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PubMedDate not supplied

The stabilization of L-ascorbic acid in aqueous solution and water-in-oil-in-water double emulsion by controlling pH and electrolyte concentration.

This study presents a new approach that can stabilize effectively L-ascorbic acid in water-in-oil-in-water (w/o/w) double emulsions. Basically, the behavior of L-ascorbic acid in the aqueous phase was observed, considering its molecular deformation. Then, it was found that the stability determined in the aqueous phase by high-performance liquid chromatography (HPLC) showed that the collapse of ionization of L-ascorbic acid played a crucial role in protecting the molecular deformation. Then, the stable aqueous system was incorporated into the internal aqueous phase of the double emulsions. From the HPLC analysis, it was observed that the L-ascorbic acid in an appropriate system showed high molecular stability for a long time. Moreover, in the measurement of in vitro skin permeation, the L-ascorbic acid stabilized in this study showed considerable skin permeation ability, indicating its potential applicability in pharmaceutics and cosmetics.

Animals↗
PubMed2002

Rapid ion chromatography of L-ascorbic acid, nitrite, sulfite, oxalate, iodide and thiosulfate by isocratic elution utilizing a postcolumn reaction with cerium(IV) and fluorescence detection.

Rapid separation and determination of mixtures of L-ascorbic acid, nitrite, sulfite, oxalate, iodide and thiosulfate by conventional ion chromatography is often difficult due to incomplete separation of L-ascorbic acid and nitrite from the water peak when using eluents giving short elution times for iodide and thiosulfate. Separation of the six species within about 15 min has been achieved by isocratic elution using a resin-based ion-exchange column with a carbonate eluent containing a trace amount of 1,3,5-benzenetricarboxylic acid (BTA) and fluorescence measurement of cerium(III) formed via postcolumn reactions of the separated sample species with cerium(IV). Calibration plots of peak height versus concentration were linear up to 10.0 microM (1.76 ppm) for L-ascorbic acid, 8.0 microM (0.37 ppm) for nitrite, 8.0 microM (0.70 ppm) for oxalate, 80.0 microM (10.2 ppm) for iodide and 25.0 microM (2.80 ppm) for thiosulfate, whilst the sulfite calibration was linear up to 25.0 microM (2.00 ppm) when peak area was plotted against concentration. Detection limits (defined as S/N = 3) were 18 ppb for L-ascorbic acid, 4 ppb for nitrite, 16 ppb for sulfite, 7 ppb for oxalate, 72 ppb for iodide and 37 ppb for thiosulfate. The proposed method was applied successfully to the determination of L-ascorbic acid, nitrite, sulfite, oxalate, iodide or thiosulfate in water samples.

Anions↗
PubMed1990

Ascorbic acid: a useful reductant to avoid oxidation of catecholamines in electrophysiological experiments in vitro?

The actions of the reductant ascorbic acid on rat neocortical neurons in vitro was investigated by means of intracellular recordings. At a concentration (500 microM), which reduced the magnitude of dopamine degradation in oxygen-saturated saline solutions by about 50%, ascorbic acid reversibly depressed synaptic potentials and enhanced direct excitability of cortical neurons. The latter effect was not reversible within the observation period. Ascorbic acid did not alter membrane potential and input resistance of the neurons. On the basis of our results we conclude that ascorbic acid is not a useful reductant to avoid oxidation of catecholamines in oxygen-saturated solutions used in electrophysiological experiments in vitro.

Animals↗
PubMed1981

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

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

2,2'-Dipyridyl↗
PubMed1998

Effects of Ascorbic Acid on the Light-Induced Riboflavin Degradation and Color Changes in Milks.

Effects of ascorbic acid (0.025, 0.05, and 0.1%, w/v) on the light-induced riboflavin degradation and color changes in whole and skim milks were studied during 10 h fluorescent light illumination at 7 +/- 2 degrees C. As the time of light illumination increased, the riboflavin content in milks greatly decreased, resulting in 30.1 and 59.1% reduction of riboflavin in whole milk and skim milk after 10 h exposure to fluorescent light, respectively. The ascorbic acid treatment effectively protected the photodegradation of riboflavin in both whole milk and skim milk, and its effectiveness is concentration dependent. The 0.1% ascorbic acid treatments resulted in 50.0 and 25.5% inhibition of riboflavin reduction in whole milk and skim milk after 10 h fluorescent light illumination, respectively. The color parameters of lightness (L), greenness (-a), and yellowness (b) in both whole milk and skim milk decreased after light illumination. Ascorbic acid treatment also protected effectively the changes in greenness and yellowness in both milks during the light illumination.

Journal Article↗
PubMed1980

Ascorbic acid transport by isolated bovine adrenal cortical cells.

Viable, ACTH-sensitive, bovine adrenal cortical cells have the ability to accumulate [1-14C]ascorbic acid. Transport of the vitamin displays saturation kinetics (Km = 16.6 microM), requires Ca2+, and is inhibited maximally by ACTH at the same concentrations of the hormone necessary for maximal stimulation of steroidogenesis. Despite the transport of quantities of radioactive ascorbate amounting to approximately 25% of the total intracellular pool, no change in the ascorbate concentration in the cells can be detected by chemical methods. Transport of the vitamin is apparently a membrane carrier-mediated exchange process, since although intracellular ascorbate concentrations are 60- to 90-fold higher than those in the incubation medium, accumulated label can only be displaced when the cells are incubated in the presence of unlabeled ascorbic acid or metabolic inhibitors. Furthermore, ACTH fails to deplete ascorbic acid from [1-14C]ascorbate-loaded cells. It is hypothesized that the vitamin exists in two pools only one of which can be depleted by ACTH. This ACTH-depletable pool is no longer present in the isolated cell. In fact, as much as 66% of the ascorbic acid is lost from rat adrenals incubated for 15 min post adrenalectomy. The remaining pool of adrenal ascorbate is not depleted by ACTH and is also maintained against a concentration gradient.

Adrenal Cortex↗
PubMed1982

The effect of megadose ascorbic acid ingestion on the absorption and retention of vitamin B12 in man.

Radiotracer B12 analogues, hydroxy- and cyano-cobalamin have been used to study the effects of megadose L-ascorbic acid (vitamin C) ingestion on vitamin B12 metabolism in man. By employing whole body counter techniques it has been shown that, while ascorbic acid can partially inactivate both the important dietary analogue, hydroxycobalamin, and the gastric secretion, intrinsic factor which is essential for B12 absorption, the rapid binding of the B12 analogue to intrinsic factor protects the hydroxycobalamin from attack. As a result, the absorption of hydroxcobalamin is unaffected by the simultaneous ingestion of 1 g ascorbic acid. The absorption of cyanocobalamin, the most stable analogue but not found in quantity in the diet, is slightly increased by ascorbic acid. Whole body retention studies on normal subjects ingesting 2 g ascorbic acid per day show no significant evidence of in vivo destruction of body B12 stores.

Anemia, Pernicious↗
PubMed2002

Redifferentiation of human gastric cancer cells induced by ascorbic acid and sodium selenite.

OBJECTIVE: To explore the effects and mechanisms of ascorbic acid (AA) and sodium selenite (SS) on growth inhibition and redifferentiation in human gastric cancer cells. METHODS: In the present study, trypan blue dye exclusion method was used to determine the cell growth curve and mitotic index, cell electrophoresis and colonogenic potential were used as the indexes of redifferentiation. In order to find out the mechanisms of redifferentiation, the activities of superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT) were assayed, the content of malondialdehyde (MDA), reduced glutathione (GSH) and H2O2 were evaluated. RESULTS: After treatment with AA 3 mol/L + SS 2 mu mol/L, the growth rate and mitotic index of human gastric cancer cells (MGc-803) decreased remarkably. The indexes related with cell malignancy were alleviated. For example, cell surface charge was obviously decreased, the electrophoresis rate was dropped from 2.21 to 1.15 mu m.s-1.V-1.cm-1. The indexes related with cell redifferentiation were promoted. For example, the colonogenic potential was decreased to 93.5%. These results indicated that redifferentiation of human gastric cancer cells was successfully induced by AA + SS. The activities of SOD and GPX were significantly higher, while the activity of CAT was slower in treated group than that in the control. The content of MDA was slightly decreased, GSH was sharply decreased, and H2O2 content was dramatically increased. CONCLUSION: These results indicated that combination of ascorbic acid and sodium selenite may induce the redifferentiation of human gastric cancer cells and inhibit cell growth by virtue of enhancing the activities of antioxidative enzymes and inducing the formation of H2O2, and altering the cell redox status. Combination of ascorbic acid and sodium selenite may be a potent anticancer agent for human gastric cancer.

Antioxidants↗
PubMed2004

Combined effect of selenium and ascorbic acid on alcohol induced hyperlipidemia in male guinea pigs.

Alcoholics usually suffer from malnutrition and are especially deficient in micronutrients like vitamin C, selenium and Zn. In the present study, combined effects of selenium and ascorbic acid on alcohol-induced hyperlipidemia were studied in guinea pigs. Four groups of male guinea pigs were maintained for 45 days as follows: control (1 mg ascorbate (AA)/100 g body mass/day), ethanol (900 mg ethanol/100 g body mass + 1 mg AA/100 g body mass/day), selenium+ascorbic acid [(25 mg AA + 0.05 mg Se)/100 g body mass/day], ethanol+selenium+ascorbic acid [(25 mg AA + 0.05 mg Se + 900 mg ethanol)/100 g body mass/day]. Co-administration of selenium and ascorbic acid along with alcohol reduced the concentration of all lipids, as also evidenced from the decreased activities of hydroxymethylglutaryl-CoA reductase and enhanced activities of plasma lecithin cholesterol acyl transferase and lipoprotein lipase. Concentrations of bile acids were increased. We conclude that the supplementation of Se and ascorbic acid reduced alcohol induced hyperlipidemia, by decreased synthesis and increased catabolism.

Animals↗
PubMed2000

[The effect of ascorbic acid on the antibacterial activity of selected antibiotics and synthetic chemotherapeutic agents in in vitro conditions].

The study was aimed to determine the ability of selected antibiotics and synthetic chemotherapeutic agents to interact with ascorbic acid by means of spectrophotometric measurements and the evaluation of the effect of the presence of ascorbic acid on antimicrobial activity of the substances in which the interaction was detected. Out of 13 chemotherapeutical agents tested, ofloxacine, N-succinimidylofloxacine, fleroxacine, tetracycline, 6-thiatetracycline, and doxycycline reacted with ascorbic acid with the development of the superoxide radical (O2.-). Heatley's method revealed that in the presence of ascorbic acid the antibacterial effect of substances was decreased by 9.6 to 40.7% and 10.1 to 45.1% in Staphylococcus aureus and Escherichia coli, respectively. The kinetics of the process of the survival of cells within 24 hours demonstrated that a combination of ofloxacine as well as tetracycline with ascorbic acid produced a statistically significant increase in log10 of CFU/ml in S. aureus as well as E. coli.

Anti-Bacterial Agents↗
PubMed2003

Oral administration of ascorbic acid attenuates endothelial dysfunction after short-term cigarette smoking.

Short-term cigarette smoking is associated with persistent endothelial dysfunction. Data on the reversibility of this effect with per os antioxidants after short-term smoking are lacking. This study examines the effect of orally administered ascorbic acid on cigarette smoking-induced endothelial dysfunction. In the present double-blind, randomized, crossover study, 19 healthy subjects (28.7 +/- 6.8 years, mean +/- SD) were examined by high-resolution ultrasonography of the brachial artery before and 0, 30, 60, 90, and 120 minutes after smoking a cigarette. Flow-mediated dilatation (FMD) was used as a method to examine endothelial function. Measurements were performed on two different days, 2 hours after oral administration of 2 g of ascorbic acid or placebo. FMD was similar for each subject between the two visits at baseline. FMD was significantly decreased after smoking with both placebo and ascorbic acid. However, there was a significant beneficial effect of ascorbic acid on the FMD change over time after smoking. After smoking, the FMD dropped to less than half of the baseline value. Thereafter in the placebo group, FMD increased to 70% of baseline value in 90 minutes, but in the ascorbic acid group the FMD increased to 70% of baseline value in 46 minutes. Oral administration of ascorbic acid attenuates endothelial dysfunction after short-term cigarette smoking by shortening its duration.

Administration, Oral↗
PubMed2001

Real-time detection of L-ascorbic acid and hydrogen peroxide in crude food samples employing a reversed sequential differential measuring technique of the SIRE-technology based biosensor.

Detection of the common electrochemical interferents, ascorbic acid and hydrogen peroxide, using a SIRE (Sensors based on Injection of the Recognition Element) technology based biosensor in reverse mode operation is reported. The differential measuring principle employed in the SIRE biosensor during operation in reverse mode is such that the sample is measured first in the presence of enzyme (yielding matrix signal only), and then measured again in the absence of enzyme (yielding signal from matrix+analyte). Subtraction of the signal obtained in the presence of enzyme from the signal obtained in the absence of enzyme gives a specific signal for the analyte only and correlates directly to its concentration in solution. The linear range for the determination of ascorbic acid and hydrogen peroxide was 0-3 mM and 0-2 mM, respectively, with an enzyme concentration of 25 U ascorbate oxidase/ml and 1000 U catalase/ml. The reproducibility was 5% for ascorbic acid (R.S.D. n=15) and 10% for hydrogen peroxide (R.S.D. n=18). The cost per measurement was 0.28 USD for ascorbic acid analysis and 0.0008 USD for hydrogen peroxide analysis. The degradation of ascorbic acid in cereal was followed in real-time, as was the stabilization of low pH on the degradation process.

Ascorbate Oxidase↗
PubMed2006

Influence of temperature, electrical conductivity, power and pH on ascorbic acid degradation kinetics during ohmic heating using stainless steel electrodes.

Degradation kinetics of ascorbic acid was determined in pH 5.7 buffer solution using an isothermal batch ohmic heater with stainless steel electrodes. Variables included in this study were temperature (40, 60 and 80 degrees C); power (0, 100,150 and 300 W); and electrical conductivity (varied using 0.25%, 0.5% and 1.0% NaCl). Ascorbic acid concentration was detected by using a HPLC technique. The results indicate that ascorbic acid degradation can be described successfully by a first order model during both conventional and ohmic heating. The Arrhenius relation showed negative values for temperature coefficient (E(T)) during most ohmic treatments, due to a combination of factors that may alter the reaction mechanism. In particular, it appears that at a given power level, higher electric field strengths are conducive to increased incidence of faradaic reactions. Increasing NaCl concentration appears to significantly influence reaction rates via its influence on dissolved oxygen, and through its participation in electrolytic reactions. Contrary to expectations, increasing temperature tended to significantly reduce reaction rate, likely due to decreased dissolved oxygen concentration at high temperature. The results indicate the importance of using inert electrodes in ohmic heating processes.

Ascorbic Acid↗
PubMed1989

Myocardial salvage with trolox and ascorbic acid for an acute evolving infarction.

Both Trolox (a water-soluble analogue of alpha-tocopherol) and ascorbic acid were more effective than superoxide dismutase or catalase in protecting myocyte cell cultures from free radical attack (induced by hypoxanthine and xanthine oxidase). In a canine model of two hours of left anterior descending coronary artery occlusion followed by four hours of reperfusion, Trolox and ascorbic acid reduced the area of infarction within the area at risk. The Trolox group received 500 mL of deoxygenated saline solution containing 2.0 g of Trolox, 3.0 g of ascorbic acid, and 18 mg of EDTA (ethylenediaminetetraacetic acid) infused into the ascending aorta 30 seconds before and four minutes after reperfusion. Saline controls received 500 mL of deoxygenated saline solution containing 18 mg of EDTA. The angioplasty group had unmodified reperfusion by simple release of the occlusion. The area at risk and the area infarcted were estimated with Evans blue and triphenyl tetrazolium hydrochloride stains, respectively. The ratio of the area infarcted to the area at risk was significantly lower with Trolox (angioplasty, 30.4% +/- 5.1%; saline, 20.8% +/- 2.9%; and Trolox, 8.7% +/- 4.0%; p less than 0.01). In summary, the antioxidants Trolox and ascorbic acid effectively reduced myocardial necrosis after ischemia.

Animals↗
PubMed1975

The concentration of ascorbic acid in the posterior and anterior chambers of the rhesus monkey (Macaca mulatta).

The ascorbic acid concentration in the posterior and anterior chambers of the rhesus monkey (Macaca mulatta) eye was determined, and found to be significantly higher in the posterior chamber. Monkeys anesthetized with pentobarbital sodium had a higher posterior chamber ascorbic acid concentration than monkeys sedated with phencyclidine. The ascorbic acid diffusion coefficient, calculated from the posterior and anterior chamber data, was 0.0012 min.-1 for monkeys given phencyclidine and 0.0010 min.-1 for pentobarbital-anesthetized monkeys.

Anesthesia, Intravenous↗
PubMed1995

Randomized clinical trial of ascorbic acid in the treatment of pressure ulcers.

The objective of this study was to assess the effects of ascorbic acid supplementation, 500 mg twice daily in the treatment of pressure ulcers as an adjunct to standardized treatment. The design consisted of a multicenter blinded randomized trial. The control group received 10 mg of ascorbic acid twice daily. Patients from 11 nursing homes and 1 hospital participated. Main outcome measures included wound survival, healing rates of wound surfaces, and clinimetric changes over 12 weeks. Eighty-eight patients were randomized. Intention-to-treat analysis showed that the wound closure probability per unit time (i.e., the closure rate) was not higher in the intervention group than in the control group (Cox hazard ratio of 0.78 [90% precision interval, 0.44-1.39]). Mean absolute healing rates were 0.21 and 0.27 cm2/week in the intervention and control group, respectively (PI of the adjusted difference: -0.17 to 0.13). Relative healing rates and healing velocities did not show favorable results of ascorbic acid supplementation, either. A panel scored slides of the ulcers with a report mark between 1 (bad) and 10 (excellent). The improvement was 0.45 and 0.72 points per week in the intervention and control group, respectively (PI of the adjusted difference: -0.50 to 0.20). With another clinimetric index we could not show any differences, either. These data do not support the idea that ascorbic acid supplementation (500 vs. 10 mg twice daily) speeds up the healing of pressure ulcers.

Ascorbic Acid↗