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PubMed2004

A human sodium-dependent vitamin C transporter 2 isoform acts as a dominant-negative inhibitor of ascorbic acid transport.

Vitamin C is transported as ascorbic acid (AA) through the sodium-ascorbate cotransporters (SVCT1 and -2) and as dehydroascorbic acid (DHA) through the facilitative glucose transporters. All cells have glucose transporters and take up DHA that is trapped intracellularly by reduction and accumulated as AA. SVCT2 is widely expressed in cells and tissues at the mRNA level; however, only specialized cells directly transport AA. We undertook a molecular analysis of SVCT2 expression and discovered a transcript encoding a short form of human SVCT2 (hSVCT2-short) in which 345 bp is deleted without a frame shift. The deletion involves domains 5 and 6 and part of domain 4. cDNA encoding this isoform was isolated and expressed in 293T cells, where the protein was detected on the plasma membrane. Transport studies, however, revealed that hSVCT2-short gave rise to a nonfunctional transporter protein. hSVCT2-short arises by alternative splicing and encodes a protein that strongly inhibited the function of SVCT2 and, to a lesser extent, SVCT1 in a dominant-negative manner, probably by protein-protein interaction. The expression of hSVCT2-short varies among cells. PCR analysis of cDNA isolated from melanocytes capable of transporting AA revealed a predominance of the full-length isoform, while HL-60 cells, which express SVCT2 at the mRNA level and were incapable of transporting AA, showed a predominance of the short isoform. These findings suggest a mechanism of AA uptake regulation whereby an alternative SVCT2 gene product inhibits transport through the two known AA transporters.

Biological Transport, Active↗
PubMed1993

Testicular and plasma ascorbic acid levels in mice following dietary intake: a high-performance liquid chromatographic analysis.

A modified buffer system is reported for the analysis of vitamin C in mouse plasma and testes, on a reversed-phase high-performance liquid chromatographic column with ultraviolet detection. The buffer, consisting of 0.1 M NaH2PO4 and 0.2 mM Na2EDTA adjusted to pH 3.1 with orthophosphoric acid, resolved the ascorbic acid (AA) peak allowing clear quantitation of the chemical. The method is also applicable to the assay of dehydroascorbic acid after its reduction to ascorbic acid, and overcomes problems of AA stability encountered in previously reported procedures. Using the present technique, variations in the vitamin levels of plasma and testes are studied from 3 to 29 days after the commencement of feeding a vitamin C-rich diet (1%, w/w) in mice. The plasma AA levels were elevated above the controls by a factor of 2.5 by day 8. Contrary to this, testicular AA levels increased marginally (1.2-fold) by day 12 and were maintained at levels close to the control values thereafter. It appears that the feedback inhibition mechanism which is effective in plasma is not operational in the testes. The findings are of clinical significance in that testicular AA levels do not change significantly as a result of dietary intake of vitamin C, whereas plasma AA levels do show an increase.

Animals↗
PubMed2003

Ascorbic acid spares alpha-tocopherol and decreases lipid peroxidation in neuronal cells.

Ascorbic acid is considered an antioxidant in the central nervous system, but direct evidence that ascorbate protects neuronal cells from oxidant stress is lacking. Differentiated SH-SY5Y cells in culture took up ascorbic acid on the sodium-dependent vitamin C transporter Type 2 and retained it much more effectively than dehydroascorbic acid. Intracellular ascorbate spared alpha-tocopherol, both in cells loaded with alpha-tocopherol in culture and in cells under oxidant stress due to extracellular ferricyanide. Sparing of alpha-tocopherol in response to ferricyanide was associated with protection against lipid peroxidation in cell membranes. These results show that neuronal cells concentrate ascorbate, and that intracellular ascorbate, either directly or through sparing of alpha-tocopherol, protects them against oxidant stress.

Ascorbic Acid↗
PubMed1975

Chemistry of nonaqueous titration of chlopromazine.

The chemistry of the red color formed during perchloric acid titration of chlorpromazine hydrochloride in acetic acid in the presence of mercuric acetate is discussed. Addition of ascorbic acid prevents the color formation and allows titration using a crystal violet end-point. Ascorbic acid addition also sharpens the potentiometric end-point. Ascrobic acid and its oxidation product, dehydroascorbic acid, being neutral to perchloric acid, do not interfere with the titration.

Ascorbic Acid↗
PubMed1992

Chromium (VI) reducing capacity of ascorbic acid and of human plasma in vitro.

In the metabolism of chromium(VI) its reduction in human plasma is of importance; an extracellular reduction of Cr(VI) is regarded as a detoxification step. Ascorbic acid has been suggested to represent the majority of the Cr(VI)-reducing capacity of human plasma. Therefore the kinetics of the reaction of Cr(VI) with ascorbic acid, at biologically realistic concentrations were studied. Ascorbic acid, in 0.2 M HEPES buffer and at concentrations ranging from 14.2 to 113.6 nmol ml-1 (2.5-20.0 microgram ml-1), was mixed with Cr(VI) (0.4-1.5 nmol ml-1) and incubated at pH 7.4 and 37 degrees C. In addition, chromate solutions at different concentrations [1.5-100 nmol ml-1 Cr(VI)], were incubated at 37 degrees C with freshly drawn blood. From these incubates, ascorbic acid and its oxidized form, dehydroascorbic acid, were simultaneously analyzed by HPLC and post-column derivatization. Chromate was determined by flow injection analysis. The reaction kinetics of ascorbic acid in HEPES buffer with Cr(VI) is of pseudo-first order at higher concentrations, whilst apparently at lower concentrations kinetics are consistent with an autocatalyzed reaction. Results obtained after spiking human plasma are similar. However, when Cr(VI) was reacted with human plasma, no changes in the intrinsic contents of ascorbic acid of the plasma samples occurred. Also, comparing different plasma samples the intrinsic plasma contents of ascorbic acid and the reduction capacities for Cr(VI) [ranging between 0.48 and 0.63 nmol ml-1 Cr(VI) to be reduced] did not correlate. This shows that the reduction of Cr(VI) in native human plasma is complex and is not only determined by the plasma ascorbic acid levels. This is in contrast to the situation in lung lavage fluids (Suzuki 1988; Suzuki and Fukuda 1990) where the concentrations of ascorbic acid are much higher than in blood.

Ascorbic Acid↗
PubMed2000

Flow injection spectrophotometric determination of ascorbic acid in soft drinks and beer.

Two spectrophotometric methods, a photochemical and a non-photochemical, for the determination of ascorbic acid in soft drinks and beer using a flow-injection system are proposed. The non-photochemical method is based on the redox reaction that takes place between ascorbic acid and Fe(III), yielding dehydroascorbic acid and Fe(II). Fe(II) reacts with 1,10-phenantroline, originating the reddish orange Fe(phen)3(2+) complex (ferroin). This complex is spectrophotometrically monitored at 512 nm, and the signal is directly related to the concentration of ascorbic acid in the sample. The photochemical method has the same basis, nevertheless, uses the irradiation with visible light to enhance the redox reaction and so achieve higher sensitivities in the analysis. The non-photochemical method shows a linear range between 5 and 80 microg mL(-1), with a relative standard deviation of 1.6% (n = 11), a detection limit of 2.7 microg mL(-1) and a sample throughput of 60 samples h(-1). The photochemical method shows a linear range between 1 and 80 microg mL(-1), with a relative standard deviation of 1.0% (n = 11 ), a detection limit of 0.5 microg mL(-1) and a sample throughput of 40 samples h(-1).

Ascorbic Acid↗
PubMed2000

Ascorbic acid reduction of active chlorine prior to determining Ames mutagenicity of chlorinated natural organic matter (NOM).

Many potable water disinfection byproducts (DBPs) that result from the reaction of natural organic matter (NOM) with oxidizing chlorine are known or suspected to be carcinogenic and mutagenic. The Ames assay is routinely used to assess an overall level of mutagenicity for all compounds in samples from potable water supplies or laboratory studies of DBP formation. Reduction of oxidizing disinfectants is required since these compounds can kill the bacteria or react with the agar, producing chlorinated byproducts. When mutagens are collected by passing potable water through adsorbing resins, active chlorine compounds react with the resin, producing undesirable mutagenic artifacts. The bioanalytical and chemoanalytical needs of drinking water DBP studies required a suitable reductant. Many of the candidate compounds failed to meet those needs, including 2,4-hexadienoic (sorbic) acid, 2,4-pentanedione (acetylacetone), 2-butenoic (crotonic) acid, 2-butenedioic (maleic and fumaric) acids and buten-2-ol (crotyl alcohol). Candidates were rejected if they (1) reacted too slowly with active chlorine, (2) formed mutagenic byproducts, or (3) interfered in the quantitation of known chlorination DBPs. L-Ascorbic acid reacts rapidly and stoichiometrically with active chlorine and has limited interactions with halogenated DBPs. In this work, we found no interference from L-ascorbic acid or its oxidation product (dehydroascorbic acid) in mutagenicity assays of chlorinated NOM using Salmonella typhimurium TA100, with or without metabolic activation (S9). This was demonstrated for both aqueous solutions of chlorinated NOM and concentrates derived from the involatile, ether-extractable chlorinated byproducts of those solutions.

Ascorbic Acid↗
PubMed2001

Fluorimetric determination of total ascorbic acid by a stopped-flow mixing technique.

A simple, rapid and automatic fluorimetric method for the determination of total ascorbic acid is described. The method makes use of the stopped-flow mixing technique in order to achieve the rapid oxidation of ascorbic acid by dissolved oxygen to dehydroascorbic acid, which then reacts with o-phenylenediamine to form a fluorescent quinoxaline. The initial rate and fluorescence signal of this system are directly proportional to the ascorbic acid concentration. The calibration graph was linear over the range 0.1-30 microg ml(-1) (kinetic method) and 0.25-34 microg ml(-1) (equilibrium method). The precision (% RSD) was close to 0.5%. The method has been used for the determination of ascorbic acid in pharmaceutical formulations, fruit juices, soft drinks and blood serum.

Ascorbic Acid↗
PubMed1991

Characteristics of ascorbic acid uptake by isolated ox neurohypophyseal nerve terminals and the influence of glucocorticoid and tri-iodothyronine on uptake.

Isolated nerve endings (neurosecretosomes) from ox neurohypophyses took up L-[14C]ascorbic acid by a process or processes which showed energy dependence and which could be inhibited by unlabelled ascorbic acid in micromolar concentrations and by isoascorbic acid in millimolar concentrations, whereas dehydroascorbic acid only inhibited in concentrations of about 100 mM. The uptake showed saturation with increasing concentration of ascorbic acid and a Km value of 97 microM. Uptake was inhibited by increasing glucose concentration in the medium or by adding cytochalasin B, phloridzin, ethanol or probenecid to the medium. The uptake was inhibited by lowering the sodium concentration and by lack of calcium. These facts suggest the presence of both a glucose-dependent uptake and a sodium-dependent uptake. Cortisol and tri-iodothyronine inhibited uptake. This effect of cortisol, but not of tri-iodothyronine, was dependent on the presence of sodium in the medium. For both hormones it was still present when phloridzin or probenecid was added to the medium.

Animals↗
PubMedDate not supplied

[Vitamin K1 and C metabolism in uremia during hemodialysis].

Plasma concentrations of vitamin K1, ascorbic acid and its derivatives were investigated in uremic patients during a session of systemic hemodialysis at the dialyzers input, output and in dialyzing solution. The data showed practically unchanged clearances of vitamin C and diketogulonic acid during the session of hemodialysis. In the course of its passage through the dialyzer, plasma ascorbic acid was partially oxidized to dehydroascorbic acid, partially it converted to a dialysate, partially it returned to the human body. Plasma level of vitamin K1 in uremic patients was 1.8 times lower than that in the healthy; 24-hour its excretion in uremic patients and in the healthy was similar. It is supposed that the vitamin K1 decrease correlates with lipoid changes in uremia. During a session of hemodialysis no significant vitamin K1 losses were revealed.

Ascorbic Acid↗
PubMed1989

[Effect of temperature on the aerobic degradation of vitamin C in citric fruit juices].

By means of the method of the 2,4-dinitrophenylhydrazine the total ascorbic acid content in lima, lemon, tangerine and grapefruit juices, fresh and kept at four temperatures and different times, was determined. It was confirmed that in all the cases, the aerobic degradation of ascorbic acid follows a kinetic first order and that the values of the reaction rate are different between species and even between varieties of lemon and tangerine. The values of the equation terms are reported, and examples of application given. Within a range from 20 degrees to 92 degrees C, the effect of temperature on the velocity of the ascorbic acid degradation is described satisfactorily following the Arrhenius equation, in accordance with which, the corresponding values of activation energy are calculated to compare them with other published values. With the simple application of the method, in two steps, and considering that the L-ascorbic acid and the L-dehydroascorbic acid are predominant, the results can be used to calculate the vitamin C losses in citric fruit juices, indicated when they are processed by traditional thermal treatments.

Ascorbic Acid↗
PubMed1999

Efflux of hepatic ascorbate: a potential contributor to the maintenance of plasma vitamin C.

Ascorbate (AH, the reduced form of vitamin C) is an important radical scavenger and antioxidant in human plasma; the resulting ascorbyl radical can disproportionate to AH and dehydroascorbic acid (DHA). Here we address potential maintenance mechanism(s) for extracellular AH by examining the ability of cells to convert extracellularly presented DHA to AH. DHA was rapidly transported into human liver (HepG2), endothelial and whole blood cells in vitro by plasma membrane glucose transporters and reduced intracellularly. Liver cells displayed the highest capacity to release the intracellularly accumulated AH. The proteins responsible for DHA uptake and AH release could be distinguished by inhibitor studies. Thus, unlike DHA uptake, AH efflux was largely insensitive to cytochalasin B and thiol-reactive agents but was inhibited by phloretin, 4,4'-di-isothiocyanostilbene-2,2'-disulphonate and isoascorbate. Efflux of AH from cells was temperature-sensitive and saturable with a low affinity (millimolar, intracellular) for AH. In addition to isolated liver cells, perfusion of intact rat and guinea-pig liver with DHA resulted in AH in the circulating perfusate. Our results show that hepatocytes take up and reduce DHA and subsequently release part of the AH formed, probably via a membrane transporter. By converting extracellular DHA to extracellular AH, the liver might contribute to the maintenance of plasma AH, a process that could be important under conditions of oxidative stress.

Animals↗
PubMed1991

The glycation-associated crosslinking of lens proteins by ascorbic acid is not mediated by oxygen free radicals.

The reaction by which ascorbic acid (ASA) causes the glycation and crosslinking of lens proteins displays a rigid requirement for the presence of oxygen, and is inhibited by the presence of glutathione. Oxygen is required to oxidize ASA to dehydroascorbic acid (DHA) and other products which are the active glycating species. No evidence could be found to support a role for oxidative protein crosslinking by a free radical mechanism. Crosslinking was not inhibited by blocking protein sulfhydryl groups with iodoacetamide, nor were the protein crosslinks dissociated by boiling with 2% mercaptoethanol prior to SDS-PAGE. The addition of a variety of oxygen free radical quenchers had no effect on the extent of protein crosslinking. In fact, the removal of oxygen from the reaction mixture had no effect on either protein glycation, protein crosslinking or the modification of lysine residues, provided DHA was used as the glycating agent. All of these activities were inhibited, however, if ASA was the glycating agent. This confirms that oxygen is required only to convert ASA to DHA.

Animals↗
PubMed1979

Maternal-fetal transfer of ascorbic acid in the guinea pig.

Placental transfer of ascorbic acid was studied in the guinea pig using an in situ placental perfusion technique. A total of 14 animals were studied during their last week of gestation. The fetus was shown to have higher plasma total ascorbic acid (TAA) levels than the mother prior to maternal ascorbic acid infusion. However, following maternal venous infusion this normal gradient for TAA (fetal greater than maternal) disappeared and a new gradient was established (maternal greater than fetal). As maternal plasma TAA levels rose, the level of TAA in the placental perfusate steadily increased to a maximal concentration of approximately 0.85 mg/dl. This occurred when maternal plasma TAA levels were above 3.0 mg/dl. These results demonstrate that a saturable or carrier-mediated transport mechanism is involved in the placental transfer of ascorbic acid in this species. The apparent Vmax (the maximal transport rate by the saturable system per gram placenta) and the Kt (or one-half saturation concentration) were estimated to be 8.3 nmoles/minute and 0.12 mM, respectively. Additional results are presented to suggest that dehydroascorbic acid (DHA) may be the predominant form of the vitamin crossing the guinea pig placenta.

Animals↗
PubMed1983

Renin release and lipid peroxidation by ascorbic acid in the renin granule fraction of rat kidney cortex.

This study was carried out to investigate the effect of lipid peroxidation in the renin granule fraction on renin release from the granules. Ascorbic acid was used to cause lipid peroxidation in the renin granule fraction prepared from rat kidney cortex homogenate. Renin activity was measured by radioimmunoassay and lipid peroxidation was estimated by means of the thiobarbituric acid test. Ascorbic acid, at the concentrations from 5 to 100 microM, produced a dose-dependent increase in lipid peroxidation during incubation of the renin granule fraction at 37 degrees C for 30 min, accompanied by increased release of renin from the granules. On the other hand, dehydroascorbic acid showed no effects on lipid peroxidation and renin release. The simultaneous increases in lipid peroxidation and renin release induced by ascorbic acid in the renin granule fraction were markedly suppressed by the addition of disodium ethylenediaminetetra-acetic acid and antioxidants such as N,N'-diphenyl-p-phenylenediamine and hydroquinone. These findings indicate that lipid peroxidation in the renin granule fraction results in the stimulation of renin release from the granules.

Animals↗
PubMed2001

Selenium spares ascorbate and alpha-tocopherol in cultured liver cell lines under oxidant stress.

The selenoenzyme thioredoxin reductase (TR) can recycle ascorbic acid, which in turn can recycle alpha-tocopherol. Therefore, we evaluated the role of selenium in ascorbic acid recycling and in protection against oxidant-induced loss of alpha-tocopherol in cultured liver cells. Treatment of HepG2 or H4IIE cultured liver cells for 48 h with sodium selenite (0-116 nmol/l) tripled the activity of the selenoenzyme TR, measured as aurothioglucose-sensitive dehydroascorbic acid (DHA) reduction. However, selenium did not increase the ability of H4IIE cells to take up and reduce 2 mM DHA, despite a 25% increase in ascorbate-dependent ferricyanide reduction (which reflects cellular ascorbate recycling). Nonetheless, selenium supplements both spared ascorbate in overnight cultures of H4IIE cells, and prevented loss of cellular alpha-tocopherol in response to an oxidant stress induced by either ferricyanide or diazobenzene sulfonate. Whereas TR contributes little to ascorbate recycling in H4IIE cells, selenium spares ascorbate in culture and alpha-tocopherol in response to an oxidant stress.

Animals↗
PubMed1998

Enzyme-dependent ascorbate recycling in human erythrocytes: role of thioredoxin reductase.

Human erythrocytes efficiently reduce dehydroascorbic acid (DHA) to ascorbate, which helps to maintain the ascorbate content of blood. Whereas erythrocyte DHA reduction is thought to occur primarily through a direct chemical reaction with GSH, this work addresses the role of enzyme-mediated DHA reduction by these cells. The ability of intact erythrocytes to recycle DHA to ascorbate, estimated as DHA-dependent ferricyanide reduction, was decreased in parallel with GSH depletion by glutathione-S-transferase substrates. In contrast, the sulfhydryl reagent phenylarsine oxide inhibited DHA reduction to a much greater extent than it decreased GSH in intact cells. DHA reduction in excess of that due to a direct chemical reaction with GSH was also observed in freshly prepared hemolysates. Hemolysates likewise showed NADPH-dependent reduction of DHA that appeared due to thioredoxin reductase, because this activity was inhibited 68% by 10 microM aurothioglucose, doubled by 5 microM E. coli thioredoxin, and had an apparent Km for DHA (1.5 mM) similar to that of purified thioredoxin reductase. Additionally, aurothioglucose-sensitive, NADPH-dependent DHA reductase activity was decreased 80% in hemolysates prepared from phenylarsine oxide-treated cells. GSH-dependent DHA reduction in hemolysates was more than 10-fold that of NADPH-dependent reduction. Nonetheless, the ability of phenylarsine oxide to decrease DHA reduction in intact cells with little effect on GSH suggests that enzymes, such as thioredoxin reductase, may contribute more to this activity than previously considered.

Arsenicals↗