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PubMedDate not supplied

The role of reactive oxygen species in diabetes-induced anomalies in embryos of Cohen diabetic rats.

The role of the antioxidant defense mechanism in diabetes-induced anomalies was studied in the Cohen diabetes-sensitive (CDs) and -resistant (CDr) rats, a genetic model of nutritionally induced type 2 diabetes mellitus. Embryos, 12.5-day-old, of CDs and CDr rats fed regular diet (RD) or a diabetogenic high-sucrose diet (HSD) were monitored for growth retardation and congenital anomalies. Activity of superoxide dismutase (SOD) and catalase-like enzymes and levels of ascorbic acid (AA), uric acid (UA), and dehydroascorbic acid (DHAA) were measured in embryonic homogenates. When fed RD, CDs rats had a decreased rate of pregnancy, and an increased embryonic resorption. CDs embryos were smaller than CDr embryos; 46% were maldeveloped and 7% exhibited neural tube defects (NTDs). When fed HSD, rate of pregnancy was reduced, resorption rate was greatly increased (56%; P < .001), 47.6% of the embryos were retrieved without heart beats, and 27% exhibited NTD. In contrast, all the CDr embryos were normal when fed RD or HSD. Activity of SOD and catalase was not different in embryos of CDs and CDr rats fed RD. When fed HSD, levels of AA were significantly reduced, the ratio DHAA/AA was significantly increased, and SOD activity was not sufficiently increased when compared to embryos of CDr. The reduced fertility of the CDs rats, the growth retardation, and NTD seem to be genetically determined. Maternal hyperglycemia seems to result in environmentally induced embryonic oxidative stress, resulting in further embryonic damage.

Animals↗
PubMed1995

Cortical ablation and drug-induced changes in striatal ascorbic acid oxidation and behavior in the rat.

Rats whose frontoparietal cortex had been bilaterally ablated were allowed 21 days for recovery and then treated with apomorphine (APO), 1 mg/kg SC or scopolamine (SCOP), 0.6 mg/kg SC. Soon after a behavioral test, dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), ascorbic acid (AA), and dehydroascorbic acid (DHAA) levels were determined by HPLC/EC in striatal synaptosomes (left side) and whole striatum (right side). SCOP behavioural effects were attenuated by cortical ablation, while those of APO were affected to a lesser extent. In the striatum of unoperated and sham-operated rats DHAA contents and DHAA/AA ratio resulted increased after drugs administration. No change in AA oxidation was observed in the striatum of ablated rats. In the synaptosomes of unoperated and sham-operated rats both drugs led to a decrease in DHAA contents and DHAA/AA ratio. In unoperated and sham-operated rats APO and SCOP caused a decrease of the DOPAC/DA ratio in the whole striatum and striatal synaptosomes. In ablated rats APO caused a decrease of DOPAC/DA ratio in the whole striatum and synaptosomes, while SCOP effects on DA turnover resulted attenuated in the whole striatum and abolished in synaptosomes. We conclude that drug-induced AA oxidation is likely to occur in the extracellular space and requires intact corticostriatal glutamatergic pathways. The latter may play an enabling role in SCOP behavioral effects.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2002

Determination of vitamin C in plasma and dialysate from uremia patients by high performance liquid chromatography with electrochemical detection.

A convenient and valid method for the determination of ascorbic acid(AA) and dehydroascorbic acid(DHAA) in plasma and dialysate from patients with uremia by high performance liquid chromatography with electrochemical detection is described. A mixture of 0.8 g/L metaphosphoric acid and 18% (volume fraction) perchloric acid was used as a protein precipitant and the extractant for AA from biosamples. It was also a good stabilizer for AA in samples. The proposed method is satisfied for routine screening of vitamin C in clinical applications with a correlation coefficient of more than 0.99 in the range of 2 mumol/L-40 mumol/L AA. The within-day precision was less than 8.9% and 10.55% for AA and DHAA, respectively. The recoveries of AA in plasma and dialysate were over 95% and 78%, respectively.

Ascorbic Acid↗
PubMed2004

Ascorbic acid recycling by cultured beta cells: effects of increased glucose metabolism.

Ascorbic acid is necessary for optimal insulin secretion from pancreatic islets. We evaluated ascorbate recycling and whether it is impaired by increased glucose metabolism in the rat beta-cell line INS-1. INS-1 cells, engineered with the potential for overexpression of glucokinase under the control of a tetracycline-inducible gene expression system, took up and reduced dehydroascorbic acid to ascorbate in a concentration-dependent manner that was optimal in the presence of physiologic D-glucose concentrations. Ascorbate uptake did not affect intracellular GSH concentrations. Whereas depletion of GSH in culture to levels about 25% of normal also did not affect the ability of the cells to reduce dehydroascorbic acid, more severe acute GSH depletion to less than 10% of normal levels did impair dehydroascorbic acid reduction. Culture of inducible cells in 11.8 mM D-glucose and doxycycline for 48 h enhanced glucokinase activity, increased glucose utilization, abolished D-glucose-dependent insulin secretion, and increased generation of reactive oxygen species. The latter may have contributed to subsequent decreases in the ability of the cells both to maintain intracellular ascorbate and to recycle it from dehydroascorbic acid. Cultured beta cells have a high capacity to recycle ascorbate, but this is sensitive to oxidant stress generated by increased glucose metabolism due to culture in high glucose concentrations and increased glucokinase expression. Impaired ascorbate recycling as a result of increased glucose metabolism may have implications for the role of ascorbate in insulin secretion in diabetes mellitus and may partially explain glucose toxicity in beta cells.

Animals↗
PubMed1998

Ascorbate-mediated transplasma membrane electron transport in pulmonary arterial endothelial cells.

Pulmonary endothelial cells are capable of reducing certain electron acceptors at the luminal plasma membrane surface. Motivation for studying this phenomenon comes in part from the expectation that it may be important both as an endothelial antioxidant defense mechanism and in redox cycling of toxic free radicals. Pulmonary arterial endothelial cells in culture reduce the oxidized forms of thiazine compounds that have been used as electron acceptor probes for studying the mechanisms of transplasma membrane electron transport. However, they reduce another commonly studied electron acceptor, ferricyanide, only very slowly by comparison. In the present study, we examined the influence of ascorbate [ascorbic acid (AA)] and dehydroascorbate [dehydroascorbic acid (DHAA)] on the ferricyanide and thiazine reductase activities of the bovine pulmonary arterial endothelial cell surface. The endothelial cells were grown on microcarrier beads so that the reduction of ferricyanide and methylene blue could be studied colorimetrically in spectrophotometer cuvettes and in flow-through cell columns. The ferricyanide reductase activity could be increased 80-fold by adding DHAA to the medium, with virtually no effect on methylene blue reduction. The DHAA effect persisted after the DHAA was removed from the medium. AA also stimulated the ferricyanide reductase activity but was less potent, and the relative potencies of AA and DHAA correlated with their relative rates of uptake by the cells. The results are consistent with the hypothesis that AA is an intracellular electron donor for an endothelial plasma membrane ferricyanide reductase and that the stimulatory effect of DHAA is the result of increasing intracellular AA. Adding sufficient DHAA to markedly increase extracellular ferricyanide reduction had little effect on the plasma membrane methylene blue reductase activity, suggesting that pulmonary arterial endothelial cells have at least two separate transplasma membrane electron transport systems.

Animals↗
PubMed1998

A simple fluorometric determination of vitamin C.

A simple and accurate method for determination of vitamin C (ascorbic acid (AsA) and dehydroascorbic acid (DHA)) using 4,5-dimethyl-o-phenylenediamine (DMPD) was investigated. It was found that DMPD is a useful fluorescent reagent. The reaction product of DMPD with DHA showed strong and stable fluorescence (Ex; 360 nm, Em; 440 nm). Fluorometric derivatives were extracted with isobutanol or n-butanol. Extraction with isobutanol was superior to that with n-butanol in terms of specificity, since fluorometric derivatives of keto acids were extracted with n-butanol, together with DHA. The fluorescence intensity of DMPD derivatives was absolutely stable in isobutanol for at least 24 h. The sensitivity of determination of vitamin C was improved by removing several non-fluorometric compounds coexisting in the samples. The derivative derived from AsA was easily separated from those of keto acids by an HPLC method. The determination of vitamin C in natural products was thus improved by extraction and the HPLC method.

1-Butanol↗
PubMed1958

The effect of ascorbic acid oxidation on the incorporation of sulfate by slices of calf costal cartilage.

A marked inhibition of the incorporation of S(35)-sulfate by normal calf costal cartilage was produced by potassium ascorbate in the presence of catalytic amounts of cupric ions. The effect of the various components of the ascorbic acid oxidizing system (potassium ascorbate, cupric ions, cuprous ions, hydrogen peroxide, dehydroascorbic acid) was investigated. The results of experiments in which hydrogen peroxide, catalase, or sodium azide were used singly or in combination suggest that the inhibition produced by the ascorbic acid oxidizing system is due, to a considerable extent, to the production of hydrogen peroxide. Dehydroascorbic acid was also found to inhibit the incorporation of S(35)-sulfate by cartilage slices. However, the gradual fall in pH which resulted from the addition of dehydroascorbic acid could account to a large extent for the inhibitory effect observed because the incorporation of S(35)-sulfate by cartilage slices decreases sharply as the pH is lowered. The incorporation of S(35)-sulfate by cartilage slices is inhibited also by increasing the concentration of phosphate.

Animals↗
PubMed1988

The precipitation and cross-linking of lens crystallins by ascorbic acid.

Bovine lens beta-crystallin was incubated with increasing concentrations of sugars and sugar derivatives for a period of 2 weeks in the dark at 37 degrees C. Marked protein precipitation and a browning reaction was observed with both ascorbic acid (ASA) and dehydroascorbic acid (DHA), but little or no reaction was seen with several other sugars and sugar analogs. Similar incubations were carried out with 20 mM ASA, 20 mM DHA and 20 mM glucose, but with increasing amounts of the individual crystallins. Glucose was capable of precipitating gamma-crystallin in the presence of air, but this reaction was decreased if dithiothreitol and a chelating agent were added prior to incubation. ASA and DHA produced precipitation and browning with gamma- and beta-crystallin, but not with alpha-crystallin or lens soluble proteins. Similar reactivities were observed both in air and under reducing conditions. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis of these reaction mixtures showed little or no cross-linking with any of the lens proteins by glucose. ASA and DHA caused detectable dimer formation with gamma-crystallin, but produced the formation of dimers as well as highly polymerized proteins at the top of the gel with all the other crystallins and with lens soluble proteins. A time-course experiment with alpha-crystallin in the presence of air showed no cross-linking with 100 mM glucose over a 6-week period; however, 10 mM ASA caused definite cross-linking at 2 weeks, and at 6 weeks a dark smear of protein was visible throughout the gel. ASA was still capable of inducing cross-linking under low oxygen conditions but the protein smearing was markedly diminished. Further, the cross-linking pattern was similar to that seen in the water-insoluble fraction from older human lenses and cataracts. This reaction may be significant in vivo because cross-linking was observed under low-oxygen conditions with as little as 2 mM ASA, which is the level of ASA normally present in human lenses.

Animals↗
PubMed1992

The effects of cortical ablation on d-amphetamine-induced changes in striatal dopamine turnover and ascorbic acid catabolism in the rat.

Dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), ascorbic acid (AA) and dehydroascorbic acid (DHAA) levels were determined by HPLC in the striatal synaptosomal fraction and in the whole striatum of rats, whose fronto-parietal cortex had been bilaterally ablated, after a single injection of d-amphetamine (2.0 mg/kg i.p.). d-Amphetamine significantly increased the DHAA/AA ratio in unoperated and sham-operated rats, but failed to increase it in ablated rats, as compared to pertinent saline-treated groups. In the synaptosomal fraction, d-amphetamine significantly decreased the DHAA/AA ratio in unoperated, sham-operated and ablated rats. d-Amphetamine significantly decreased the DOPAC/DA ratio in the whole striatum and significantly increased it in the striatal synaptosomal fraction in all experimental groups. Cortical ablation greatly increased d-amphetamine-induced motor hyperactivity. We conclude that the d-amphetamine-induced increase in AA striatal oxidation requires integrity of the cortico-striatal glutamatergic pathways. Further, AA oxidation occurs in the extracellular space. The cortico-striatal glutamatergic pathways exert an inhibitory modulation on d-amphetamine behavioral effects.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2004

6-Bromo-6-deoxy-L-ascorbic acid: an ascorbate analog specific for Na+-dependent vitamin C transporter but not glucose transporter pathways.

Vitamin C intracellular accumulation is mediated by Na(+)-dependent vitamin C transporters SVCT1 and -2 and dehydroascorbic acid transporters GLUT1 and -3. It is unclear which pathways dominate in vivo. As a new step to resolve this issue, we identified and tested 6-bromo-6-deoxy-L-ascorbic acid as a specific candidate for SVCTs. In high performance liquid chromatography and electron paramagnetic resonance analyses, the reduced compounds ascorbic acid and 6-bromo-6-deoxy-L-ascorbic acid were similar. The oxidized products 6-bromo-6-deoxy dehydroascorbic acid (BrDHA) and dehydroascorbic acid (DHA) had comparable stabilities, based on reduction recoveries. Upon expression of GLUT1 or GLUT3 in Xenopus oocytes, BrDHA was neither transported nor bound, in contrast to robust transport of DHA. The findings were not explained by differences in the oocyte reduction of DHA and BrDHA because lysed oocytes reduced both compounds equally. Further, there was no transport of the reduced compound, 6-bromo-6-deoxy-L-ascorbic acid, by GLUT1 or GLUT3. As a prerequisite for investigating 6-bromo-6-deoxy-L-ascorbic acid transported by SVCTs, SVCT2 transport activity in oocytes was enhanced 14-fold by construction and use of a vector that added a fixed poly(A) tail to the 3' end of cRNA. For SVCT1 and SVCT2 expressed in oocytes, similar K(m) and V(max) values were observed for ascorbic acid and 6-bromo-6-deoxy-L-ascorbic acid. In human fibroblasts, predicted to have SVCT-mediated ascorbate accumulation, K(m) and V(max) values were again comparable for ascorbic acid and 6-bromo-6-deoxy-L-ascorbic acid. Using activated human neutrophils, predicted to have ascorbate accumulation mediated predominantly by DHA and GLUT transporters, 6-bromo-6-deoxy-L-ascorbic acid accumulation was <1% of accumulation when compared with ascorbic acid. We conclude that 6-bromo-6-deoxy-L-ascorbic acid is the first transport substrate identified as completely specific for SVCTs, but not GLUTs, and provide a new strategy to determine the contribution of each pathway to ascorbate accumulation.

Animals↗
PubMed1989

The bactericidal effect of isoascorbic acid combined with mild heat.

The thermal inactivation of Salmonella thompson, Escherichia coli, Staphylococcus aureus, Clostridium perfringens, Candida zeylanoides, Enterococcus faecium and E. faecalis was accelerated by the addition of sodium isoascorbate (1 mmol/l) to phosphate-buffer heating medium but not to complex food mixtures. The lethal effect of isoascorbate was nullified by heating under anaerobic conditions or by the addition of catalase. The scavengers of hydroxyl radicals, mannitol and formate were not protective whereas histidine was. Histidine may have protected by slowing the rate of isoascorbate autoxidation, a property common to other amino acids tested. Superoxide dismutase was not protective. Dehydroascorbic acid also enhanced heat killing and its action was also reversed by catalase. The bactericidal effects of mild heat plus isoascorbate or dehydroascorbic acid both apparently depend on oxidative processes but their relative effectiveness was not related to their respective rates of oxygen consumption or peroxide production. We speculate that site-specific redox reactions, involving amino-carbonyl intermediates are involved in the inactivation mechanism.

Anaerobiosis↗
PubMed2006

Reversible reduction of nitroxides to hydroxylamines: roles for ascorbate and glutathione.

Biological applications of stable nitroxyl radicals, NR, include their use as contrast agents for magnetic resonance imaging, spin labels, superoxide dismutase mimics, and antioxidants. The rapid reduction of NR in biological samples into hydroxylamines (HA) significantly limits their application. In turn, reoxidation of HA back to the NR has been used for detection of reactive oxygen species (ROS). In this work comparative studies of the reduction of pyrrolidine, imidazoline, and imidazolidine NR by ascorbate were performed taking advantage of recently synthesized tetraethyl-substituted NR with much higher stability toward reduction both in vitro and in vivo. Surprisingly, these NR kept 10-50% of initial intensity of electron paramagnetic resonance signal for about 1 h in the presence of 100-fold excess of ascorbate. To explain these data, reoxidation of the corresponding HA by ascorbate radical and dehydroascorbic acid back to the NR was proposed. This hypothesis was supported by direct measurement of the NR appearance from the HA on ascorbate radical generation by ascorbate oxidase, or in the presence of the dehydroascorbic acid. The reversible reaction between NR and ascorbate was observed for the various types of NR, and the rate constants for direct and reverse reactions were determined. The equilibrium constants for one-electron reduction of the tetraethyl-substituted NR by ascorbate were found to be in the range from 2.65x10(-6) to 10(-5) which is significantly lower than corresponding values for the tetramethyl-substituted NR (more or about 10(-4)). This explains the establishment of an EPR-detectable quasi-equilibrium level of tetraethyl-substituted NR in the presence of an excess of ascorbate. The redox reactions of the NR-HA couple in ascorbate-containing media were found to be significantly affected by glutathione (GSH). This effect was attributed to the reduction of ascorbate radicals by GSH, and the rate constant of this reaction was found to be equal to 10 M-1 s-1. In summary, the data provide new insight into the redox chemistry of NR and HA, and significantly affect interpretation and strategy of their use as redox- and ROS-sensitive probes, or as antioxidants.

Ascorbate Oxidase↗
PubMed1995

Altered ascorbic acid status in the mucosa from inflammatory bowel disease patients.

Attempts to establish the presence of oxidant stress and tissue damage in inflammatory bowel disease (IBD) have relied on determining the capacity of peripheral blood inflammatory cells to produce reactive oxygen species (ROS) and other indirect indices. These approaches have failed to address whether or not there are adequate chemical antioxidant defences to prevent oxidative injury in the inflamed mucosa. In this investigation we have determined the mucosal concentrations of reduced and total ascorbic acid and the redox status in paired non-inflamed and inflamed mucosa using colonic biopsies from IBD patients. In inflamed mucosa from Crohn's disease (CD) patients, reduced and total ascorbic acid content decreased by 35% (p = 0.014 and p = 0.009, respectively). In ulcerative colitis (UC) patients, mucosal total ascorbic acid content decreased by 73% (p = 0.069) and reduced ascorbic acid by 41% (p = 0.014). The proportion of total ascorbic acid present in its reduced form in histologically normal mucosa from CD patients was unusually low at approximately 30%. In the paired-inflamed mucosa from CD patients, the redox ratio was also approximately 30% despite the loss of 35% of total ascorbate. In UC patients, the ascorbate redox ratio in the non-inflamed mucosa was 23% which increased to 51% in paired inflamed mucosa. This increase reflected the loss (73%) of total ascorbate. Reduction of dehydroascorbic acid by GSH/NADPH dependent dehydroascorbic acid reductase decreased significantly (p = 0.046) in inflamed mucosa from UC patients, suggesting that the capacity of the inflamed mucosa to maintain the concentration of reduced ascorbic acid is also diminished. HPLC analysis of mucosal preparations for diketogulonic acid, the decomposition product of dehydroascorbic acid, did not account for the loss of total ascorbate in the inflamed mucosa suggesting that ascorbate equivalents underwent further decomposition reactions or were excreted to the colonic lumen. We conclude that the normal luminal environment is strongly oxidising in character and that oxidant stress derived from inflammatory cells contributes to the loss of 35-73% total and reduced ascorbate. In absolute terms, the overall loss of this antioxidant buffering capacity would decrease the capacity of the inflamed mucosa to prevent oxidative tissue damage and hinder recovery of the inflamed mucosa.

2,3-Diketogulonic Acid↗
PubMedDate not supplied

[Content of different forms of ascorbic acid in the tissues of rabbits with experimental myocardial infarct].

It was established that experimental myocardial infarction leads to a decrease in the ascorbic acid content in the left heart ventricle in the ischemic are and to a negligible rise in the dehydroascorbic acid concentration within the first hours after artery ligation followed by its lowering at the 24th hour. Meanwhile 24 hours after the operation the right heart ventricle manifests a 22% increase in the ascorbic acid content along with the rise of the deketogulonic acid level, whereas the content of dehydroascorbic acid does not appreciably change. The concentration of ascorbic acid in the liver of animals with experimental myocardial infarction drops by 27% as compared with intact animals. The data obtained attest to upset ascorbic acid metabolism in the acute stage of experimental myocardial infarction thus suggesting that it is desirable to apply vitamin C to the treatment of patients with myocardial infarction.

Animals↗
PubMed2004

Oxidative decomposition of vitamin C in drinking water.

We have previously shown that vitamin C (ascorbic acid) can initiate hydroxyl radical formation in copper contaminated household drinking water. In the present study, we have examined the stability of vitamin C in copper and bicarbonate containing household drinking water. In drinking water samples, contaminated with copper from the pipes and buffered with bicarbonate, 35% of the added vitamin C was oxidized to dehydroascorbic acid within 15 min. After 3h incubation at room temperature, 93% of the added (2 mM) ascorbic acid had been oxidized. The dehydroascorbic acid formed was further decomposed to oxalic acid and threonic acid by the hydrogen peroxide generated from the copper (I) autooxidation in the presence of oxygen. A very modest oxidation of vitamin C occurred in Milli-Q water and in household water samples not contaminated by copper ions. Moreover, addition of vitamin C to commercially sold domestic bottled water samples did not result in vitamin C oxidation. Our results demonstrate that ascorbic acid is rapidly oxidized to dehydroascorbic acid and further decomposed to oxalic- and threonic acid in copper contaminated household tap water that is buffered with bicarbonate. The impact of consuming ascorbic acid together with copper and bicarbonate containing drinking water on human health is discussed.

Ascorbic Acid↗
PubMed2001

Mitochondrial uptake and recycling of ascorbic acid.

Mitochondria generate reactive oxygen species as by-products of oxidative metabolism. Since ascorbic acid can scavenge such destructive species, we studied the ability of mitochondria from rat liver and muscle to take up, recycle, and oxidize ascorbate. Freshly prepared mitochondria contain ascorbate, as do mitoplasts that lack the outer mitochondrial membrane. Both mitochondria and mitoplasts rapidly take up oxidized ascorbate as dehydroascorbic acid and reduce it to ascorbate. Ascorbate concentrations in mitochondria and mitoplasts rise into the low millimolar range during dehydroascorbic acid uptake, although uptake and reduction is opposed by ascorbate efflux. Mitochondrial dehydroascorbic acid reduction depends mainly on GSH, but mitochondrial thioredoxin reductase may also contribute. Reactive oxygen species generated within mitochondria oxidize ascorbate more readily than they do GSH and alpha-tocopherol. These results show that mitochondria can recycle ascorbate, which in turn might help to prevent deleterious effects of oxidant stress in the organelle.

Animals↗
PubMed1994

Dehydroascorbate reduction.

Dehydroascorbic acid is generated in plants and animal cells by oxidation of ascorbic acid. The reaction is believed to occur by the one-electron oxidation of ascorbic acid to semidehydroascorbate radical followed by disproportionation to dehydroascorbic acid and ascorbic acid. Semidehydroascorbic acid may recycle to ascorbic acid catalyzed by membrane-bound NADH-semidehydroscorbate reductase. However, disproportionation of the free radical occurs at a rapid rate, 10(5) M-1 s-1, accounting for measurable cellular levels of dehydroascorbate. Dehydroascorbate reductase, studied earlier and more extensively in plants, is now recognized as the intrinsic activity of thioltransferases (glutaredoxins) and protein disulfide isomerase in animal cells. These enzymes catalyze the glutathione-dependent two-electron regeneration of ascorbic acid. The importance of the latter route of ascorbic acid renewal was seen in studies of GSH-deficient rodents (Meister, A. (1992) Biochem. Pharmacol. 44, 1905-1915). GSH deficiency in newborn animals resulted in decreased tissue ascorbic acid and increased dehydroascorbate-to-ascorbate ratios. Administration of ascorbic acid daily to GSH-deficient animals decreased animal mortality and cell damage from oxygen stress. A cellular role is proposed for dehydroascorbate in the oxidation of nascent protein dithiols to disulfides catalyzed in the endoplasmic reticulum compartment by protein disulfide isomerase.

Animals↗
PubMed2004

Cellular vitamin C accumulation in the presence of copper.

Under the cell-free condition, copper is known to oxidize ascorbic acid (the active form of vitamin C) and the event leads to the loss of vitamin C. However, the biological consequence of this interaction was never examined in the presence of cells. We demonstrated in intestinal epithelial cells that dehydroascorbic acid (the oxidized form of ascorbic acid), when generated from ascorbic acid in the presence of copper, can be efficiently transported into the cells and reduced back to ascorbic acid. We also observed in other types of cells the transport and intracellular reduction of dehydroascorbic acid in the presence of copper. In the presence of iron, a metal that also oxidizes ascorbic acid, we observed similar oxidation-related accumulation in intestinal cells. Other metals that do not interact with ascorbic acid had little effect on vitamin C transport. A nonmetal pro-oxidant, hydrogen peroxide, is known to oxidize ascorbic acid and we observed that the oxidation is also accompanied by an increased intracellular accumulation of vitamin C. The efficient coupling between dehydroascorbic acid transport and intracellular reduction could help to preserve the important nutrient when facing oxidative metals in the intestine.

Animals↗