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PubMed1969

Ascorbic acid and copper in linoleate oxidation. II. Ascorbic acid and copper as oxidation catalysts.

Both ascorbic acid and copper were strong prooxidants in the oxidation of linoleate in a buffered (pH 7.0) aqueous dispersion at 37 degrees C. Minimum concentrations at which catalytic activity was detected were 1.3 x 10(-7) m for copper and 1.8 x 10(-6) m for ascorbic acid. For concentrations up to 10(-3) m, the increase in rate of oxidation with increase in concentration of catalyst was greater for ascorbic acid than for copper. Ascorbic acid had maximum catalytic activity at 2.0 x 10(-3) m, but was still prooxidant at the highest concentration tested (5.0 x 10(-2) m). Dehydroascorbic acid was a weaker prooxidant than ascorbic acid. Further degradation products of ascorbic acid were not prooxidant. In early stages of the oxidation autocatalytic behavior was observed with copper, but not with ascorbic acid. Ascorbic acid functioned as a true catalyst, i.e., it accelerated the reaction but it was not oxidized simultaneously with the linoleate. It is proposed that the dehydroascorbic acid radical initiates the linoleate oxidation reaction.

Alkenes↗
PubMedDate not supplied

Routine analysis of ascorbic acid in citrus juice using capillary electrophoresis.

A procedure to monitor citrus juice samples was established to quantitate vitamin C by capillary electrophoresis using a previously developed method. Dilution and filtration were the only preparation requirements and separation was achieved with an uncoated capillary using a 35mM sodium borate buffer (pH 9.3) containing 5% (v/v) acetonitrile at 21 kV and 23 degrees C. Detection was performed by high speed scanning between 200 and 360 nm. From the multiwave length scan, the electropherogram at 270 nm was extracted and used to quantitate ascorbic acid. The ascorbic acid concentration was calculated with an internal standard method, with ferulic acid as internal standard. The level of ascorbic acid during analysis was stabilized with ethylenediaminetetraacetic acid and dithiothreitol was used to reduce dehydroascorbic acid to ascorbic acid to estimate the total vitamin C level. Results were similar to those obtained by liquid chromatography and the method is now used to determine routinely the level of ascorbic acid in citrus juices.

Acetonitriles↗
PubMed1992

Unequivocal evidence in support of the nonenzymatic redox coupling between glutathione/glutathione disulfide and ascorbic acid/dehydroascorbic acid.

Experiments were performed to evaluate the nonenzymatic reaction between glutathione (GSH) and dehydroascorbic acid (DHA). Though both ascorbic acid and glutathione disulfide (GSSG) are formed from this reaction, previous work has focused almost exclusively on measurements of ascorbic acid. In contrast, there is very little information about the formation of GSSG under the same conditions as those used to produce ascorbic acid. The emphasis on ascorbic acid stems from the fact that a spectrophotometric technique is available for its measurement, whereas 1H-NMR or an amino acid analyzer has been used to measure GSSG. The present experiments use a simple, rapid method for accurately and precisely measuring the concentrations of GSSG in a solution. The spectrophotometric (340 nm) procedure uses NADPH and glutathione reductase; analysis time is very short, many replicate samples can be tested and as little as 0.05-0.1 mM GSSG can be detected. Using this method, it is shown that there is an equimolar production of GSSG and ascorbic acid from GSH and DHA and that the decrease in GSH is stoichiometrically related to the increase in the concentration of GSSG. The present findings provide additional insight into the interaction between the GSH/GSSG redox couple and the ascorbic acid/DHA redox couple.

Ascorbic Acid↗
PubMed2004

Vitamin C inhibits hypoxia-induced damage and apoptotic signaling pathways in cardiomyocytes and ischemic hearts.

Reactive oxygen species play a central role in myocardial ischemic injury and are a target for therapeutic intervention. Vitamin C is an essential antioxidant yet difficult to deliver in pharmacologic concentration to the myocardium. We found that adult rat cardiomyocytes accumulate vitamin C by transporting dehydroascorbic acid (DHA), the oxidized form of vitamin C, but do not transport ascorbic acid. Loading cells with vitamin C by DHA treatment resulted in resistance to hypoxia- and hypoxia/reoxygenation-induced cell death associated with the quenching of reactive oxygen species. When rats were injected with DHA before coronary occlusion, the ascorbic acid content in the heart was six to eight times higher than in untreated controls and myocardial infarction was reduced by 62%. DHA also provided significant protection when administered intravenously 2 h after coronary occlusion. In cardiomyocytes subjected to hypoxia/reoxygenation, DHA treatment resulted in decreased apoptosis associated with inhibition of Bax expression, caspase-3 activation, and cytochrome c translocation into the cytoplasm. DHA treatment also inhibited Jak2, STAT1, and STAT5 phosphorylation, and increased STAT3 phosphorylation, in hypoxic cardiomyocytes and ischemic myocardial tissue. Our findings suggest that DHA may be useful as a cardioprotectant in ischemic heart disease.

Animals↗
PubMed1987

Vitamin C metabolites and microangiopathy in diabetes mellitus.

Recent evidence has suggested that diabetic microangiopathy is associated with increased free radical induced oxidative damage. Ascorbic acid (AA) is a free radical scavenger and using a specific HPLC method we have investigated its concentration and that of its oxidized metabolite dehydroascorbic acid (DHAA) in diabetic patients and matched normal controls. The findings have been related to the presence of microangiopathy and to glycaemic control. Ascorbic acid levels were significantly lower in diabetics (mean +/- SD 42.5 +/- 26.2 mumol/l) compared with controls (58 +/- 21 mumol/l p less than 0.02). Although there was no differences in DHAA levels between the groups the ratio DHAA/AA was increased in diabetics (0.72 +/- 0.8) compared with controls (0.4 +/- 0.2 p less than 0.05). There were no significant differences between insulin and non-insulin dependent patients in these measurements and there was no association with the presence of microangiopathy or poor glycaemic control. The plasma ratio DHAA/AA may be a reflection of increased oxidative stress and our results suggest that diabetics may be less able to prevent oxidative damage occurring due to their lower AA concentrations.

Ascorbic Acid↗
PubMed1976

[Glutathatione-dehydrogenase of wheat flour. Purification and properties (author's transl)].

Glutathione: dehydroascorbic acid oxidoreductase (EC 1.8.5.1) has been purified to essential homogeneity by precipitation with (NH4)2SO4, and ion-exchange chromatography on CM-Sephadex and DEAE-cellulose. The molecular weight is 24200 Dalton as determined by SDS-PAG-electrophoresis. The amino acid composition was analysed. The esed. The enzyme ist specific for glutathione as H-donor and it reduces the L-threo-diasteromer faster than the L-erythro- and D-erythro-dehydroascorbic acid. The enzyme is inhibited by iode acetic acid and N-ethyl-maleinimide. Zero-order kinetics was only observed for the hydrogen-acceptor but not for glutathione.

Oxidoreductases↗
PubMed1981

A specific method for determination of total ascorbic acids in urine by the alpha,alpha'- dipyridyl method.

Application ot the alpha,alpha'- dipyridyl method for determination of ascorbic acid in urine is described. The urine sample was acidified with trichloracetic acid and shaken with activated carbon to remove interfering substances. The acid filtrate was first neutralized (pH 7.0) by adding Na2HPO4. The dehydroascorbic acid was then reduced back to ascorbic acid by incubation with dithiothreitol. After removal of the excess dithiothreitol with N-ethylmaleimide, ascorbic acid was determined by measuring the reduction of ferric ion. The ferrous ion produced was coupled to alpha,alpha'-dipyridyl in the presence of H3PO4. Ferrous ion in urine samples, which theoretically interferes with the method, was removed by a combination of Na2HPO4 and H3PO4.

2,2'-Dipyridyl↗
PubMed2003

Elevated carbon dioxide increases contents of antioxidant compounds in field-grown strawberries.

The effects of elevated CO2 concentrations on the antioxidant capacity and flavonoid content in strawberry fruit (Fragaria x ananassa Duch.) were studied under field conditions. Increased CO(2) (300 and 600 micromol mol(-1) above ambient) concentrations resulted in increases in ascorbic acid (AsA), glutathione (GSH), and ratios of AsA to dehydroascorbic acid (DHAsA) and GSH to oxidized glutathione (GSSG), and a decrease in DHAsA in strawberry fruit. High anthocyanin and phenolic content were also found in fruit of CO(2) treated plants. Growing strawberry plants under CO(2) enrichment conditions significantly enhanced fruit p-coumaroylglucose, dihydroflavonol, quercetin 3-glucoside, quercetin 3-glucuronide, and kaempferol 3-glucoside contents, as well as cyanidin 3-glucoside, pelargonidin 3-glucoside, and pelargonidin 3-glucoside-succinate content. Fruit of strawberry plants grown in the CO(2) enrichment conditions also had high oxygen radical absorbance activity against ROO(*), O(2)(*-), H(2)O(2), OH(*), and (1)O(2) radicals.

Antioxidants↗
PubMed1994

Ascorbic acid increases synaptosomal potassium-induced dopamine release.

On synaptosomes prepared from striata of mice, increasing concentrations of ascorbic acid (from 0.01 mM to 0.5 mM) did not modify the 3H-dopamine uptake. However, at the 0.1 mM concentration, ascorbic acid increased the potassium-induced release of 3H-dopamine by synaptosomes previously loaded with the amine. This effect was dependent on the presence of Ca2+ in the superfusion medium and was not shared by dehydroascorbic acid (from 1 mM to 0.01 mM). This effect of ascorbic acid, which occurs in the range of its endogenous concentrations, suggests that it is a putative modulator of dopaminergic transmission.

Animals↗
PubMed1994

Vitamin C concentration in gastric juice before and after anti-Helicobacter pylori treatment.

OBJECTIVES: To investigate the change of vitamin C concentration (ascorbic and dehydroascorbic acid) in gastric juice after anti-Helicobacter pylori treatment, and to relate any observed change to gastric pH, inflammatory compromise of the gastric mucosa, plasma vitamin C concentration, and smoking habits. METHODS: Plasma and gastric juice vitamin C, fasting gastric juice pH, gastric histology, and smoking status were studied in 70 patients with H. pylori-associated gastritis before and after therapy. RESULTS: Gastric juice ascorbic acid increased significantly after H. pylori clearance. For the most part, this change was confined to patients who experienced reduction of gastric pH. It was also related to improvement of the compromise of the gastric epithelium, reduction of the proportion of vitamin C composed by dehydroascorbic acid, and increase of the gastric juice/plasma vitamin C concentration gradient. Smokers had lower vitamin C concentrations in plasma and gastric juice before and after H. pylori clearance than nonsmokers. CONCLUSIONS: The findings are consistent with a causal association between H. pylori infection and low ascorbic acid levels in gastric juice, and support two mechanisms for this association: increased oxidation and a decreased secretion of ascorbic acid.

Amoxicillin↗
PubMed1976

Effect of reductones on glyoxalase I1.

The effect of some reductones on glyoxalase I prepared from animal and microbial origins has been studied. The enzyme was extracted from ox liver or baker's yeast and partially purified by ammonium sulfate fractionation, gel filtration and ion exchange chromatography. Aliphatic reductones such as ascorbic acid, ascorbic acid 3-phosphate and triose reductone showed strong to medium inhibition, while dehydroascorbic acid showed no inhibition. Kinetic analysis indicated that the inhibition mechanism of ascorbic acid was uncompetitive. Varying extents of inhibition were observed among three kinds of diphenols belonging to aromatic reductones. They were in the order of increasing inhibitory power resorcinol, hydroquinone and catechol for the ox liver enzyme, and catechol, resorcinol and hydroquinone for the yeast enzyme. p-Benzoquinone, an oxidized reductone, exhibited marked inhibition on both enzymes. Its action seemed due to reaction with amino and/or sulfhydryl functions of enzyme protein and those of glutathione, one of the substrates.

Animals↗
PubMed1998

Decrease in vitamin C concentration in human lenses during cataract progression.

Cataract formation is believed to result from an oxidative insult which decreases the antioxidant defense of the lens, particularly the vitamin C concentration. Upon oxidation, vitamin C contributes with glucose to protein glycation. It also favours tryptophan oxidation, resulting in fluorescent peptide cross-links and protein insolubilisation. The relationship between cataract and lenticular vitamin C was analysed in 48 cataractous lens nuclei classified into four severity grades, considering the sum of the colour and opacity. Ascorbic and dehydroascorbic acids were quantified by HPLC-fluorescence. The Amadori product was measured by means of furosine, advanced glycation end products by their fluorescence and tryptophan concentration by HPLC-UV. The lens vitamin C concentration significantly decreased with cataract severity, but mostly in severe brown cataracts (around 88 mumol/100 g lens in mild cataracts, and 50 mumol/100 g in dark brown lenses). The dehydroascorbic acid concentration was always low and stable (1.9 +/- 0.9 mumol/100 g), as was the furosine concentration (0.4 +/- 0.1 mumol/g). The fluorescence of insoluble advanced glycated end products was significantly higher in severe cataracts than in milder ones. The peptide tryptophan content was stable but the tryptophan to tyrosine ratio decreased and was highly correlated to the ascorbic acid concentration. Vitamin C content appears to be a good indicator of cataract severity, suggesting that oxidation could take part in cataract progression.

Ascorbic Acid↗
PubMed2001

Direct inhibition of the hexose transporter GLUT1 by tyrosine kinase inhibitors.

The facilitative hexose transporter GLUT1 is a multifunctional protein that transports hexoses and dehydroascorbic acid, the oxidized form of vitamin C, and interacts with several molecules structurally unrelated to the transported substrates. Here we analyzed in detail the interaction of GLUT1 with a group of tyrosine kinase inhibitors that include natural products of the family of flavones and isoflavones and synthetic compounds such as the tyrphostins. These compounds inhibited, in a dose-dependent manner, the transport of hexoses and dehydroascorbic acid in human myeloid HL-60 cells, in transfected Chinese hamster ovary cells overexpressing GLUT1, and in normal human erythrocytes, and blocked the glucose-displaceable binding of cytochalasin B to GLUT1 in erythrocyte ghosts. Kinetic analysis of transport data indicated that only tyrosine kinase inhibitors with specificity for ATP binding sites inhibited the transport activity of GLUT1 in a competitive manner. In contrast, those inhibitors that are competitive with tyrosine but not with ATP failed to inhibit hexose uptake or did so in a noncompetitive manner. These results, together with recent evidence demonstrating that GLUT1 is a nucleotide binding protein, support the concept that the inhibitory effect on transport is related to the direct interaction of the inhibitors with GLUT1. We conclude that predicted nucleotide-binding motifs present in GLUT1 are important for the interaction of the tyrosine kinase inhibitors with the transporter and may participate directly in the binding transport of substrates by GLUT1.

Adenosine Triphosphate↗
PubMed1977

Semiautomated method for the fluorometric determination of total vitamin C in food products.

A simple method employing simultaneous extraction and oxidation has been developed for the semiautomated determination of ascorbic and dehydroascorbic acids in food products. Recovery studies were conducted on ready-to-eat breakfast cereals and both fresh and canned fruits and vegetables, with average recoveries of 101, 100, and 102%, respectively. Reproducibility data were generated showing a relative standard deviation of 3.5%. The automated method was compared with the manual AOAC fluorometric method and with indophenol titration; correlation coefficients were 0.9960 and 0.9926, respectively. The hydrolysis product of dehydroascorbic acid, 2,3-diketogulonic acid, a reported interference in this method, was prepared and shown not to form an interfering fluorescent derivative.

Ascorbic Acid↗
PubMed1998

Ascorbate function and metabolism in the human erythrocyte.

Ascorbic acid, or vitamin C, is an important antioxidant in plasma, where it consumes oxygen free radicals and helps to preserve alpha-tocopherol (vitamin E) in lipoproteins. Erythrocytes, as the most plentiful cell in blood, help to preserve ascorbate in the blood plasma. In contrast to nucleated cells, which avidly concentrate ascorbate, the erythrocyte ascorbate concentration is the same as that in plasma. Erythrocytes nonetheless have a high capacity to regenerate the vitamin from its two electron-oxidized form, dehydroascorbic acid (DHA). DHA is rapidly taken up by these cells on the abundant glucose transport protein, GLUT1. Intracellular DHA is rapidly reduced to ascorbate by GSH in a direct chemical reaction, although enzyme-dependent mechanisms involving both glutaredoxin and thioredoxin reductase have also been demonstrated. Ascorbate, which carries a negative charge at physiologic pH, enters and leaves the cells slowly. Nonetheless, this slow release of ascorbate from erythrocytes can preserve both the plasma concentration of the vitamin, and prevent oxidation of alpha-tocopherol in low-density lipoprotein. In addition, intracellular ascorbate can spare and possibly recycle alpha-tocopherol in the erythrocyte membrane. In turn, alpha-tocopherol protects the cell membrane from lipid peroxidation. The ability of erythrocytes to recycle ascorbate, coupled with the ability of ascorbate to protect alpha-tocopherol in the cell membrane and in lipoproteins, provides a potentially important mechanism for preventing lipid peroxidative damage in areas of inflammation in the vascular bed, such as those involved with atherosclerosis.

Antioxidants↗
PubMed2006

On the mechanism of the ascorbic acid-induced release of nitric oxide from N-nitrosated tryptophan derivatives: scavenging of NO by ascorbyl radicals.

During the past years, there has been increasing interest in endogenous nitric oxide storage compounds. Recently, we briefly reported on the ascorbate-dependent release of nitric oxide ((.)NO) from N-nitrosotryptophan derivatives. In the present study, the underlying mechanism of (.)NO release is studied in more detail, primarily utilizing N-acetyl-N-nitrosotryptophan (NANT) as a model compound. The initial rate of the ascorbate-induced release of nitric oxide has been found to correspond to the rate of NANT decay. In this process, N-acetyltryptophan (NAT) is produced almost quantitatively. The final yield of nitrite amounted to around 90 % with respect to the applied amount of NANT. However, the total release of nitric oxide was only 60 %, as determined by using an FNOCT-4(fluorescent nitric oxide cheletropic trap number 4) assay. Besides nitric oxide, a second volatile product, dinitrogen oxide (N(2)O), has been identified by using (15)N NMR spectrometry, strongly indicating the intermediacy of nitroxyl (HNO). The formation of intermediate ascorbyl radical anions during the NANT-ascorbate reaction has been monitored by using ESR spectrometry. Unexpectedly, it was found that the primary oxidized product of vitamin C, dehydroascorbic acid (DHA), efficiently consumes nitric oxide. Since ESR spectrometry further revealed that ascorbyl radical anions are also generated during the spontaneous decay of DHA, the DHA-nitric oxide reaction is related to recombination of (.)NO with the thus formed ascorbyl radical anions. A conclusively established mechanism of the NANT-ascorbate reaction is presented, with O-nitrosoascorbate as a key intermediate, as additionally supported by CBS-QB3 calculations. The present study suggests that vitamin C and its oxidation products can chemically counterbalance endogenous nitric oxide levels.

Ascorbic Acid↗
PubMed2006

Degradation kinetics of the antioxidant additive ascorbic acid in packed table olives during storage at different temperatures.

The kinetics of ascorbic acid (AA) loss during storage of packed table olives with two different levels of added AA was investigated. Three selected storage temperatures were assayed: 10 degrees C, ambient (20-24 degrees C), and 40 degrees C. The study was carried out in both pasteurized and unpasteurized product. The effect of pasteurization treatment alone on added AA was not significant. In the pasteurized product, in general AA degraded following a first-order kinetics. The activation energy calculated by using the Arrhenius model averaged 9 kcal/mol. For each storage temperature, the increase in initial AA concentration significantly decreased the AA degradation rate. In the unpasteurized product, AA was not detected after 20 days in samples stored at room temperature and AA degradation followed zero-order kinetics at 10 degrees C, whereas at 40 degrees C a second-order reaction showed the best fit. In both pasteurized and unpasteurized product, the low level of initial dehydroascorbic acid disappeared during storage. Furfural appeared to be formed during storage, mainly at 40 degrees C, following zero-order kinetics.

Ascorbic Acid↗
PubMed1998

Tissue ascorbic acid and polyol pathway metabolism in experimental diabetes.

Previous studies demonstrating reduced plasma concentrations of ascorbic acid (AA) in diabetes and interactions between this vitamin and biochemical mechanisms such as synthesis of structural proteins, oxidative stress, polyol pathway and nonenzymatic glycation of proteins suggest that disturbed AA metabolism may be important in the pathogenesis of diabetic microangiopathy. However, limited information is available on the concentration of AA in tissues which develop diabetic complications. This study demonstrates reduced renal but not sciatic nerve or plasma AA concentration in two animal models of insulin-dependent diabetes mellitus, namely the STZ-diabetic rat and the spontaneously diabetic BB rat. Decreased lens AA concentration was also observed in STZ-diabetic rats. Improvement of glycaemic control by insulin treatment (albeit insufficient to achieve normoglycaemia) partially corrected lens and renal AA concentration in STZ-diabetic rats. AA treatment increased kidney and lens AA concentrations of STZ-diabetic and non-diabetic rats and corrected the abnormalities observed for untreated diabetic rats. Sciatic nerve AA concentration was not increased by AA treatment in any group. Tissue ratios of dehydroascorbic acid (DHAA)/AA, one index of oxidative stress, were not different between the diabetic and non-diabetic groups and were unaltered by AA supplementation. AA treatment of STZ-diabetic rats had no effect on elevated tissue concentrations of glucose, sorbitol and fructose or reduced myo-inositol concentration. The effect of reduced tissue AA levels in diabetes on either collagen synthesis or ability to combat increased free radical production is not known. However, correction of abnormal kidney and lens AA concentrations in experimental diabetes by AA supplementation suggests that if AA does have a role in the development or progression of the renal and ocular complications of diabetes, this treatment could be beneficial.

Animals↗