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Results for “Dehydroascorbic Acid”

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PubMed1996

Protective action of dehydroascorbic acid on the Ah receptor-dependent and receptor-independent induction of lipid peroxidation in adipose tissue of male guinea pig caused by TCDD administration.

The effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on lipid peroxidation, 3H-Me-glucose (3H-Me-glu), and 14C-dehydroascorbic acid (14C-DHA) uptakes were studied in adipose tissue of male guinea pig. Under in vitro test conditions, using isolated adipose tissue in a culture medium (explant culture), TCDD reduced the uptake of 3H-Me-glu and 14C-DHA in a dose- and time-dependent fashion. The IC50 values of TCDD's action were 0.04 and 2 nM on 14C-DHA and 3H-Me-glu uptakes, respectively. TCDD (10 nM) also suppressed glucose transporting activity within 15 minutes in explant-cultured adipocytes. Cytochalasin B (CB) and nonlabeled D-glucose inhibited 14C-DHA uptake also in a dose-dependent manner. In addition, TCDD was found to induce lipid peroxidation in explant-cultured adipose tissue. This effect of TCDD was similar to that of a typical lipid peroxidation inducer, CCl4, and it was dose and time dependent. TCDD caused a statistically significant rise in lipid peroxidation at a concentration as low as 0.1 nM after 60 minutes of treatment in explant culture. Unexpectedly, the Ah receptor partial antagonists, 4,7-phenanthroline and alpha-naphthoflavone, did not fully antagonize TCDD-induced lipid peroxidation in explant-cultured adipocytes. In vivo treatment of TCDD also induced lipid peroxidation. Among seven organs of male guinea pig tested, the levels of lipid peroxidation in adipose tissue and in liver increased at 1 and 40 days following a single i.p. dose of TCDD (1 microgram/kg). The results of an in vivo time-course study indicated that such an effect of TCDD was most pronounced after 40 days of treatment. Finally, we have tested the protective role of some antioxidants on TCDD-induced lipid peroxidation under explant-culture conditions. The results indicated that DHA, but not ascorbic acid, could completely abolish TCDD-induced lipid peroxidation. The protective effect of DHA on TCDD-induced lipid peroxidation was stronger than that of alpha-tocopherol and uric acid, and this effect was blocked by CB. We conclude from these studies that TCDD acts in this guinea pig tissue through two different routes: one is the Ah receptor-dependent route causing the reduction of the level of glucose transporters and subsequent decrease of cellular uptake of DHA and the other, the Ah receptor-independent route causing the overall lipid peroxidation. Nevertheless, it appears likely that both events are antagonized by DHA.

Adipose Tissue↗
PubMed2002

Sepsis inhibits reduction of dehydroascorbic acid and accumulation of ascorbate in astroglial cultures: intracellular ascorbate depletion increases nitric oxide synthase induction and glutamate uptake inhibition.

Sepsis is associated with oxidative stress and impaired glutamatergic transmission in brain. We investigated whether sepsis impairs accumulation of the antioxidant, ascorbate, and uptake of glutamate by astrocytes. Bacterial endotoxin (Escherichia coli lipopolysaccharide, LPS) and the inflammatory cytokine, interferon-gamma (IFNgamma), were applied to primary astrocyte cultures to model sepsis. In the absence of ascorbate, the combination of LPS and IFNgamma (LPS + IFNgammay) up-regulated inducible nitric oxide synthase (iNOS) and decreased the initial rate of glutamate uptake by 50% within 24 h. Cell viability and facilitated glucose transport activity were not affected at 24 h. Pre-treatment with ascorbate-2-O-phosphate increased intracellular ascorbate concentration and attenuated the induction of iNOS and inhibition of glutamate uptake caused by LPS + IFNgamma. Subsequent experiments examined the mechanisms by which cells accumulate ascorbate. LPS + IFNy decreased slightly the initial rate of uptake of ascorbate and inhibited markedly the rate with which intracellular dehydroascorbic acid (DHAA) was reduced to ascorbate. We conclude that septic insult impairs astrocytic clearance of DHAA from the extracellular fluid and decreases intracellular ascorbate concentration. Furthermore, sepsis induces iNOS and inhibits glutamate uptake by astrocytes through mechanisms that can be modulated by intracellular ascorbate. These results indicate treatments that increase intracellular ascorbate concentration may be beneficial for patients at risk for neurologic complication in sepsis.

Animals↗
PubMed2001

Degradation of dehydroascorbic acid in parenteral nutrition mixtures.

The degradation of ascorbic acid (AA) stored in parenteral nutrition (PN) regimens is initially by oxidation, catalysed by trace elements, in particular copper. After prolonged storage the concentration of AA remains relatively constant, with little variation, due to the lack of available oxygen. The initial degradation product is dehydroascorbic acid (DHAA). This is generated in an anaerobic environment, and is hypothesised to degrade by hydrolysis. It is the purpose of this investigation to ascertain the effect of temperature and trace elements on the anaerobic degradation of DHAA, and to identify the kinetics of the reaction. A stability-indicating reversed-phase HPLC assay was used. The column contained C(18) reverse-phase packing (Luna), mean diameter 5 microm. The column dimensions were 15 cm long with an internal diameter of 0.4 cm. The mobile phase consisted of methanol: phosphate buffer (pH 7.8: 0.067 mol dm(-3)) at a ratio of 40: 60 (v/v) and also included Cetrimide (mixed alkyltrimethylammonium bromide) (0.05 mol dm(-3)) as an ion pair reagent. The flow rate was 0.7 ml min(-1) and detection was by ultra-violet light absorption at 278 nm. This assay was used to monitor the degradation rate of DHAA in PN mixtures with and without trace elements over a range of temperatures (5-35 degrees C). Results indicated a first order reaction that was temperature-dependent but trace elements independent.

Dehydroascorbic Acid↗
PubMed1984

Effects of ascorbic and dehydroascorbic acid on the multiplication of tumor ascites cells in vitro.

The effects of AA and DHA on ATP C+ cell multiplication in vitro were studied by measuring incorporation of 3H thymidine into DNA. The results obtained demonstrate that both AA and DHA have the same effects: they favor cell multiplication at low doses and inhibit it at high doses. Experiments carried out with serial doses of both these substances revealed that AA is more efficient in determining both stimulating and inhibiting effects. The lesser efficiency of DHA may be attributed to its limited stability in culture medium. Studies on the effect of high doses of AA and DHA added to the culture medium in single or fractionated doses revealed that fractionated administration is more efficient in inhibiting cell multiplication than single administration.

Animals↗
PubMed1975

Determination of vitamin C (ascorbic and dehydroascorbic acids) in foods and feeds.

Ascorbic acid (ASC) is separated by percolating the extract solution through an anionic Sephadex column. After one or two washings with water, the vitamin is oxidized on the column by a p-benzoquinone solution to dehydroascorbic acid (DASC). This latter being actually no acid is eluted as it is formed. The DASC containing eluate is treated with a new colorimetric reagent: 4-Nitro-1,2-Phenylenediamine (NPD). After extraction of the excess reagent with ethyl acetate, the optical extinction is measured at 375 nm. DASC, if present in the extract solution, can be reduced to ASC by dimercaptopropanol prior to chromatography. The method is very specific. The rather simple chromatographic purification can be effected semi-automatically with series of 10 colums (or more).

Ascorbic Acid↗
PubMed2000

A single calibration graph for the direct determination of ascorbic and dehydroascorbic acids by electrogenerated luminescence based on Ru(bpy)(3)2+ in aqueous solution

Ascorbic (H2A) and dehydroascorbic (DA) acids were for the first time directly determined in a single chromatographic run by means of the tris(2,2'-bipyridine)ruthenium(II) (Ru(bpy)(3)2+) based electrogenerated chemiluminescence (ECL) detection. For the first time, it was demonstrated that DA, a nonelectroactive compound, is ECL active and is responsible for the ECL behavior of H2A. This fact, together with the lack of a DA standard, suggested the use of a calibration graph obtained for H2A, for determining both analytes. The proven ECL activity of DA, together with literature data relative to the standard redox potentials of the different species coming from H2A, led to a reconsideration of the proposed ECL reaction mechanism for H2A. The role of the OH- ion in the reaction mechanism of the two analytes appeared to be crucial. H2A and DA could be separated by a suitable C18-reversed-phase HPLC column using an aqueous 30 mM H3PO4 solution as the mobile phase. The optimal ECL response was achieved by polarizing the working electrode at 1.150 Vvs SCE (standard calomel electrode) (oxidation diffusion limiting potential for both H2A and Ru(bpy)(3)2+). The Ru(bpy)(3)2+ solution, at pH 10 for carbonate buffer, was mixed to the eluent solution in a postcolumn system, obtaining, still at pH 10, the final 0.25 mM Ru(bpy)(3)2+ concentration. The detection limit found for the two analytes was 1 x 10(-7) M. The method was successfully applied to the determination of the analytes in a commercially available orange fruit juice.

Journal Article↗
PubMed1999

Identification of the dehydroascorbic acid reductase and thioltransferase (Glutaredoxin) activities of bovine erythrocyte glutathione peroxidase.

Bovine erythrocyte glutathione (GSH) peroxidase (GPX, EC 1.11.1.9) was examined for GSH-dependent dehydroascorbate (DHA) reductase (EC 1.8.5.1) and thioltransferase (EC 1.8.4.1) activities. Using the direct assay method for GSH-dependent DHA reductase activity, GPX had a kcat (app) of 140 +/- 9 min-1 and specificity constants (kcat/Km(app)) of 5.74 +/- 0.78 x 10(2) M-1s-1 for DHA and 1.18 +/- 0.17 x 10(3) M-1s-1 for GSH based on the monomer Mr of 22,612. Using the coupled assay method for thioltransferase activity, GPX had a kcat (app) of 186 +/- 9 min-1 and specificity constants (app) of 1. 49 +/- 0.14 x 10(3) M-1s-1 for S-sulfocysteine and 1.51 +/- 0.18 x 10(3) M-1s-1 for GSH based on the GPX monomer molecular weight. GPX has a higher specificity constant for S-sulfocysteine than DHA, and both assay systems gave nearly identical specificity constants for GSH. The DHA reductase and thioltransferase activities of GPX adds to the repertoire of functions of this enzyme as an important protector against cellular oxidative stress.

Animals↗
PubMedDate not supplied

[The antiacidotic and cardioprotective effects of fructose-1,6-diphosphate and dehydroascorbic acid].

The antiacidotic and cardioprotective effects of dehydro-L-ascorbic acid and fructose-1,6-diphosphate were compared in experiments of rats. It was found that the both compounds exhibit the antiacidotic effect on the model of metabolic acidosis in the isolated hypoxic heart, decrease the excess-lactate degree, increase ATP level in the myocardium and reduce the size of the necrosis area 4 hours after the modelling of myocardial infarction. The significance of the antiacidotic component in the mechanism of the cardioprotective action of the energy-supplying agents is concluded.

Acidosis↗
PubMed1999

Ascorbic acid-dehydroascorbate induces cell cycle arrest at G2/M DNA damage checkpoint during oxidative stress.

Reactive oxygen species induce cellular damage and have been implicated as mediators for cellular signaling pathways. However, a linkage between the cellular redox status and cell cycle progression has not been demonstrated. We previously demonstrated, using the Chinese hamster ovary cell line AS52, that the cytotoxic and mutagenic effects of oxidative stress is prevented by ascorbic acid (AA), but only when cells are treated with AA prior to treatment with the stressor. To elucidate the mechanism(s) responsible for this effect, we determined the effect of AA on cell cycle progression during oxidative stress. Flow cytometric analyses demonstrated that treatment of AS52 cells with AA (50 microM), prior to treatment with a radical generating system (RGS), enhanced cell cycle arrest at the G2/M DNA damage checkpoint when compared to cells treated with RGS. AA had no effect on cell cycle progression in the absence of oxidative stress. Furthermore, under conditions that prevent the reduction of dehydroascorbate (DHA), the oxidized form of AA, cell cycle arrest was also induced at the G2/M DNA damage checkpoint. These observations demonstrate that during periods of oxidative stress, AA functions as an antioxidant and DHA enhances transient arrest at the G2/M checkpoint by delaying the activation of cyclin B-cdc2. These results suggest the presence of a unique redox mechanism for the regulation of cell cycle progression and also demonstrate a novel mechanism by which AA protects cells from damage due to oxidative stress.

Animals↗