Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Dehydroascorbic Acid”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources
PubMed1982

Hexavalent chromium and ascorbic acid interaction on proliferation of the human cell line NHIK3025.

When cells from the human cell line NHIK3025 were cultured for 4 days, with hexavalent chromium (K2Cr2O7) at a concentration of 8 . 10(-7)M, the relative cell number was reduced to 38%. This effect of hexavalent chromium was abolished if ascorbic acid and chromate were added simultaneously to the incubation medium, but not if ascorbic acid was added 24 h prior to chromate addition. Dehydroascorbic acid was not able to reduce the effect of K2Cr2O7 either when added simultaneously or when added 24 h prior to chromate exposure. Therefore, the cells could only be protected against the toxic effect of hexavalent chromium when ascorbic acid was added at the same time as K2Cr2O7.

Ascorbic Acid↗
PubMed2001

Inactivation of protein farnesyltransferase by active-site-targeted dicarbonyl compounds.

Upon farnesylation by protein farnesyltransferase (FTase), key proteins become compartmentalized in cells. For example, cell membrane localization is essential for the mitogenic role of mutant Ras protein, which acts as a switch for cancer cell proliferation. We report that alpha-dicarbonyl compounds derived from the isoprenoid skeleton or other hydrophobic groups potently obstruct farnesylation of a Ras model peptide by human recombinant FTase in vitro. A geranyl-derived isoprenoid diketone, 5,9-dimethyl-8-decene-2,3-dione, at 17 microM caused a 62% reduction in FTase activity after 30 minutes. A farnesyl-derived isoprenoid diketone, 5,9,13-trimethyl-8,12-tetradecadiene-2,3-dione, at 93 microM caused a 94% reduction after 30 minutes. Other dicarbonyl compounds found to be effective against FTase in vitro were (+/-)-6-(camphorquinone-10-sulfonamido)-hexanoic acid, 4,4'-biphenyldiglyoxaldehyde, dehydroascorbic acid 6-palmitate, 2-oxododecanal, and phenylglyoxal. Higher concentrations of the alpha-dicarbonyl compound resulted in more rapid and more extensive inactivation. These findings demonstrate that alpha-dicarbonyl compounds targeted to FTase interfere with protein farnesylation in vitro and may lead to derivatives that have utility as chemotherapeutic agents.

Alkenes↗
PubMed1996

Effects of morphine treatment and withdrawal on striatal and limbic monoaminergic activity and ascorbic acid oxidation in the rat.

Since ascorbic acid (AA) reportedly suppresses tolerance to and dependence on morphine in humans and rodents, levels of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 3-methoxytyramine (3-MT), 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), AA, dehydroascorbic acid (DHAA), uric acid, xanthine, hypoxanthine, glutamate and gamma-aminobutyric acid (GABA) were determined by high-pressure liquid chromatography (HPLC) in the striatum and in the limbic forebrain of the rat following morphine treatment (single or repeated) and withdrawal. Single morphine administration (20 mg/kg s.c.) increased DOPAC + HVA/DA, 5-HIAA/5-HT and DHAA/AA ratios, uric acid levels, and decreased xanthine, hypoxanthine, glutamate and GABA levels in both regions. 3-MT levels were decreased in the striatum and increased in the limbic forebrain. After 7 days of morphine treatment, striatal DOPAC + HVA/DA and DHAA/AA ratios and uric acid levels were still higher and striatal and limbic xanthine levels still lower than in controls, while all other parameters were in the range of control values in both regions. Morphine treatment also increased the glutamate/GABA ratio in the striatum. In all morphine-treated rats, individual striatal DOPAC + HVA/DA and DHAA/AA ratio values were directly correlated. After a 48 h withdrawal period, both striatal AA oxidation and glutamate/GABA ratio further increased; limbic 3-MT levels further decreased, while all other parameters did not differ from control values. We conclude that: (i) tolerance to morphine-induced increase in hypoxanthine, xanthine and AA oxidation develops in the limbic forebrain faster than in the striatum; (ii) the morphine-induced increase in striatal and limbic AA oxidation may be considered a consequence of increased formation of reactive oxygen species due to increased DA, hypoxanthine and xanthine oxidative metabolism; (iii) a striatal excitotoxic imbalance characterizes the withdrawal state and may be taken into account to explain the further increase in striatal AA oxidation.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

Cellular defence mechanisms in the striatum of young and aged rats subchronically exposed to manganese.

A deficiency of striatal dopamine (DA) is generally accepted as an expression of manganese (Mn) toxicity in experimental animals. Since compromised cellular defence mechanisms may be involved in Mn neurotoxicity, we investigated the response of the neuronal antioxidant system [ascorbic acid (AA) oxidation, glutathione (GSH) and uric acid levels] and neurochemical changes in the striatum in aged rats exposed to Mn. Levels of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), AA, dehydroascorbic acid (DHAA), GSH and uric acid were determined after subchronic oral exposure to MnCl2 200 mg/kg (3-month-old rats) and 30-100-200 mg/kg (20-month-old-rats). Aged rats had basal levels of striatal DA, DOPAC, HVA, 5-HT, 5-HIAA, GSH and AA lower than those of young rats. In the striatum of aged rats, Mn induced biphasic changes in the levels of DA, DOPAC, HVA (an increase at the lower dose and a decrease at the higher dose) and DHAA (opposite changes). Mn decreased GSH levels and increased uric acid levels both in the striatum and in synaptosomes in all groups of aged rats. All of these parameters were affected to a lesser extent in young rats. In conclusion, the response of cellular defence mechanisms in aged rats is consistent with a Mn-induced increase in the formation of reactive oxygen species. An age-related impairment of the neuronal antioxidant system may play an enabling role in Mn neurotoxicity.

Aging↗
PubMed1995

Whole body X-ray irradiation to mice decreases ascorbic acid concentration in bone marrow: comparison between ascorbic acid and vitamin E.

The change in the ascorbic acid concentration in the bone marrow after whole body X-ray irradiation was compared with that in the vitamin E concentration. The ascorbic acid concentration in the bone marrow significantly decreased by 30% 1 h after exposure to 3 Gy of X-rays, whereas the vitamin E concentration in the bone marrow was significantly decreased 5 h after exposure, when the level of ascorbic acid was less than 10% of that in the control. At 24 h after exposure, the ascorbic acid concentration in the bone marrow was significantly decreased by 80% after exposure to 0.5 Gy, whereas the vitamin E concentration was significantly decreased after exposure to 1 Gy or more. In the bone marrow, the decrease in the ascorbic acid concentration was accompanied by a marked increase in the concentration of dehydroascorbic acid, an oxidized form of ascorbic acid. X-ray irradiation did not decrease either the ascorbic acid or vitamin E concentration in the serum or intestine. These findings suggest that the bone marrow is more highly susceptible to oxidative damage by radiation and that ascorbic acid plays an important defense role against it. On Day 8 after irradiation, the decreases in the vitamin E and ascorbic acid concentrations in the bone marrow showed recovery after exposure to 3 Gy, but not after the exposure to 6 Gy.

Animals↗
PubMed2006

Coenzyme Q(1) depletes NAD(P)H and impairs recycling of ascorbate in astrocytes.

Ascorbate is an important antioxidant in the brain. Astrocytes are capable of recycling ascorbate by taking up and then reducing its oxidation product dehydroascorbic acid (DHAA) using reducing equivalents derived from NAD(P)H. Astrocytes also contain NAD(P)H-dependent quinone reductases, such as NAD(P)H:quinone oxidoreductase (NQO1), which are capable of reducing coenzyme Q and its analogs. Short-chain coenzyme Q analogs have been proposed as therapeutic agents for neurodegenerative illnesses, but they may cause oxidative stress by non-enzymatic redox cycling or enzyme-dependent depletion of NAD(P)H. Therefore, we tested the hypothesis that the short-chain coenzyme Q analog coenzyme Q(1) (CoQ(1), ubiquinone-5) decreases intracellular NAD(P)H levels in astrocytes and impairs the ability of these cells to replace extracellular DHAA with ascorbate (i.e., ascorbate recycling). We observed that CoQ(1) inhibited the production of intra- and extracellular ascorbate by primary rat astrocytes incubated with DHAA in glucose-free medium. Reduction of CoQ(1) to CoQ(1)H(2) by astrocytes was partially blocked by the NQO1 inhibitor dicumarol but was not affected by DHAA. The inhibition of ascorbate recycling by CoQ(1) was attenuated by dicumarol and was abolished by glucose. CoQ(1) lowered intracellular levels of reactive oxygen species, as measured by oxidation of 2',7'-dichlorofluorescin but also produced marked decreases in the concentrations of NADH and NADPH. We conclude that in astrocytes CoQ(1) recycling depletes NAD(P)H and inhibits ascorbate recycling when glucose metabolism is limited. Because DHAA can cause cell-lethal oxidative stress in neurons and ascorbate produced by astrocytes may be neuroprotective, coenzyme Q analogs may adversely affect brain function through this novel mechanism.

Animals↗
PubMed2005

Sepsis inhibits recycling and glutamate-stimulated export of ascorbate by astrocytes.

Sepsis causes brain dysfunction. Because neurotransmission requires high ascorbate and low dehydroascorbic acid (DHAA) concentrations in brain extracellular fluid, the effect of septic insult on ascorbate recycling (i.e., uptake and reduction of DHAA) and export was investigated in primary rat and mouse astrocytes. DHAA raised intracellular ascorbate to physiological levels but extracellular ascorbate only slightly. Septic insult by lipopolysaccharide and interferon-gamma increased ascorbate recycling in astrocytes permeabilized with saponin but decreased it in those with intact plasma membrane. The decrease was due to inhibition of the glucose transporter (GLUT1) that translocates DHAA because septic insult slowed uptake of the nonmetabolizable GLUT1 substrate 3-O-methylglucose. Septic insult also abolished stimulation by glutamate of ascorbate export. Specific nitric oxide synthase (NOS) inhibitors and nNOS and iNOS deficiency failed to alter the effects of septic insult. Inhibitors of NADPH oxidase generally did not protect against septic insult, because only one of those tested (diphenylene iodonium) increased GLUT1 activity and ascorbate recycling. We conclude that astrocytes take up DHAA and use it to synthesize ascorbate that is exported in response to glutamate. This mechanism may provide the antioxidant on demand to neurons under normal conditions, but it is attenuated after septic insult.

3-O-Methylglucose↗
PubMed2002

Effect of processing techniques at industrial scale on orange juice antioxidant and beneficial health compounds.

Phenolic compounds, vitamin C (L-ascorbic acid and L-dehydroascorbic acid), and antioxidant capacity were evaluated in orange juices manufactured by different techniques. Five processes at industrial scale (squeezing, mild pasteurization, standard pasteurization, concentration, and freezing) used in commercial orange juice manufacturing were studied. In addition, domestic squeezing (a hand processing technique) was compared with commercial squeezing (an industrial FMC single-strength extraction) to evaluate their influences on health components of orange juice. Whole orange juice was divided into soluble and cloud fractions after centrifugation. Total and individual phenolics were analyzed in both fractions by HPLC. Commercial squeezing extracted 22% more phenolics than hand squeezing. The freezing process caused a dramatic decrease in phenolics, whereas the concentration process caused a mild precipitation of these compounds to the juice cloud. In pulp, pasteurization led to degradation of several phenolic compounds, that is, caffeic acid derivatives, vicenin 2 (apigenin 6,8-di-C-glucoside), and narirutin (5,7,4'-trihydroxyflavanone-7-rutinoside) with losses of 34.5, 30.7, and 28%, respectively. Regarding vitamin C, orange juice produced by commercial squeezing contained 25% more of this compound than domestic squeezing. Mild and standard pasteurization slightly increased the total vitamin C content as the contribution from the orange solids parts, whereas concentration and freezing did not show significant changes. The content of L-ascorbic acid provided 77-96% of the total antioxidant capacity of orange juice. Mild pasteurization, standard pasteurization, concentration, and freezing did not affect the total antioxidant capacity of juice, but they did, however, in pulp, where it was reduced by 47%.

Antioxidants↗
PubMed2004

Varietal difference in vitamin C content in the fruit of kiwifruit and other actinidia species.

Vitamin C content in the fruit of various cultivars of kiwifruit and other Actinidia species was estimated by determination of L-ascorbic acid and L-dehydroascorbic acid using ion-pair reversed-phase high-performance liquid chromatography. Fruit of A. deliciosa cv. Hayward, the most common commercially available cultivar, contained 65.5 mg/100 g fresh weight (FW) vitamin C. Vitamin C content in A. deliciosa fruit varied from 29 mg/100 g FW to 80 mg/100 g FW. In most cultivars of A. chinensis, vitamin C content in fruit was higher than that of Hayward. In particular, vitamin C content in cv. Sanuki Gold fruit reached more than 3-fold that of Hayward on a weight for weight basis. In A. argutafruit, there was wide variation in vitamin C content, with concentrations ranging from 37 to 185 mg/100 g FW. In cv. Gassan, Issai, and Mitsuko, vitamin C content of the fruit was much higher than that of Hayward. In A. arguta fruit, the ratio of L-ascorbic acid to total ascorbic acid tended to be higher than that of other species.

Actinidia↗
PubMed1990

Determination of L-ascorbic acid in fruit and vegetable juices by flow injection with immobilised ascorbate oxidase.

Ascorbate oxidase was immobilised on cyanogen bromide activated-Sepharose 4B and incorporated in a flow-injection system with amperometric detection at a glassy carbon electrode at +0.6 V. On passage through the immobilised ascorbate oxidase a fraction of the L-ascorbic acid was converted into dehydroascorbic acid and the decrease in signal was measured. This could be directly related to the amount of L-ascorbic acid present. The calibration graph was linear over the range 0-400 ng ml(-1) with a correlation coefficient of 0.9994. The detection limit (2 sigma) in phosphate buffer (0.08 M, pH 5.5) was 4.0 ng ml(-1). The relative standard deviation for a 200 ng ml(-1) standard was 1.0% (n = 10) and the sampling throughput was 30 samples h(-1). The method was used for the simple and rapid determination of L-ascorbic acid in fruit and vegetable juice.

Ascorbate Oxidase↗
PubMed2001

Alterations in intragastric nitrite and vitamin C levels during acid inhibitory therapy.

Most nitrite entering the healthy acid-secreting stomach is derived from dietary nitrate. The latter is absorbed from the small intestine, 25% then being secreted by the salivary glands into the mouth. Buccal organisms subsequently convert 20% of this nitrate to nitrite. When this nitrite is swallowed, the ascorbic acid in the acidic gastric juice reduces it to nitric oxide, which is absorbed by the mucosa. In the process, the ascorbic acid is oxidized to dehydroascorbic acid. When the intragastric pH is elevated by powerful anti-secretory agents, this gastric chemistry is profoundly modified. At a neutral pH, the swallowed nitrite does not react with ascorbic acid but accumulates in the stomach. The level of nitrite in the gastric juice during treatment with anti-secretory medication is particularly high after a nitrate-containing meal. Powerful anti-secretory medication also lowers the intragastric concentration of ascorbic acid and total vitamin C, probably because of the relative instability of the vitamin at a higher pH. These changes in the intragastric concentrations of nitrite and ascorbic acid are most marked in Helicobacter pylori -infected subjects on proton pump inhibitor therapy. It is recognized that an elevated nitrite-to-ascorbic acid ratio predisposes to the formation of potentially carcinogenic N -nitroso compounds. It is, however, unclear at present whether such compounds are formed within the human stomach.

Anti-Ulcer Agents↗
PubMed2004

Evaluation of the hepatic reduction of a nitroxide radical in rats receiving ascorbic acid, glutathione or ascorbic acid oxidase by in vivo electron spin resonance study.

BACKGROUND: A nitroxide radical, 4-hydroxyl-2,2,6,6-tetramethylpiperidin-1-oxyl (TEMPOL), is directly reduced to hydroxylamine by ascorbic acid (AsA). Ascorbic acid is oxidized to dehydroascorbic acid (DHA) by ascorbic acid oxidase (AAOx), and DHA is reduced to AsA by glutathione (GSH). In the present study, in vivo and ex vivo reduction of TEMPOL in the rat liver under various conditions of AsA supply was investigated using an electron spin resonance (ESR) spectrometer equipped with a surface coil-type resonator. METHODS: To investigate in vivo hepatic reduction of TEMPOL, an ESR study of the liver of living rats which orally received AsA or intravenously received GSH or AAOx was made. To investigate direct interactions between TEMPOL and GSH or AAOx, an in vitro ESR study was conducted. To investigate TEMPOL reduction in the hepatic homogenate, an ex vivo ESR study was performed. RESULTS: Ascorbic acid and GSH administration increased the in vivo hepatic reducing ability of TEMPOL. In contrast, AAOx administration decreased the reducing ability. In vitro TEMPOL was not reduced by GSH and hydroxylamine was not oxidized by AAOx. Reducing ability in the hepatic homogenate of AAOx-treated rats decreased, but that for GSH-treated rats was unchanged. CONCLUSION: Ascorbic acid administration directly increases hepatic reducing ability. Ascorbic acid, which increased in the plasma due to GSH administration, entered the liver and enhanced the hepatic reducing ability. Administration of AAOx impaired the hepatic reducing ability by oxidizing AsA in the plasma and/or the liver.

Animals↗
PubMed1983

Ascorbic acid inhibition of Campylobacter jejuni growth.

The inhibitory effect of ascorbic acid on Campylobacter jejuni is described. In vitro growth of clinical strains, as measured spectrophotometrically, was inhibited by 0.5 mg of freshly prepared L-ascorbic acid per ml. Alkaline-treated or aged L-ascorbic acid increased inhibition, as did copper; however, L-cysteine, L-cystine, and glutathione prevented inhibition. Biochemical analysis of the medium and cultures indicated that one or more of the oxidation products of L-ascorbic acid, e.g., L-dehydroascorbic acid or L-diketogulonic acid, were more effective inhibitors than was reduced L-ascorbic acid.

Ascorbic Acid↗
PubMed2001

Reduction of dehydroerythorbic acid in vitamin C-deficient guinea pigs.

A reduction of dehydroerythorbic acid (DERA) to erythorbic acid (ERA) in vitamin C-deficient guinea pigs was evaluated and compared with that of dehydroascorbic acid (DASA). Thirty-six guinea pigs were fed with vitamin C-deficient diets for 18 days. On day 19, the guinea pigs were divided into four groups for the administration of 100 mg of DERA, ERA, ascorbic acid (ASA), or DASA every day. After 12 days of oral administration, the concentration of DERA, ERA, ASA, and DASA in the liver, adrenal, spleen, kidney, and plasma of guinea pigs was determined by HPLC. A recovery from scurvy was measured in terms of weight gain and serum alkaline phosphatase activity. All four groups showed similar recovery, indicating that the oral administration of relatively high concentrations of DERA reversed the effects of scurvy in vitamin C-deficient guinea pigs. In spite of DERA or DASA administration, ERA or ASA was mainly detected in the tissues. The reduction ratios of DEAR and DASA were similar (approximately 80%) in all tissues except spleen. These results suggest that both DASA and DERA are taken up and reduced to ASA or ERA in vivo.

Animals↗
PubMed1999

[Determination of vitamin C in selected fruit and vegetable products].

A simple method was described to determine vitamin C as L-ascorbic acid (after reduction of dehydroascorbic acid by means of dithiothreitol) in fruit juices, fruit and vegetable-fruit nectars. Ascorbic acid was analyzed by RP-HPLC technique with UV detection (254 nm). The average recovery of ascorbic acid was 92-103% and limits of identification and detection were 0.003 and 0.009 mg/ml of products respectively.

Ascorbic Acid↗
PubMed2005

Use of ascorbate-rich dialysate to attenuate oxidative stress in maintenance hemodialysis patients.

BACKGROUND: Oxidative stress exists in uremic milieu, particularly in maintenance hemodialysis (MHD) patients, and accounts for certain long-term complications. Yet little is known about whether supplementation of ascorbic acid (vitamin C, or vitC) via extracorporeal circuit has substantial effects on minifying oxidative impairment. SUBJECTS AND METHODS: The entire experiment consisted of three sections: 1) Practicing ascorbate dialysate among 8 MHD patients in a single dialysis session, compared with a conventional hemodialysis session and another one with intravenous injection of vitC. In each session, oxidative stress markers--namely, plasma total ascorbic acid (TAA), ratio of dehydroascorbic acid (DHAA) to TAA (DHAA/TAA), vitamin E (vitE), and malondialdehyde (MDA)--in both plasma and erythrocytes were measured. 2) A relatively long-term application of ascorbate dialysate in 12 of 23 MHD patients, who were randomly allocated to experimental group (n = 12), and control group (n = 11). Oxidative stress markers and main hematological and biochemical indices were determined at the beginning and end of the period. 3) Application of ascorbate dialysate in 10 MHD patients with intravenous iron treatment, performed in similar procedures as section 1. In addition to determining the aforementioned oxidative stress markers, area under the curve (AUC0-180 min) of ratio of plasma MDA to cholesterol (MDA:Cho) was calculated to evaluate the extent of lipoperoxidation. RESULTS: 1) Plasma TAA gradually decreased during dialysis, whereas a mild increase appeared in MDA. A protruding TAA concentration peak, as well as an extreme DHAA/TAA reduction, followed the injection of vitC, but soon a precipitous fall in DHAA/TAA ensued. Stable plasma TAA and slightly raised vitE were observed when applying ascorbate dialysate. 2) Plasma TAA augmented (27.4 +/- 13.3 vs. 16.8 +/- 9.5 mg/dL, P < .05) and plasma low-density lipoprotein (oxLDL) became two-thirds of baseline data (32.6 +/- 25.2 vs. 83.8 +/- 56.5 micromol/L, P < .05) in the experimental group, whereas oxLDL in the control group reduced quantitatively but not significantly in statistics. (3) As iron sucrose was infused, the decline of TAA and ascending of MDA would be abated not only by intravenous drop of vitC, but also by ascorbate dialysate; however, TAA or MDA curve manifested totally distinguished in the two modalities. AUC0-180 min in ascorbate dialysate group was significantly less than that in control group (400.25 +/- 28.54 vs. 487.25 +/- 109.82). CONCLUSION: Plasma ascorbic acid diminished a great deal during hemodialysis, and at the same time oxidative stress formed and intensified, which will be exacerbated by a remedy of frequent intravenous iron. Ascorbate supplementation, by means of either infusion or extracorporeal circuit, can lessen the loss and therefore attenuate oxidative stress. The latter pattern takes the advantage of retaining the approximate internal balance instead of exquisite change in vivo due to administration of intravenous vitC.

Ascorbic Acid↗
PubMed2004

Chromatographic study of photolysis of aqueous cyanocobalamin solution in presence of vitamins B and C.

Aqueous cyanocobalamin solutions (pH 1-7) have been photolysed in the presence of individual B (thiamine HCl, riboflavin, nicotinamide and pyridoxine HCl) and C (ascorbic acid) vitamins with visible light. The degraded solutions were subjected to thin-layer chromatography using several solvent systems and the Rf values of the vitamins and their photoproducts were determined. The major photoproducts have been identified by comparison of their Rf values with those of the authentic compounds. Cyanocobalamin leads to the formation of hydroxocobalamin. Thiamine HCl gives rise to 4-methyl-5-(Beta-hydroxyethyl) thiazole and 2-methyl-4-amino-5-hydroxymethyl-pyrimidine in trace amounts whereas riboflavin degrades extensively to formylmethylflavin and lumichrome, and to a smaller extent to lumiflavin and carboxymethylflavin. Ascorbic acid is oxidized to dehydroascorbic acid. Nicotinamide and pyridoxine HCl do not undergo any degradation. The extent of degradation depends upon the pH.

Journal Article↗