosporine. Genistein inhibited the uptake of deoxyglucose and dehydroascorbic acid in Chinese hamster ovary (CHO) cells overexpressing GLUT1 in a similar dose-dependent manner. Genistein also inhibited the uptake of deoxyglucose in human erythrocytes indicating that its effect on glucose transporter function is cell-independent. The inhibitory action of genistein on transport was instantaneous, with no additional effect observed in cells preincubated with it for various periods of time. Genistein did not alter the uptake of leucine by HL-60 cells, indicating that its inhibitory effect was specific for the glucose transporters. The inhibitory effect of genistein was of the competitive type, with a Ki of approximately 12 microM for inhibition of the transport of both methylglucose and deoxyglucose. Binding studies showed that genistein inhibited glucose-displaceable binding of cytochalasin B to GLUT1 in erythrocyte ghosts in a competitive manner, with a Ki of 7 microM. These data indicate that genistein inhibits the transport of dehydroascorbic acid and hexoses by directly interacting with the hexose transporter GLUT1 and interfering with its transport activity, rather than as a consequence of its known ability to inhibit protein-tyrosine kinases. These observations indicate that some of the many effects of genistein on cellular physiology may be related to its ability to disrupt the normal cellular flux of substrates through GLUT1, a hexose transporter universally expressed in cells, and is responsible for the basal uptake of glucose.

Amino Acids↗
PubMed1986

Uptake of dehydroascorbic acid and ascorbic acid to isolated nerve terminals and secretory granules from ox neurohypophyses.

When uptake of L-[14C]ascorbic acid ([14C]AA) to various organs in guinea-pigs was studied after intracardiac injection, the adenohypophysis, pars intermedia, and the neurohypophysis had an uptake per milligramme protein which was about half of the uptake to the adrenals. Adrenal uptake was 20 +/- 2.8 pmol mg-1 protein microCi-1 injected. The uptake to the different parts of the hypophysis was considerably higher than the uptake to pancreas, liver, kidney, spleen and other organs. When isolated nerve endings (neurosecretosomes) from ox neurohypophyses were incubated with a medium containing labelled dehydroascorbic acid ([14C]DHA), the uptake was much slower than when the medium contained labelled ascorbic acid. The uptake of [14C]DHA showed a linear dependence on concentration, and was not influenced by addition of Mg2+ and ATP. Addition of Mg2+ + ATP, omission of Ca2+ and Mg2+ or exchange of Na+ in the medium with K+ had no effect on the uptake of ascorbic acid. When isolated secretory granules from ox neurohypophyses were incubated with a medium containing [14C]DHA, uptake was considerably faster than the uptake when they were incubated in a medium containing [14C]AA. The uptake of dehydroascorbic acid was linear with the concentration in the medium and was not changed by addition of Mg2+ ATP. Addition of 10 mM NH4Cl or exchange of 120 mM K+ in the incubation medium with Na+ did not change the uptake of dehydroascorbic acid. The contents of copper, zinc, iron and cobalt were determined in isolated nerve endings (A) and membranes (B) as well as in lysate (C) from isolated neurosecretory granules. The results (in nmol mg-1 protein) were for Cu: (A): 0.25 +/- 0.01 (SEM), (B): 0.67 +/- 0.16, (C): 0.22 +/- 0.06; for Zn: (A): 0.53 +/- 0.13, (B): 6.97 +/- 0.75, (C): 1.8 +/- 0.53; and for Fe: (A): 15.6 +/- 1.9, (B): 6.92 +/- 0.32, (C): 3.15 +/- 0.43. In all preparations the cobalt content was below the detection limit (less than 5 pmol mg-1 protein).

Animals↗
PubMed1989

Liquid chromatographic and fluorescent derivative aerobic degradation studies of dehydroascorbic acid in aqueous solution at elevated temperatures.

The aqueous degradation of dehydroascorbic acid (DHA) has been studied in the temperature range 52-90 degrees C. The DHA was determined by reversed-phase liquid chromatography and by derivatisation of DHA with o-phenylenediamine to form the fluorescent quinoxaline. The pseudo-first-order degradation of DHA has been verified and rate constants for the process are presented. The role of DHA in the degradation of ascorbic acid and previous DHA solution stability studies are discussed.

Ascorbic Acid↗