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PubMed1996

Inhibition by L-ascorbic acid and other antioxidants of the 2.2'-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) oxidation catalyzed by peroxidase: a new approach for determining total antioxidant status of foods.

The accumulation of 2.2'-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS) radical catalyzed by peroxidase can be inhibited by the presence of L-ascorbic acid in the reaction medium, this inhibition delaying the accumulation of the ABTS radical and giving rise to a lag time. A kinetic approach to explain this lag time is presented, which also makes it possible to determine the amount of L-ascorbic acid in the reaction medium. The stoichiometry of the system was determined as 1 mol of L-ascorbic reducing 2 mol of ABTS radicals. L-Ascorbic acid is not the only compound to have this ability, since other antioxidant compounds also react with the ABTS radical. We studied the ABTS/H2O2/horseradish peroxidase system in the presence of L-ascorbic acid and other antioxidant compounds. The influence of such factors as pH, enzyme concentration, and L-ascorbic acid concentration was studied. A good correlation between the lag time and the L-ascorbic acid present in the medium was observed, and under optimal conditions, the method could determine as little as 0.65 nmol of L-ascorbic acid. Based on our findings, we propose a method to measure the total antioxidant activity of different compounds related to L-ascorbic acid and apply this method to determining the total antioxidant activity present in fruit juices.

Antioxidants↗
PubMed2001

Dihydropyridine calcium channel blockers inhibit ascorbic acid accumulation in human intestinal Caco-2 cells.

We investigated the effect of commonly used medications on the accumulation of ascorbic acid in human intestinal Caco-2 cells. Although ascorbic acid is negatively charged at physiological pH, anionic compounds including drugs and metabolites had little effect on its accumulation. On the other hand, hydrophobic 1,4-dihydropyridine compounds (nifedipine and nicardipine), but not other structurally unrelated calcium channel blockers, were found to be potent inhibitors. They inhibited both Na+-dependent and Na+-independent (K+ substituting Na+) accumulation of ascorbic acid. The inhibition was non-competitive with a Ki of 108 microM and 9 microM for nifedipine and nicardipine, respectively. The efflux of ascorbic acid from cells was not affected. Previously, we reported a similar inhibition of ascorbic acid accumulation by estrogens. When nifedipine and estrogens were included in the buffer together, the combined inhibitory effect was less than additive implying that they may act through the same mechanism. The potential clinical significance of dihydropyridine usage on ascorbic acid status in human needs to be considered.

Ascorbic Acid↗
PubMed2005

Formation of furan from carbohydrates and ascorbic acid following exposure to ionizing radiation and thermal processing.

This study was conducted to investigate the formation of furan from sugars, ascorbic acid, and organic acids as affected by ionizing radiation and thermal treatments. Results showed that both thermal treatments and irradiation induced formation of furan from ascorbic acid, fructose, sucrose, or glucose. Little furan was produced from malic acid or citric acid. The pH and concentration of sugars and ascorbic acid solutions had profound influences on furan formation due to either irradiation or thermal treatment. The rate of irradiation-induced furan formation increased with decreasing pH from 8 to 3. Approximately 1600 times less furan was formed at pH 8 as apposed to pH 3. At the same pHs, the amounts of furan formed from irradiation of ascorbic acid, fructose, and sucrose were always higher than from glucose. As pH decreased from 7 to 3, an increase in thermally induced furan was observed for sucrose and ascorbic acid solutions, but for glucose solution, less furan was formed at pH 3 than at pH 7. The levels of sugars commonly found in fruits and fruit juices, upon irradiation, would be high enough to potentially produce low parts per billion (ppb) levels of furan. The concentration of ascorbic acid at which a maximum of furan was produced upon irradiation was about 0.5 mg/mL, a level commonly found in some foods. Five furan derivatives were tentatively identified in thermally treated ascorbic acid solution, while one furan derivative was tentatively found in both irradiated and thermally treated samples.

Ascorbic Acid↗
PubMed2004

Antioxidative effects of glycosyl-ascorbic acids synthesized by maltogenic amylase to reduce lipid oxidation and volatiles production in cooked chicken meat.

Glycosylated ascorbic acids were synthesized by using the transglycosylation activity of Bacillus stearothermophilus maltogenic amylase with maltotriose to show effective antioxidative activity with enhanced oxidative stability. The modified ascorbic acids comprised mono- and di-glycosyl transfer products with an alpha-(1,6)-glycosidic linkage. The antioxidative effects of the glycosyl derivatives of ascorbic acid on the lipid oxidation of cooked chicken breast meat patties were compared, and the synergistic effect when combined with alpha-tocopherol was determined in terms of thiobarbituric acid-reactive substances (TBARS) and volatiles production during storage. The results indicate that the glycosylated ascorbic acids had very effective antioxidative activity in preventing lipid oxidation, and were better in their synergistic effect in comparison to authentic ascorbic acid, with maltosyl-ascorbic acid being the most effective. Volatiles production was highly correlated with the TBARS values in the lipid oxidation of cooked meat. The antioxidative effect preventing the production of volatiles was particularly strong on pentanal, fairly strong on propanal and butanal, and not at all on ethanal. Propanal, pentanal, and the total volatiles thus provided a good representation of the lipid oxidation status of cooked chicken meat.

Aldehydes↗
PubMed1990

Ascorbic acid: effect on ongoing iron absorption and status in iron-depleted young women.

The effect of ascorbic acid on iron retention from a diet with predicted low iron bioavailability (containing minimal meat and ascorbic acid) was investigated in iron-depleted premenopausal women. Eleven women were depleted of storage iron (indicated by serum ferritin) through a combination of diet (5.0 mg Fe/2000 kcal for 67-88 d) and phlebotomy. They then consumed a diet containing 13.7 mg Fe/2000 kcal, supplemented with placebo or ascorbic acid three times daily (1500 mg total) with meals for 5.5 wk. Ascorbic acid improved apparent iron absorption (balance method) [38 +/- 2% (means +/- SEM) vs 27 +/- 2%]. Ascorbic acid also improved hemoglobin, erythrocyte protoporphyrins, and serum iron but not hematocrit, serum ferritin, iron-binding capacity, or transferrin saturation. In iron-depleted women consuming a diet with predicted poor iron availability, ascorbic acid supplementation enhanced body iron retention for 5.5 wk.

Adult↗
PubMed1994

Ascorbic acid, but not glutathione, is taken up by brain slices and preserves cell morphology.

1. We have determined the ascorbic acid (ascorbate) and glutathione (GSH) content of cortical and hippocampal slices from rat brain after prolonged (6h) incubation and have correlated these levels with the histological quality of the slices. Ascorbate and GSH levels in control and sliced tissue were determined by high performance liquid chromatography (HPLC) with electrochemical detection. Cell morphology of incubated slices was compared with that of intact tissue in cresyl violet stained tissue sections. 2. Roughly 70% of tissue ascorbate and GSH was lost from slices during incubation in vitro. Normal in vivo levels of ascorbate (2-3 mumol g-1 tissue wet weight) could be maintained by including 200-400 microM ascorbate (typical extracellular concentration) in the incubation media. By contrast, the loss of GSH could not be prevented by incubation with GSH. 3. The morphology of cells in hippocampal slices incubated under conditions that maintained ascorbate content and compartmentalization were similar to those of intact tissue. Ascorbate protected pyramidal cells in CA1 and CA3 regions of the hippocampus from the degeneration that was seen in slices incubated in ascorbate-free media. 4. These data suggest that loss of endogenous antioxidants may be a major factor in neuronal loss in vitro and support the notion that ascorbate is an endogenous neuroprotective agent.

Animals↗
PubMed1999

The effect of ascorbic acid supplementation on the blood lead levels of smokers.

BACKGROUND: The study subjects were 75 adult men (20 to 30 years of age), who smoked one pack of cigarettes per day (minimum) and had no clinical signs of ascorbic acid deficiency or lead toxicity. None had a history of industrial exposure to lead, and the blood-lead levels were anticipated to be below 1.45 micromol/L, the minimum blood level associated with toxicity symptoms. METHODS: The men were randomly assigned to three study groups of 25, and each group was provided a four-week supply of one level of daily ascorbic acid supplements (placebo, 200 mg or 1000 mg of ascorbic acid). We measured baseline and weekly serum and urine ascorbic-acid levels as well as blood and urine lead levels. The weekly group means and variations of the measured data were statistically compared by means of ANOVA and Pearson's correlation. RESULTS: The serum ascorbic-acid levels of the groups receiving ascorbic acid increased significantly after one week (p< or =.001). There was no effect of placebo or 200 mg ascorbic-acid supplementation on the blood or urine lead levels. However, there was a 81% decrease in blood-lead levels in the 1000 mg ascorbic acid group after one week of supplementation (p< or =.001). CONCLUSIONS: Daily supplementation with 1000 mg of ascorbic acid results in a significant decrease of blood-lead levels associated with the general population. Ascorbic acid supplementation may provide an economical and convenient method of reducing blood-lead levels, possibly by reducing the intestinal absorption of lead.

Adult↗
PubMed1977

Effects of ascorbic acid on glucose-6-phosphate dehydrogenase-deficient erythrocytes: studies in an animal model.

There is little information available concerning the possible effects of ascorbic acid on glucose-6-phosphate dehydrogenase (G-6-PD) -deficient erythrocytes. We therefore studied the survival of G-6-PD-deficient cells, incubated with ascorbic acid, in rats with partial reticuloendothelial and complement blockade. Animals were pretreated with ethyl palmitate and cobra venom factor. They were then transfused with 51Cr-labeled erythrocytes which had been incubated in the presence or absence of ascorbic acid. G-6-PD-deficient cells, incubated with ascorbic acid, had impaired survival when compared to that of controls. G-6-PD-deficient cells, in the absence of ascorbic acid, had survival times equal to those of normal control erythrocytes. At the concentrations used, ascorbic acid did not appear to alter the survival of normal cells. Ascorbic acid causes premature loss of G-6-PD-deficient human erythrocytes in this rat model. On the basis of previous clinical and experimental observations, as well as this study, caution should be used when administering ascorbic acid in large doses to individuals who might be G-6-PD deficient.

Animals↗
PubMed1998

5-HT1A receptors mediate inhibition of ethanol-induced ascorbic acid release in rat striatum studied by microdialysis.

Our previous study showed that the serotonergic system was involved in the ethanol-induced striatal ascorbic acid release in rat. In the present study, the 5-HT1A agonists and antagonists were used to analyze the possible mechanism of ethanol-induced ascorbic acid release in rat striatum. The results showed that ethanol (3.0 g/kg, i.p.) significantly increased striatal ascorbic acid release. Buspirone (5.0 mg/kg, s.c.), a partial agonist of 5-HT1A receptors, and 8-OH-DPAT (0.5 mg/kg, s.c.), a selective agonist of 5-HT1A receptors, showed no effect on basal ascorbic acid release in striatum, but both drugs significantly antagonized the ascorbic acid release induced by ethanol in striatum. WAY 100635 (0.5 mg/kg, s.c.), a selective antagonist of 5-HT1A receptors, affecting neither the basal nor the ethanol-induced ascorbic acid release per se, antagonized the suppressing effect of 8-OH-DPAT on ethanol-induced ascorbic acid release in striatum. This study gives the first evidence that activation of 5-HT1A receptors is involved in ethanol-induced ascorbic acid release in rat striatum.

Animals↗
PubMed1975

Effects of ascorbic acid on health parameters in guinea pigs.

The maximal response of a selection of ascorbic-acid-dependent parameters to a range of intakes of ascorbic acid has been shown to occur at virtually one level of intake in the present experiments. Further, this response occurred with intakes that produced only 1/2 saturation or less of tissues with ascorbic acid. Excessive intakes did not enhance effects, and, as in the case of serum copper levels, may have a detrimental effect. In view of the known factors that may influence requirements and the intralaboratory variability in experimental conditions, the more reasonable approach to the interpretation of dose response data is likely to relate the response to the accompanying degree of tissue saturation, rather than to an absolute level of ascorbic acid intake.

Animals↗
PubMed1996

Ascorbic acid and total vitamin C concentrations in plasma, gastric juice, and gastrointestinal mucosa: effects of gastritis and oral supplementation.

Epidemiological evidence suggests that high dietary ascorbic acid reduces gastric cancer risk. It may do this by either reducing N-nitroso compound formation in gastric juice, or by scavenging reactive oxygen species in gastric mucosa. The aim of this study was to discover if potential ascorbic acid protection might be increased by supplementation. Thirty two patients were supplemented with ascorbic acid, 500 mg twice daily for two weeks. Gastric juice, plasma, and upper gastrointestinal biopsy ascorbate concentrations were measured and compared with values in 48 unsupplemented patients. It was found that ascorbic acid and total vitamin C concentrations were considerably higher in biopsy specimens from oesophagus, body, antrum, duodenum, and rectum, compared with values in plasma or gastric juice. Plasma and mucosal concentrations were unaffected by the presence of chronic gastritis but gastric juice concentrations were substantially lower in patients with chronic gastritis than in patients with normal histological assessment (p < 0.01). Patients receiving ascorbic acid supplements had higher ascorbic acid concentrations in plasma (p < 0.001), gastric juice (p < 0.001), and at all biopsy sites in the upper gastrointestinal tract (p < 0.05). Gastric juice ascorbic acid and total vitamin C concentrations in gastritic patients, however, were still less after supplementation than in normal subjects (p < 0.01). These data suggest that high ascorbic acid intake could reduce gastric cancer risk, but its protective effect might be greater if gastritis is treated (for example, by Helicobacter pylori eradication).

Adult↗
PubMed1989

A comparative study of ascorbic acid entry into aqueous and vitreous humors of the rat and guinea pig.

The transport rates of radiolabeled ascorbic acid and dehydroascorbic acid, as well as, labeled 3-O-methyl-D-glucose and L-glucose from a central plasma compartment into aqueous and vitreous humors and cerebrospinal fluid were studied in vivo. Normal, male albino Sprague-Dawley rats and English Short Haired guinea pigs were used to explore the mechanism of ascorbic acid entry into ocular humors in a species that can produce ascorbate (the rat) and one that cannot and, like humans, is dependent on dietary sources (the guinea pig). In vivo kinetic studies allowed for the calculation of entry rate constants, Ki (min-1), in double-labeled experiments using L-glucose as an internal passive control. Parallel TLC chromatographic studies were performed to monitor intraocular labeled molecules deriving from the plasma-introduced test molecule. In addition, resting levels of ascorbic acid and D-glucose were determined in order to obtain more reliable data than previously available. Resting levels of D-glucose revealed a consistent pattern of lower levels in aqueous and vitreous humors and CSF than found in plasma for both rat and guinea pig. However, ascorbate levels differed significantly, with the guinea pig demonstrating high ascorbate levels in the aforementioned humors: 58, 77 and 22, respectively, times the circulating plasma value of 0.2 +/- 0.2 mg/dl. In contrast, the rat, like the guinea pig, had low plasma ascorbate levels (3.3 +/- 0.8 mg/dl) compared to glucose (162 +/- 8 mg/dl), with even lower aqueous and vitreous values in a pattern similar to that of D-glucose. In vivo aqueous, vitreous and CSF transport results from the guinea pig indicate active transport mechanisms for ascorbic acid that prefer the ascorbate over the dehydroascorbate moiety and are probably different from the carrier-facilitated diffusion mechanisms for D-glucose, which do not move molecules against a concentration gradient. TLC studies, performed under nitrogen, revealed that only (14C)-ascorbic acid was present in aqueous or vitreous humors regardless of whether the radiolabeled pulse was of ascorbic or dehydroascorbic acid. The rat demonstrated little or no carrier involvement, with ascorbic acid crossing into ocular humors at rates very close to those of L-glucose, which is similar in size and is considered to cross the barriers studied via passive diffusion. Saturation studies with unlabeled glucose and glucose inhibitor drugs phloretin (10(-3) M) and phloridzin (10(-1)) had no apparent effect on ocular entry rates. Dehydroascorbic acid movement was also found to be passive.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Ascorbic acid levels in aqueous and vitreous humors of the rabbit: effects of inflammation and ceruloplasmin.

A HPLC method for determination of ascorbic acid and dehydroascorbic acid in plasma and aqueous and vitreous humors of rabbits is described. Values for total ascorbic acid concentration found in this study are in agreement with those of previous investigators. Endotoxin-induced ocular inflammation caused a decrease in the concentration of ascorbic acid in the aqueous humor and an increase in the vitreous humor. The additional lack of correlation between levels of ascorbic acid in normal aqueous and vitreous humors from the same uninflamed eye indicates that the aqueous humor is not the source of vitreal ascorbic acid. The copper concentration of the aqueous humor is increased during ocular inflammation, most likely due to the influx of ceruloplasmin from plasma when the blood-aqueous barrier is disrupted. Ceruloplasmin caused a decrease in the amount of ascorbic acid in the aqueous humor in vitro and the vitreous humor in vivo. The presence of ceruloplasmin in the aqueous humor during inflammation thus may contribute to the decreased concentration of ascorbic acid in this fluid.

Animals↗
PubMed2002

Ascorbic acid in diet supplements: loss in the manufacturing process and storage.

The ascorbic acid content was determined in 25 different diet supplements commercially available to the consumer in two pharmaceutical forms (pills and ampoules). These products are widely consumed by several population groups (elderly people, sportsmen, adolescents, children, etc.). High-performance liquid chromatography was used as the analytical technique. The proposed method has been validated with good linearity, reproducibility, recovery and accuracy, and can be used in routine analyses and in quality control. The ascorbic acid content in pills ranged from 15.62 to 50.16 mg/g, and in that ampoules from 2.12 to 8.83 mg/ml. Depending on the dosage rates, these levels would represent approximately 20-50% of the daily dietary intake recommended by the National Research Council. Possible losses in the manufacturing process and stability during storage for 30 days at 40 +/- 2 degrees C without light, were tested. In relation to the ascorbic acid concentrations stated on the labels, a loss of 12.0-21.9% in pills and of 11.7-18.0% in ampoules was detected. In relation to the stability conditions, the losses are of 1.8-24.8% in pills and of 10.4-19.3% in ampoules. The pasteurisation and sterilisation processes produced a mean loss of ascorbic acid in ampoules of 2.1 and 1.4%, respectively. A statistically significant direct correlation was observed between ascorbic acid loss and content in proteins, humidity, ash, and fructose. The influence of the pharmaceutical form was also tested. Data revealed that the control of losses during the manufacturing and commercialisation process of these products is necessary to ensure the intake of vitamin C from these products by the consumer.

Ascorbic Acid↗
PubMed1993

Carbon tetrachloride-induced alterations in hepatic glutathione and ascorbic acid contents in mice fed a diet containing ascorbate esters.

The effects of L-ascorbyl stearate and L-ascorbyl palmitate on carbon tetrachloride-induced alterations in glutathione and ascorbic acid content in mouse livers were investigated. Powdered food containing 1% ascorbate ester was given to mice for 3 days before and 1 day after a single injection of CCl4 (0.1 ml/kg, i.p.). Biochemical parameters were determined 1 day after the CCl4 administration. The ascorbate esters markedly attenuated CCl4-induced alterations such as reductions in ascorbate content and hepatic glutathione S-transferase (GST) activity, and increases in glutathione and calcium content and serum GST activity. The CCl4-induced rise in thiobarbituric acid-reactive substances, an index of lipid peroxidation, was not affected by ascorbate feeding. These findings suggest that exogenous ascorbate, in addition to endogenous glutathione, is available to maintain the intracellular milieu in a reduced state, and that this system operates more effectively in aqueous compartments than in membrane lipid bilayers.

Animals↗
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↗
PubMed2002

Ascorbic acid assays of individual neurons and neuronal tissues using capillary electrophoresis with laser-induced fluorescence detection.

Ascorbic acid is an important cellular metabolite involved in many biochemical pathways. A method to quantitate ascorbic acid and dehydroascorbic acid in individual neurons and neuronal tissues is described with detection limits of 320 pM (430 zmol). The method uses microvial sampling, derivatization with 4,5-dimethyl-1,2-phenylenediamine, capillary electrophoresis separation, and laser-induced fluorescence detection and quantifies the ascorbic acid and dehydroascorbic acid levels with less than a 15-min total analysis time including sample preparation and derivatization. Ascorbic acid and dehydroascorbic acid levels are measured using functionally characterized and identified neurons of Aplysia californica, Pleurobranchaea californica, and Lymnaea stagnalis -three well-recognized models in cellular and system neuroscience. Multiple assays of a particular identified neuron (e.g., metacerebral cells from Aplysia) show a high level of reproducibility, while endogenous intracellular concentrations of ascorbate are neuron-specific. Ascorbic acid concentrations in the neurons studied range from 0.19 to 6.2 mM for Aplysia and 0.12 to 0.22 mM for Lymnaea. In contrast, concentrations of ascorbic acid observed in heterogeneous tissues such as ganglia (with connective tissues, glia, blood vessels, neuropile, and areas with intercellular spaces), 4-190 microM, are significantly lower than the single-cell values.

Animals↗