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PubMed1987

[Quality changes in the storage of vegetable peas (Pisum sativum L.). 2. Nutritional physiologic quality].

In tests extending over several years the typical changes in the nutritional quality as occur during storage at defined temperatures (0 ... 18 degrees C) were determined in dependence on the duration of storage (chi in days). Due to the nutrient transfer from the pods to the seeds, a temporary major rise of the dry matter content (DM) is recorded in the latter together with a strongly inhibited reduction of the mono- and disaccharide content. Green peas stored without pods show a linear decrease in the DM content, degressively increasing DM losses and a more distinct reduction of saccharides. When stored with the pods, the typical decline of the vitamin C (ascorbic acid + dehydroascorbic acid) [changes in the content according to the equation y = alpha 0 + beta 1e-c theta chi and losses according to y = beta 1(1 - e-c theta chi)] goes back, mainly owing to an essentially lower coefficient for c theta. In addition, there are smaller losses in the total carotene content of such crops in the first stage of storage (losses of y = beta 1 chi 2). When storing peas without pods, we observe a a faster accumulation of the titratable total acid (up to 160%). The greatest influence on range and degree of the changes in the chemical constituents is exerted by the storage temperature. The form of the harvested crop, varietal characteristics and annual growing conditions have less bearing. Relationships and physiological causes are discussed.

Fabaceae↗
PubMed1998

Protection by vitamin C of loss of vitamin E in cultured rat hepatocytes.

Results from in vivo studies of the capacity of vitamin C to spare and/or recycle vitamin E are equivocal. While some in vitro and membrane models reveal an interaction between vitamins C and E, the characterization of this relationship in biologically relevant systems is lacking. Thus, we investigated this relationship using hepatocytes isolated from 3- to 6-month-old male Sprague-Dawley rats. Cells were incubated for 18-20 h in medium supplemented with 0.1-4 mM ascorbic acid. The loss of alpha-tocopherol and the formation of its primary oxidized metabolite, alpha-tocopherolquinone, was determined by HPLC. Levels of alpha-tocopherol in hepatocytes incubated without ascorbic acid declined from 390 to 35 pmol/mg protein; hepatocyte ascorbic acid levels declined from 9 to 0.5 nmol/mg protein. alpha-Tocopherolquinone was undetectable in freshly isolated hepatocytes but following incubation in ascorbate-free medium reached 10 pmol/mg protein. The formation of alpha-tocopherolquinone was not detected in hepatocytes incubated with ascorbic acid. Dehydroascorbic acid (DHA) levels represented 10-20% of the total ascorbate content in freshly isolated hepatocytes but after 3 h incubation the proportion of DHA increased to 50%; after 18-20 h incubation DHA was undetectable. Hepatocytes incubated with 1.0, 2.0, 2.5, or 4.0 mM ascorbic acid lost significantly less alpha-tocopherol (62, 69, 67, and 56%, respectively) than unsupplemented controls (90%). Twelve percent of the alpha-tocopherol lost from hepatocytes during incubation was detected in the medium of cells incubated with ascorbic acid, but vitamin E was undetectable in the medium of cells incubated without ascorbic acid. These results demonstrate an interaction between vitamins C and E in cell culture and are not inconsistent with a potential recycling of oxidized alpha-tocopherol by ascorbic acid.

Animals↗
PubMed1996

Increased oxidation resistance of atherogenic plasma lipoproteins at high vitamin E levels in non-vitamin E supplemented men.

The oxidative modification of human low density lipoprotein (LDL) has been widely investigated. However, there are no data concerning the oxidation susceptibility of combined very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and low density lipoprotein fraction, although all of them are atherogenic and contain antioxidants such as alpha-tocopherol. We investigated the oxidation susceptibility and oxidation resistance of VLDL + LDL (including IDL) fraction by induction with CuCl2 and its relation to plasma alpha-tocopherol concentration and lipid standardised alpha-tocopherol concentration in 406 non-vitamin E-supplemented men from eastern Finland. Even thought we did not give oral vitamin E or any other antioxidant supplementation to our study participants, we observed a significant, consistent relationship between measurements of oxidation resistance and plasma content of vitamin E. In the multivariate regression model, a high plasma content of vitamin E or lipid standardised vitamin E concentration were the most important determinants of lag time to maximal oxidation rate (standardised regression coefficient = 0.244, P < 0.0001 for vitamin E and 0.211, P < 0.0001 for lipid standardised vitamin E). After statistical adjustment for age, use of cigarettes, hypolipidemic medication (yes vs. no), month of the measurements, plasma concentrations of total ascorbic acid (ascorbic acid + dehydroascorbic acid), beta-carotene and phospholipids, serum concentrations of LDL cholesterol and triglycerides and dietary intake of linoleic acid, the lag time to maximal oxidation rate was 10% (95% C.I. 6.0-13.5%) longer in men in the highest fifth than in the lowest fifth of plasma vitamin E content (P < 0.0001 for trend). When the fifths of lipid standardised vitamin E were compared, the lag time to maximal oxidation rate was 6% (95% C.I. 1.8-10.1%) longer in men in the highest than in the lowest fifth (P < 0.0001 for trend). Our data suggest that alpha-tocopherol is an important antioxidant preventing the in vitro oxidation of VLDL + LDL fraction even in non-supplemented subjects.

Adult↗
PubMed1989

Manganese catalysis of dopamine oxidation.

Manganese catalysis of the oxidation of dopamine by air was studied as part of an investigation of possible manganese intoxication amongst a group of Aborigines living on manganese-rich soil on Groote Eylandt, in the Northern Territory of Australia. Manganese significantly increased the oxidation rate of dopamine, and the manganese complexes with some purines were especially efficient catalysts. An oxidation mechanism, involving a manganese(II)/(III) redox couple and a semiquinone free radical intermediate, is proposed. Stoichiometric hydrogen peroxide was produced by the oxidation, and the oxidation products of dopamine were highly toxic to the marine diatom Nitzschia closterium. Hydrogen peroxide and the superoxide radical did not oxidize dopamine at physiological pH. Some electrophilic compounds, including ascorbic acid, dehydroascorbic acid and thiamine, effectively inhibited dopamine oxidation. The Groote Eylandt Aborigines are likely to be deficient in ascorbic acid (vitamin C) and thiamine (vitamin B1), and these deficiencies, as well as their lifestyle, may predispose them to manganese intoxication.

Catalysis↗
PubMed1987

Determination of ascorbic acid in human urine by high-performance liquid chromatography coupled with fluorimetry after post-column derivatization with benzamidine.

High-performance liquid chromatography on two Asahipak GS-320 hydrophilic gel columns (50 X 0.76 cm I.D.), connected in series, with 0.015 M tartrate buffer (pH 3.0), containing 2 mM ethylenediaminetetraacetate and 0.05% beta-thiodiglycol as eluent allowed the separation of glucose, diketogulonic acid + diketogluconic acid, dehydroisoascorbic acid, dehydroascorbic acid, ascorbic acid, and isoascorbic acid within 55 min. Ascorbic acid in a urine sample was stabilized by the addition of an equal volume of 5% metaphosphoric acid solution, containing 0.5% of beta-thiodiglycol. Filtration of the mixture through a column of Dowex 50W-X8 (H+) facilitated the determination of ascorbic acid and isoascorbic acid in human urine. Samples could be analyzed every 20 min.

Ascorbic Acid↗
PubMed1973

Some EPR signals in tumour tissue.

Normal and tumour tissues from rats, blood from normal and tumour bearing rats, and normal human blood were examined using the electron paramagnetic resonance (epr) technique. At low temperature a triplet epr signal, which is known to be produced by a NO-haemoprotein complex, was detected in some tumour samples and in decaying normal liver. At room temperature all of the tumour samples examined gave a doublet signal. This signal was also detected in blood but not in other normal tissues. The signal has a g value of 2·0054 ± 0·0002 and a hyperfine splitting of 1·80 ± 0·05 G and is assigned to the ascorbyl free radical. Model experiments suggest that the appearance of detectable concentrations of this radical result from a disturbance of the normal state of the ascorbic acid, dehydroascorbic acid redox system. It was verified that cell division is not responsible for the ascorbyl radical although autolysis may be involved. A possible relationship between the formation of ascorbyl radicals and other paramagnetic species in tumours is discussed.

Animals↗
PubMed1985

Ascorbic acid mediates acetylcholine receptor increase induced by brain extract on myogenic cells.

Extracts of fetal calf brain cause a 3- to 5-fold increase in acetylcholine receptors (AcChoR) on cultured myogenic L5 cells. Purification of the substance causing the major portion of this receptor increase has been completed. Ultraviolet spectral characteristics, nuclear magnetic resonance, mass spectra, and AcChoR induction by the active factor are the same as those of commercially available ascorbic acid. The biological activity of ascorbic acid is not mimicked by reducing agents with or without sulfhydryl groups. Compounds related to ascorbic acid were tested for their ability to induce AcChoR increases on L5 cells. D-Isoascorbic acid is the only substance with identical biological activity to ascorbic acid. Dehydroascorbic acid and ascorbic acid 2-O-sulfate also induce AcChoR increases but with lower specific activity. These data show that ascorbic acid can play a role in regulating AcChoR expression in myogenic tissue, and the presence of ascorbic acid in the purified fraction from fetal calf brain accounts for its ability to increase AcChoR in L5 cells.

Animals↗
PubMed1999

Ascorbic acid inhibits apoptosis induced by X irradiation in HL60 myeloid leukemia cells.

Exposure of cells to ionizing radiation can cause apoptosis. Since antioxidants have been shown to protect against radiation-induced apoptosis, in this study we have evaluated the putative protective effect of ascorbate against radiation-induced apoptosis as well as the production of peroxides in the cells. HL60 cells transport the oxidized form of ascorbic acid, dehydroascorbic acid (DHA), and accumulate reduced ascorbate. Exposure of the cells to 5-40 Gy X radiation resulted in induction of apoptosis. Preincubation of the cells with DHA reduced the level of apoptosis after exposure to 5-20 Gy. Exposure of the cells to 5 or 20 Gy X radiation did not affect the intracellular concentration of peroxides, while phorbol myristate acetate (PMA), which is known to induce production of H(2)O(2) in cells (and served as a control), resulted in an increase in peroxides and a decrease in intracellular ascorbate. Irradiation of the cells with 1-3 Gy resulted in up-regulation of expression of BCL2 without affecting the level of apoptosis. At higher doses of radiation, enhanced BCL2 expression did not prevent radiation-induced apoptosis. Loading of the cells with ascorbate prior to their exposure to 1-3 Gy X radiation did not affect the enhanced BCL2 expression observed in the irradiated cells. At higher doses of radiation, ascorbate decreased apoptosis and restored the level of BCL2 in the cells. Exposure of the cells to 3-20 Gy X radiation enhanced the cell surface expression of TNFRSF6 (formerly known as Fas/APO-1) antigen and enhanced anti-TNFRSF6 antibody-induced apoptosis of the cells. Ascorbate loading did not affect expression of TNFRSF6 and did not overcome the anti-TNFRSF6 antibody-induced apoptosis. In conclusion, our data demonstrate that exposure of HL60 cells to radiation enhanced BCL2 and TNFRSF6 expression. Ascorbate did not affect BCL2 or TNFRSF6 expression. We therefore conclude that it protects HL60 cells against radiation-induced apoptosis, although the mechanisms of protection must still be elucidated.

Apoptosis↗
PubMedDate not supplied

Vitamin C status, glutathione and histamine in gastric carcinoma, tuberculous enteritis and non-specific ulcerative colitis.

Studies were conducted to evaluate the blood levels of ascorbic acid, dehydroascorbic acid, glutathione, and histamine in patients with gastric carcinoma, tuberculous enteritis and non-specific ulcerative colitis. Leucocyte ascorbic acid, urinary excretion of total ascorbic acid and ascorbic acid saturation test were also carried out in order to assess the ascorbic acid status of these patients. It was observed that the plasma and leucocyte content of ascorbic acid was significantly lower with markedly decreased urinary excretion in these patients. Further urinary excretion of ascorbic acid after a test dose was also found to be subnormal. Decreased levels of glutathione and significantly higher levels of histamine reflect an overall reducing status of the body is markedly deranged.

Ascorbic Acid↗
PubMed1978

The influence of irradiation and packaging on the quality of prepacked vegetables.

During storage, transport and sale of prepacked vegetables, their quality deteriorates very quickly by microbiological decay, discolouration and desiccation. The experiments described were carried out with endive (Chichorium endiva L.) as a representative of the leaf vegetables. After processing (cutting, washing and drying), the product was packed in polythene bags without and with 4 perforations of 2 mm diameter. The endive was irradiated with 0 and 100 krad gammarays and afterwards stored at 10 degrees C, thus simulating the transport and sale temperature. The quality was studied on the basis of the following parameters. The gas composition in the bags, the microbiological composition, the Vitamin C (Ascorbic acid + Dehydroascorbic acid) content and the sensory quality. The experiments showed that the modified gas composition in the non-perforated bags, caused by the respiratory activity of the cut product, improved the quality. The low O2 and high CO2 content prevented discolouration, retarded the senescence and diminished the Vitamin C losses. The initial Total Viable Count of endive was 10(6) to 10(7) and the number of Enterobacteriaceae amounted to approx. 10(5) g-1 product, and increased in a couple of days to 10(8) and 10(7) g-1 respectively, resulting in decay of the product. The contamination with aerobic and anaerobic spores was low, viz. 10(1) to 10(2) g-1 and did not increase at 10 degrees C. An irradiation treatment of 100 krad reduced the Total Viable Count and the Enterobacteriaceae with 3-4 decimals, by which the shelf life increased with about 100% and almost all the Enterobacteriaceae were eliminated, so that the hygienic quality was improved. In prepacked endive nearly half of the Total Vitamin C content was lost within two days. The retention was strongly affected by the presence or absence of perforations; the effect of an irradiation treatment was slight.

Enterobacteriaceae↗
PubMedDate not supplied

Determination of total vitamin C by ion exclusion chromatography with electrochemical detection.

A rapid and sensitive liquid chromatographic method for determination of total vitamin C in foods and beverages is described. Ascorbic acid and dehydroascorbic acid are extracted with sulfuric acid solution, and the dehydroascorbic acid in the extract is reduced to ascorbic acid by dithiothreitol at pH 7. The reduction is complete in 2 min at room temperature. The resulting total ascorbic acid is separated on an anion exclusion/high speed column with 20 mM sulfuric acid as eluant and detected amperometrically with a platinum electrode operating at +0.6-0.8 V vs Ag/AgCl reference electrode. Dithiothreitol (retention time, 3.2 min) does not interfere with the separation and detection of ascorbic acid (retention time, 1.3 min). The dehydroascorbic acid content can be estimated as the difference in ascorbic acid content measured with and without reduction by dithiothreitol. The completeness of the reduction was demonstrated by purposely allowing the oxidation of ascorbic acid in the food extract and determining the total vitamin C after reduction. The determinations of vitamin C content in selected foods and beverages were in good agreement with the expected values. Total analysis time for vitamin C is 10 min and the detection limit is 0.1 ng. The method is specific for vitamin C, and interference by other food constituents is minimal.

Ascorbic Acid↗
PubMedDate not supplied

Effects of multilayered bags vs ethylvinyl-acetate bags on oxidation of parenteral nutrition.

BACKGROUND: We evaluate the effects of multilayered bags vs ethylvinyl-acetate bags on peroxidate formation of various emulsions for all-in-one total parenteral nutrition solutions (TPN) during storage. METHODS: Twenty-four parenteral nutritions were prepared with 4 commercial i.v. lipid emulsions (Soyacal 20%, Grifols; Intralipid 20%, Fresenius-Kabi; Lipofundina 20%, Braun; and Clinoleic 20%, Clintex) and 2 different bags (multilayered [ML] bag, Miramed; and 1 ethylvinyl-acetate [EVA] bag, Miramed). Each kind of TPN was prepared in triplicate. Samples were taken at 3 different times: immediately after preparation (time 0), after 6 days at 4 degrees C and 48 hours at 37 degrees C (time 1), and finally after a total of 14 days at 37 degrees C (time 2). Oxidation of TPN was evaluated by analysis of hydroperoxides by ferrous oxidation-xylenol orange (FOX) reactive, lipoperoxides by thiobarbituric acid reactive species (TBARS), alpha-tocopherol by high-performance liquid chromatography (HPLC), and ascorbic acid and dehydroascorbic acid by HPLC. RESULTS: TPN admixtures in ML bag showed less oxidation evaluated by peroxide determination using FOX than EVA bag. Lipoperoxides by TBARS did not show significant differences between 2 bags. Ascorbic acid and dehydroascorbic acid disappeared in EVA bags at time 1. No important differences were found in alpha-tocopherol content. CONCLUSIONS: Multilayered bags minimize oxidation.

Ascorbic Acid↗
PubMed1984

HPLC analysis with fluorometric detection of vitamin C in food samples.

A high performance liquid chromatographic (HPLC) procedure has been developed for the analysis of ascorbic acid and dehydroascorbic acid in complex matrices. Separation is accomplished with an anion-exchange resin and fluorescent detection is achieved through post-column inline chemistry, involving oxidation of ascorbic acid to dehydroascorbic acid followed by reaction with o-phenylenediamine to form a fluorescent product. Lower limits of detection for both forms of vitamin C are well below the levels found in the usual food sources of this vitamin. The extraction procedures developed yield clean samples for analysis with minimal loss of the vitamers during the analytical procedures. Recoveries are in the range of 90-107%. The results obtained with this HPLC procedure agree well with those obtained with a modified version of the classical procedure of Deutsch and Weeks. A variety of foods including fruit juices, vegetables, and fruits were analyzed.

Ascorbic Acid↗
PubMed1993

Inhibition by ascorbic acid of NMDA-evoked acetylcholine release in rabbit caudate nucleus.

The interaction of ascorbic acid and of dehydroascorbic acid with acetylcholine (ACh) release in rabbit caudate nucleus was investigated. The presence of ascorbic acid in the superfusion medium decreased the release of ACh evoked by N-methyl-D-aspartate (NMDA), but not by electrical stimulation. The pH of the buffer was always maintained at 7.4. Inhibition occurred even at 570 mumol/l ascorbic acid, a concentration which is widely employed in transmitter release experiments. In vivo this concentration may be reached extracellularly in brain tissue. Both ascorbic acid and dehydroascorbic acid inhibited the NMDA-evoked ACh release to the same degree in a non-competitive manner. The nearly identical action of ascorbic acid and dehydroascorbic acid makes a mode of action by lipid peroxidation or by redox phenomena unlikely. The mechanism of action underlying the described effects is unknown.

2-Amino-5-phosphonovalerate↗
PubMed1984

Cerebrospinal fluid ascorbic acid levels in neurological disorders.

The ascorbic acid/dehydroascorbic acid system was analyzed in the cerebrospinal fluid (CSF) of 41 patients with different neurological disorders. The chi-square test of covariance analysis revealed in this sample significant differences in the CSF levels of total ascorbic acid when patients were classified by diagnostic categories. The population analyzed contained a group of 18 patients (back pain/sciatica group) in whom no overt neurological abnormalities were disclosed upon evaluation. Taking the CSF levels of total ascorbic acid and dehydroascorbic acid in these patients as the reference (3.57 +/- 0.87 (SD)/100 ml and 0.53 +/- 0.19 mg/100 ml, respectively), it was found that head-traumatized patients showed a significant reduction in the concentration of total ascorbic acid in the CSF. CSF ascorbic acid levels were also significantly lower in patients with increased intracranial pressure (noninfected hydrocephalus group) and in patients with cerebral tumors. Although the CSF concentration of dehydroascorbic acid did not correspondingly increase over the reference values in these three groups of patients, the tendency existed for dehydroascorbic acid to represent in them a higher percentage of total ascorbic acid. After examining different alternatives, it is concluded that the hypothesis of free radical damage to the central nervous system after certain types of injury (trauma, ischemia, and tumors) may provide a satisfactory explanation of our findings. A rationale for the use of vitamin C in the management of some neurological patients is also derived from this work.

Adolescent↗
PubMed1977

[On the mechanism of ascorbic acid induced methemoglobin reduction of human erythrocytes (author's transl)].

Ascorbic acid and dehydroascorbic acid penetrate the human erythrocyte membrane. In vitro methemoglobin is reduced nonenzymatically by both substances in concentrations of 10(-2) M to 10(-3) M. Dehydroascorbic acid is reduced nonenzymatically to ascorbic acid by GSH, even with low GSH-content of erythrocytes. Under physiological conditions ascorbic acid induced methemoglobin reduction is far less important than reduction by the NADH dependent methemoglobin reductase system. In methemoglobinemic conditions caused by toxic effects or by congenital methemoglobin reductase deficiency treatment with ascorbic acid is possible. However, critically increased methemoglobin content of the blood higher than 30% makes therapy with methylene blue necessary.

Ascorbic Acid↗
PubMed1996

Purification, cloning and expression of dehydroascorbic acid-reducing activity from human neutrophils: identification as glutaredoxin.

Dehydroascorbic acid-reducing activity in normal human neutrophil lysates was characterized and identified by activity-based purification and measurement of newly synthesized ascorbate by HPLC. The initial reducing activity was non-dialysable and could not be accounted for by the activity of glutathione as a reducing agent. The reducing activity was purified to homogeneity as an 11 kDa protein. The protein had a specific activity of 3 mumol/min per mg of protein and was glutathione dependent. Kinetic experiments showed that the protein had a K(m) for glutathione of 2.0 mM and a K(m) for dehydroascorbic acid of 250 microM. Dehydroascorbic acid reduction by the purified protein was pH dependent and was maximal at pH 7.5. Peptide fragments from the purified protein were analysed for amino acid sequence and the protein was identified as glutaredoxin. By using degenerate oligonucleotides based on the amino acid sequence, glutaredoxin was cloned from a human neutrophil library. Expressed purified glutaredoxin displayed reducing activity and kinetics that were indistinguishable from those of native purified enzyme. Several approaches indicated that glutaredoxin was responsible for the most of the protein-mediated dehydroascorbic acid reduction in lysates. From protein purification data, glutaredoxin was responsible for at least 47% of the initial reducing activity. Dehydroascorbic acid reduction was at least 5-fold greater in neutrophil lysates than in myeloid tumour cell lysates, and glutaredoxin was detected in normal neutrophil lysates but not in myeloid tumour cell lysates by Western blotting. Glutaredoxin inhibitors inhibited dehydroascorbic acid reduction in neutrophil lysates as much as 80%. These findings indicate that glutaredoxin plays a major role in dehydroascorbic acid reduction in normal human neutrophil lysates, and represent the first identification of dehydroascorbic acid reductase in human tissue by activity-based purification.

Amino Acid Sequence↗
PubMed1993

Determination of total vitamin C in fruits by capillary zone electrophoresis.

A simple capillary zone electrophoretic (CZE) method is described for the rapid determination of ascorbic acid and dehydroascorbic acid, the physiologically active forms of vitamin C, in fruits. The electrophoretic run was accomplished in 9 min on a coated capillary column using 20 mM phosphate buffer (pH 7.0). Total ascorbic acid was determined by first reducing the dehydroascorbic acid to ascorbic acid by treatment with DL-homocysteine. This reaction was complete in 15 min and total ascorbic acid determination was performed immediately. The data obtained by CZE were in good agreement with HPLC data.

Ascorbic Acid↗