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PubMed1999

Ascorbic acid treatment to reduce residual halogen-based oxidants prior to the determination of halogenated disinfection byproducts in potable water.

Treatment of potable water samples with ascorbic acid has been investigated as a means for reducing residual halogen-based oxidants (disinfectants), i.e. HOCl, Cl2, Br2 and BrCl, prior to determination of EPA Method 551.1A and 551.1B analytes. These disinfection byproducts include certain haloalkanes, haloalkenes, haloethanenitriles, haloaldehydes, haloketones and trichloronitromethane. When used as a dehalogenating agent immediately before analysis, only one analyte, 2,2,2-trichloroethanediol (chloral hydrate), is significantly decomposed. Ascorbic acid is superior to thiosulfate and sulfite as it does not destroy trichloroethanenitrile (trichloroacetonitrile), trichloronitromethane (chloropicrin) or dibromoethanenitrile (dibromoacetonitrile). Unlike ammonia or amines, it is not nucleophilic and cannot form hemiaminals (carbinolamines) with carboxaldehydes and ketones. Ascorbic acid treatment can rapidly consume (reduce) large amounts of active (oxidizing) halogen compounds, producing only inorganic halides and dehydroascorbic acid and not additional halogenated organic molecules.

Ascorbic Acid↗
PubMed2000

A simple and rapid method for the routine assay of total ascorbic acid in serum and plasma using ascorbate oxidase and o-phenylenediamine.

A simple and rapid analysis of total ascorbic acid (AsA) in serum and plasma and its automated analysis are described. AsA is oxidized by ascorbate oxidase (AsA oxidase) to dehydroascorbic acid that then reacts with o-phenylenediamine (OPDA) to form a quinoxaline derivative that absorbs at 340 nm. The change in absorbance is directly proportional to the total AsA concentration. The assay was validated with a linear concentration range of 0.8-80 mg/L, and the within-day and between-day assays precision did not exceed 8.6% and 12.5%, respectively. On 47 sera, the manual enzymatic procedure gave 0.2 mg/L on average lower values than those of an automated enzymatic procedure with a correlation coefficient of 0.847. On another 66 sera, results by automated enzymatic method correlated well with the HPLC method and the regression equation is Y (enzymatic, automated)=0.97 X (HPLC)+0.1, r=0.980, Sy.x=0.6 mg/L. An experienced analyst can perform about 24 manual assays per hour whereas the automated procedure gave a rate of 100 assays per hour.

Ascorbate Oxidase↗
PubMed1996

Re-evaluation of myocardial FDG uptake in hyperglycemia.

UNLABELLED: Myocardial [18F] fluorodeoxyglucose (FDG) uptake depends on several metabolic variables in vivo. The effect of different levels of experimentally induced hyperglycemia on myocardial FDG uptake was examined. METHODS: FDG uptake was studied in young Donryu rats 1 hr after intravenous injection under various pretreatments that increased serum glucose levels. Serum samples were analyzed for glucose, insulin and free fatty acids. Myocardial distribution of FDG was examined with autoradiography. RESULTS: Administration of glucose (n = 42), triiodothyronine (n = 7), epinephrine (n = 7), dehydroascorbic acid (n = 5) and 4 mg streptozotocin (Szt, n = 10) increased glucose levels to 120-200 mg/dl. Dexamethasone (Dex, n = 34) and 6 mg Szt (n = 6) increased glucose levels to 200-450 mg/dl. Myocardial FDG uptake increased proportionately with increases in serum glucose level up to 200 mg/dl. In severe hyperglycemia (serum glucose: 200-450 mg/dl), however, the FDG uptake decreased and did not correlate with blood glucose level. A study of fractional FDG uptake calibrated by the arterial FDG curve confirmed the same results. Heterogeneous distribution of FDG was observed in the myocardium, both in fasting and in severe hyperglycemic conditions. The pattern of FDG uptake by skeletal muscles was similar to that of the myocardium, although the uptake was lower than that in the myocardium. Changes in insulin and free fatty acids levels could not explain the FDG uptake pattern in severe hyperglycemia. Blood FDG uptake level remained constant regardless of glucose level. CONCLUSION: Hyperglycemia induced a biphasic pattern of myocardial FDG uptake, common with skeletal muscles. The understanding of myocardial FDG uptake characteristics and their dependence on blood glucose is helpful in interpreting myocardial FDG-PET images.

Animals↗
PubMed1996

The mechanism of uptake of ascorbic acid into osteoblasts and leukocytes.

Ascorbic acid is taken up into osteoblast cells by a saturable, stereospecific, Na(+)-dependent transporter, accumulating ascorbic acid to a level 100-fold that in the medium. The ascorbic acid uptake rate correlated with intracellular hydroxyproline synthesis. A second, distinct mechanism has also been described for accumulation of ascorbic acid into neutrophils and myeloid leukemia cells. This appears to be Na(+)-independent and relies on the glucose transporter GLUT1 to ferry dehydroascorbic acid (DHA) into cells and then to trap it as ascorbic acid to a high concentration.

Animals↗
PubMed1998

The relation between gastric vitamin C concentrations, mucosal histology, and CagA seropositivity in the human stomach.

BACKGROUND: Vitamin C may be protective against gastric cancer though infection with Helicobacter pylori is associated with a reduction in intragastric concentrations of vitamin C. AIMS: To examine the effects of H pylori infection, gastric juice pH, the severity and extent of gastric inflammation, and CagA antibody status of the individual on gastric juice and mucosal vitamin C concentrations. PATIENTS: One hundred and fifteen patients undergoing routine gastroscopy for investigation of dyspepsia. METHODS: High performance liquid chromatography was used to determine vitamin C concentrations. CagA antibody was detected by western blot analysis. RESULTS: Gastric juice ascorbic acid concentration was significantly lower in patients infected with H pylori compared with those uninfected (19.3 mumol/l (interquartile range (IQR) 10.7-44.5) versus 66.9 mumol/l (IQR 24.4-94.2), p = 0.003). The reduction in gastric juice ascorbic acid concentration was inversely related to the severity of gastritis (p = 0.01). CagA positive patients had significantly lower gastric juice ascorbic acid concentrations than CagA negative ones (14.8 mumol/1 (IQR 7.9-52.2) versus 39 mumol/l (IQR 19.9-142.2), p = 0.05). Decreased gastric juice dehydroascorbic acid concentrations were observed in patients with gastric atrophy and intestinal metaplasia. Mucosal ascorbic acid concentrations were also significantly lower in infected patients than uninfected patients (p = 0.04). CONCLUSIONS: The reduction in gastric vitamin C concentrations is related to gastric juice pH, the severity and extent of gastritis, the presence of H pylori, and the CagA antibody status of the individual. These findings may have implications in H pylori associated carcinogenesis.

Adult↗
PubMed1994

Measurement of ascorbic acid in human plasma and urine by high-performance liquid chromatography. Results in healthy subjects and patients with idiopathic calcium urolithiasis.

A simple, reliable high-performance liquid chromatographic method was developed to measure ascorbic acid (ASC), with ultraviolet detection (250 nm), in human plasma and urine. Immediately following blood withdrawal, the heparinized plasma samples were deproteinized with 10% m-phosphoric acid, while the freshly voided urine samples were diluted with m-phosphoric acid. ASC was separated on a reversed-phase column by elution with 0.1 M KH2PO4 adjusted to pH 2.35. In urine, after reduction of dehydroascorbic acid to ASC, total ASC was measured using the same mobile phase. The method was sensitive down to 0.1 and 0.4 mg ASC per litre of urine and plasma, respectively. In patients with idiopathic calcium urolithiasis, both plasma and urinary ASC were within the range observed in age-matched controls.

Adult↗
PubMed1999

Ascorbic acid metabolism in pea seedlings. A comparison of D-glucosone, L-sorbosone, and L-galactono-1,4-lactone as ascorbate precursors

L-Ascorbic acid (AsA) accumulates in pea (Pisum sativum L.) seedlings during germination, with the most rapid phase of accumulation coinciding with radicle emergence. Monodehydroascorbate reductase and dehydroascorbic acid reductase were active in the embryonic axes before AsA accumulation started, whereas AsA oxidase and AsA peroxidase activities increased in parallel with AsA. Excised embryonic axes were used to investigate the osone pathway of AsA biosynthesis, in which D-glucosone and L-sorbosone are the proposed intermediates. [U-14C]Glucosone was incorporated into AsA and inhibited the incorporation of [U-14C]glucose (Glc) into AsA. A higher D-glucosone concentration (5 mM) inhibited AsA accumulation. L-Sorbosone did not affect AsA pool size but caused a small inhibition in the incorporation of [U-14C]Glc into AsA. Oxidase and dehydrogenase activities capable of converting Glc or Glc-6-phosphate to glucosone were not detected in embryonic axis extracts. The osones are therefore unlikely to be physiological intermediates of AsA biosynthesis. L-Galactono-1,4-lactone, recently proposed as the AsA precursor (G.L. Wheeler, M.A. Jones, N. Smirnoff [1998] Nature 393: 365-369), was readily converted to AsA by pea embryonic axes. Although L-galactono-1,4-lactone did not inhibit [14C]Glc incorporation into AsA, this does not mean that it is not a precursor, because competition between endogenous and exogenous pools was minimized by its very small pool size and rapid metabolism.

Journal Article↗
PubMed2004

Nitric oxide-induced oxidant stress in endothelial cells: amelioration by ascorbic acid.

Nitric oxide has multiple beneficial effects in the blood vessel wall. However, high concentrations of nitric oxide in the presence of hydroperoxides have been shown to damage cultured cells. In this work, the effect of relatively high concentrations of nitric oxide alone on the function and antioxidant status of a human endothelial cell line (EA.hy926) was tested. Nitric oxide generated from 0.1 to 0.5mM spermine NONOate generated reactive species in the cells detected by triazole formation from diaminofluorescein and by oxidation of dihydrofluorescein. Intracellular ascorbic acid decreased this oxidant stress. Spermine NONOate also decreased intracellular ascorbate concentrations, although reduced glutathione was not affected unless cells had also been caused to reduce dehydroascorbic acid to ascorbate. Nitric oxide predictably inhibited both endothelial nitric oxide synthase and glyceraldehyde 3-phosphate dehydrogenase, and ascorbate partially prevented inhibition of the latter enzyme. These results suggest that relatively high concentrations of nitric oxide can cause oxidant stress in endothelial cells that is ameliorated by ascorbic acid.

Ascorbic Acid↗
PubMed2002

Ascorbic acid and flavonoid-peroxidase reaction as a detoxifying system of H(2)O(2) in grapevine leaves.

Biosynthesis of both ascorbic acid (AsA) and peroxidase activity were induced by light in cv. Sultana grapevine leaves. Induced peroxidase activity mainly involved basic isoenzymes of pI 9.8 and 9.6 and catalyzed the oxidation of flavonoids like quercetin and kaempferol and derivatives of hydroxycinnamic acids such as ferulic and p-coumaric acids, but not AsA. However, the peroxidase-dependent oxidation of ferulic acid and quercetin was temporarily suppressed by AsA as long as it remained in the reaction medium. Kinetics and spectroscopic results indicated that AsA was oxidized to dehydroascorbic acid only in the presence of phenols or flavonoids, and did not interfere with the catalytic activity of the peroxidase. Ascorbate peroxidase isoenzymes (APx), whose activities are widely considered central for detoxification of H(2)O(2) in most plant cells, were not detected in grape leaves extracts. The significance of light stimulus on peroxidase activity and leaf AsA content is discussed in terms of a flavonoid-redox cycle proposed as an alternative system to detoxify H(2)O(2) in grapevine leaves.

Ascorbic Acid↗
PubMedDate not supplied

[Ascorbic acid supply and cytochrome P-450 levels in guinea pig liver after dimethylformamide poisoning].

The universal solvent dimethylformamide (DMFA) administered to guinea-pigs in a dose of 400 mg/kg bw per os for 14 days produced a considerable decrease in the content of total and reduced ascorbic acid (AA) in the liver, in all forms of AA in the adrenals, and lowering of vitamin C excretion with daily urine. The liver showed an increase in the concentration of dehydroascorbic acid and diminution of the concentration of cytochrome P-450 detected in liver homogenates. Additional administration of AA (50 mg/day) recovered the lowered level of the vitamin in the liver and adrenals but did not make the daily excretion of AA with urine return to normal. Additional administration of vitamin C to guinea-pigs recovered the level of cytochrome P-450 in liver homogenates, which was reduced during DMFA poisoning. One of the reasons for the development of vitamin C deficiency during DMFA poisoning is likely to be high oxidation of AA.

Adrenal Glands↗
PubMed1966

Ascorbic acid and aging in the rat. Uptake of ascorbic acid by teeth and concentration of various forms of ascorbic acid in different organs.

1. The uptake of ascorbic acid in vitro by the teeth of rats showed a gradual decrease with age, indicating that the uptake may be related to collagen synthesis as in bone. 2. The concentration of total free ascorbic acid in various organs declined with age, but the rate of decline was different in different organs. In the spleen, however, it increased until maturity and then declined. 3. This decrease may be due to one or both of the following reasons: (a) the permeability of different tissues may decrease at different rates for ascorbic acid, or (b) the requirement for ascorbic acid may decrease at different rates. 4. The bound ascorbic acid declined with age in the skin, kidney, liver and brain after the age of 10-12 weeks, and in the spleen after the age of 26 weeks. 5. The concentration of dehydroascorbic acid and dioxogulonic acid declined with age in the skin.

Aging↗
PubMed2001

Quantification of L-ascorbic acid and total ascorbic acid in fruits and spinach by capillary zone electrophoresis.

A standard curve for the quantification of L-ascorbic acid (L-AA) by capillary zone electrophoresis (CZE) was established, and the quantification of ascorbic acid and total ascorbic acid in fruits (lemon, Sunkist, and pineapple) and spinach were performed using D-isoascorbic acid (D-IAA) as an internal standard. The minimum detection limits (MDLs) for L-AA and D-IAA were determined to be 1 and 2 microg/mL, respectively, at 265 nm. Dehydroascorbic acid (DHAA) in fruits and spinach was quantified in the presence of DL-homocysteine. The recoveries for L-AA in these juices were between 95 and 105%.

Ascorbic Acid↗
PubMed1986

Transport and stability of ascorbic acid in pituitary cultures.

Ascorbic acid uptake in AtT-20 tumor cells and primary cultures of rat anterior and intermediate pituitary was sodium-dependent and showed half-maximal saturation between 9 and 18 microM ascorbate. When incubated in [14C]ascorbic acid at concentrations similar to those in serum (50 microM), all of the cells concentrated ascorbate 20- to 40-fold, producing intracellular ascorbate concentrations of 1-2 mM. HPLC analyses showed that over 90% of the intracellular label comigrated with authentic ascorbic acid. Although ascorbate was rapidly oxidized in culture medium in the absence of cells, incubation of ascorbate in culture medium in the presence of cells stabilized the ascorbate substantially. Unlike systems that transport dehydroascorbic acid, the ascorbate transport systems in all three preparations were not inhibited by glucose. Thus all three systems possess similar saturable, high-affinity, sodium-dependent active transport systems for ascorbic acid.

Animals↗
PubMed1992

The extent of N epsilon-(carboxymethyl)lysine formation in lens proteins and polylysine by the autoxidation products of ascorbic acid.

The autoxidation of ascorbic acid (ASA) leads to the formation of compounds which are capable of glycating and crosslinking proteins in vitro. When the soluble crystallins from bovine lens were incubated with ASA in the presence of sodium cyanoborohydride, a single major adduct was observed, whose appearance correlated with the loss of lysine. When polylysine was reacted with equivalent amounts of ASA under the same conditions, this product represented half of the total lysine content after four weeks of incubation at 37 degrees C. This adduct was isolated and identified as N epsilon-(carboxymethyl)lysine (CML) by TLC, GC/MS and amino acid analysis. Several oxidation products of ASA were each reacted with polylysine in the presence of sodium cyanoborohydride to identify the reactive species. CML was the major adduct formed with either ASA and dehydroascorbic acid (DHA). Markedly diminished amounts were seen with L-2,3-diketogulonic acid (DKG), and L-threose, while no CML was formed with L-threo-pentos-2-ulose (L-xylosone). In the absence of sodium cyanoborohydride the yield of CML was similar with each of the ASA autoxidation products and required oxygen. Reactions with [1-14C]ASA gave rise to [14C]CML, but only with NaCNBH3 present. At least two routes of CML formation appear to be operating depending upon whether NaCNBH3 is present to reduce the putative Schiff base formed between lysine and DHA.

2,3-Diketogulonic Acid↗
PubMed2001

Relationships among dietary roasted soybeans, milk components, and spontaneous oxidized flavor of milk.

Relationships among dietary roasted whole soybeans (RSB), milk fatty acid profile, and the development of spontaneous oxidized flavor of milk were investigated by using 20 commercial dairy herds. Diets contained 0 to 15.3% of dry matter as RSB. Concentrations of dietary RSB were correlated positively with concentrations of C18:2 and C18:3 in milk fat. Concentrations of alpha-tocopherol, beta-carotene, and ascorbic acid in milk decreased from 0 to 3 d of storage (4 degrees C), and oxidized flavor in milk increased linearly between 0 and 8 d of storage. Milk fatty acid profile did not change during storage. The development of oxidized flavor at 8 d postsampling was correlated (r) with increased concentrations in milk fat of C18:2 (0.49), C18:3 (0.55), total polyunsaturated milk fatty acids (0.50), and dietary concentrations of RSB (0.38). Multiple regression was used to quantify relationships between variables and oxidized flavor (samples stored 8 d). All significant models included milk concentrations of Cu and dehydroascorbic acid. Concentrations of C18:2, C18:3, or total polyunsaturated fatty acids in milk fat, or dietary RSB concentrations, and interactions of those variables with Cu were included in individual models. Milk with high concentrations of polyunsaturated fatty acids and Cu were most susceptible to oxidation. Feeding RSB increased polyunsaturated fatty acid concentrations in milk fat, which increased the likelihood of oxidized flavor, especially when milk had high concentrations of Cu.

Animal Feed↗
PubMed2002

Oxidation of ferulic acid or arabinose-esterified ferulic acid by wheat germ peroxidase.

The oxidation of ferulic acid (FA) or 5-O-(trans-feruloyl)-L-arabinose (EFA) by a purified wheat germ peroxidase was followed by UV spectrophotometry and high-performance liquid chromatography using an electrochemical detection. Wheat peroxidase (POD) exhibits a ping-pong bireactant mechanism forming phenoxy radicals more rapidly from FA than from EFA in routine assay conditions. When both the free and the esterified forms of FA are present, the reverse was found. This result could be due to a nonenzymatic cooxidation of FA by the phenoxy radicals of EFA leading to the formation of phenoxy radicals of FA and the EFA regeneration. Addition of ascorbic acid (AA) provokes a delay of FA consumption. AA reduced very rapidly the phenoxy radicals formed by POD back to initial phenol avoiding the formation of ferulate dimers until it was completely oxidized in dehydroascorbic acid. Conversely, cysteine addition slowed but did not delay the FA consumption. The thiol reduced a fraction of the phenoxy radicals produced by wheat POD and was oxidized into cystine, while the other part of phenoxy radicals formed ferulate dimers. These results could be of interest to understand the POD effect on the wheat dough rheological properties.

Arabinose↗
PubMed1998

Ascorbate-induced oxidative inactivation of Zn2+-glycerophosphocholine cholinephosphodiesterase.

Zn2+-glycerophosphocholine cholinephosphodiesterase, responsible for the conversion of glycerophosphocholine into glycerol and phosphocholine, was inactivated during incubation with ascorbic acid at 38 degrees C. The inclusion of copper ions or Fe2+ accelerated the ascorbate-induced inactivation, with Cu2+ or Cu+ being much more effective than Fe2+, suggestive of ascorbate-mediated oxidation. Dehydroascorbic acid had no effect on the phosphodiesterase, but H2O2 inactivated the enzyme in a concentration-dependent manner. Also, the enzyme was inactivated partially by a superoxide anion-generating system but not an HOCl generator. In support of involvement of H2O2 in the ascorbate action, catalase and superoxide dismutase expressed a complete and a partial protection, respectively. However, hydroxy radical scavengers such as mannitol, benzoate, or dimethyl sulfoxide were incapable of preventing the ascorbate action, excluding the participation of extraneous .OH. Although p-nitrophenylphosphocholine exhibited a modest protection against the ascorbate action, a remarkable protection was expressed by amino acids, especially by histidine. In addition, imidazole, an electron donor, showed a partial protection. Separately, when Cu2+-induced inactivation of the phosphodiesterase was compared with the ascorbate-mediated one, the protection and pH studies indicate that the mechanism for the ascorbate action is different from that for the Cu2+ action. Here, it is proposed that Zn2+-glycerophosphocholine cholinephosphodiesterase is one of brain membrane proteins susceptible to oxidative inactivation.

Animals↗
PubMed2005

Vitamin C transiently arrests cancer cell cycle progression in S phase and G2/M boundary by modulating the kinetics of activation and the subcellular localization of Cdc25C phosphatase.

Regulation of cell cycle progression involves redox (oxidation-reduction)-dependent modification of proteins including the mitosis-inducing phosphatase Cdc25C. The role of vitamin C (ascorbic acid, ASC), a known modulator of the cellular redox status, in regulating mitotic entry was investigated in this study. We demonstrated that vitamin C inhibits DNA synthesis in HeLa cells and, mainly the form of dehydroascorbic acid (DHA), delays the entry of p53-deficient synchronized HeLa and T98G cancer cells into mitosis. High concentrations of Vitamin C caused transient S and G2 arrest in both cell lines by delaying the activation of the M-phase promoting factor (MPF), Cdc2/cyclin-B complex. Although vitamin C did not inhibit the accumulation of cyclin-B1, it may have increased the level of Cdc2 inhibitory phosphorylation. This was achieved by transiently maintaining Cdc25C, the activator of Cdc2, both in low levels and in a phosphorylated on Ser216 inactive form that binds to 14-3-3 proteins contributing thus to the nuclear exclusion of Cdc25C. As expected, vitamin C prevented the nuclear accumulation of Cdc25C in both cell lines. In conclusion, it seems that vitamin C induces transient cell cycle arrest, at least in part, by delaying the accumulation and the activation of Cdc25C.

Antioxidants↗