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PubMed1998

Aqueous humor uric acid and ascorbic acid concentrations and outcome of trabeculectomy.

OBJECTIVE: To determine if there is an association between the surgical outcome of trabeculectomy and uric acid and ascorbic acid concentrations in the aqueous humor at the time of the procedure. PATIENTS, MATERIALS, AND METHODS: Aqueous humor samples were collected from the eyes of 169 of 249 adult patients who underwent trabeculectomy alone for any type of glaucoma between April 1989 and July 1995. Postoperatively, all medical records were reviewed and outcomes were classified as successful, unsuccessful, or indeterminate. The ascorbic acid and uric acid concentrations were determined in masked fashion by high-pressure liquid chromatography. Factors associated with surgical outcome were determined. RESULTS: Uric acid concentration was higher in unsuccessful eyes (mean+/-SD, 0.21+/-0.08 mmol/L, n=26) than in successful eyes (0.15+/-0.09 mmol/L, n=91, 95% confidence interval for difference, 0.02-0.10 mmol/L). Ascorbic acid levels were not significantly different in the eyes with unsuccessful (1129.9+/-601.9 micromol/L) and successful (1334.3+/-511.0 micromol/L) surgery (95% confidence interval for difference, -475.2 to 66.4 micromol/L, P=.13) surgery. Other factors associated with failure were previous surgery and surgery performed at the inferior limbus. A multiple polytomous logistic regression analysis was performed, after excluding the small number of operations performed at the inferior limbus. The odds ratio for failure increased by a factor of 1.68 for every 1-mmol/L increase in uric acid (95% confidence interval, 1.16-2.43, P=.006). CONCLUSIONS: Uric acid levels were higher at the time of surgery in eyes that had unsuccessful outcomes than in those with successful outcomes. No significant difference in ascorbic acid levels was detectable. A higher uric acid level in the aqueous humor is a risk factor for trabeculectomy failure and might be tested as a prognostic indicator [corrected].

Aged↗

PubMed1984

Characterization of alkaline phosphatase inactivation by ascorbic acid.

Ascorbic acid, isoascorbic acid and dehydroascorbic acid inhibit bovine kidney alkaline phosphatase activity. Ascorbic acid free radicals seem not to be involved. Dialysis does not make the inactivation reversible. A competitive mechanism can be inferred from experiments with phosphate and substrates, which block the activity decay. The influence of temperature, pH, other inhibitors and tertiary structure modifications on the inactivation process is also investigated.

Alkaline Phosphatase↗

PubMed1997

Uric acid and ascorbic acid redox ratios in plasma and tracheal aspirate of preterm babies with acute and chronic lung disease.

This study compared plasma redox ratios of uric acid and ascorbic acid in well preterm babies with those with respiratory distress syndrome (RDS) and chronic lung disease (CLD), and investigated the relationship between these ratios and their respective measurements in tracheal aspirate. On day 1 after birth, plasma allantoin and allantoin/uric acid ratio were elevated in CLD (p < .05), and both markers of oxidative stress enabled early prediction of development of CLD (sensitivity and specificity: 54 and 83%, respectively). The relation between allantoin production and oxidative stress is supported by the correlation between the allantoin level and oxygen therapy in both RDS and CLD (p < .05). Reduced and oxidize ascorbic acid in plasma decreased postnatally in all groups and their redox ratio remained stable. Uric acid and ascorbic acid redox ratios were significantly elevated in tracheal aspirates compared to plasma samples (p < .05), and there was a strong positive correlation between both ratios (p < .005). These markers may be useful in monitoring babies with respiratory distress.

Antioxidants↗

PubMed1998

Effects of hypochlorous acid and ascorbic acid on conductance, permeability, and structure of equine colonic mucosa in vitro.

OBJECTIVES: To study effects of hypochlorous acid (HOCl) on equine colonic mucosa in vitro, and determine whether addition of ascorbic acid protects against the effects. ANIMALS: 6 healthy horses and ponies. PROCEDURE: Short-circuit current was measured in mucosa mounted in Ussing chambers. Incubation conditions were: control (no additions); 5 mM HOCl; 1 mM HOCl; same and 5 mM ascorbic acid; 3 mM HOCl; 3 mM HOCl and 5 mM ascorbic acid; 7 mM HOCl; and 7 mM HOCl plus 5 mM ascorbic acid. Permeability was measured with [3H]mannitol and, at the conclusion of each experiment, tissues were examined microscopically to assess the effects of HOCl and ascorbic acid, alone or in combination. RESULTS: Short-circuit current and conductance increased transiently in response to 1 mM HOCl. Tissues had mild surface epithelial damage, as evident by swelling and separation of isolated cells. These changes were abolished when tissues were coincubated with 5 mM ascorbic acid and 1 mM HOCl. At 3 and 7 mM concentrations, HOCl caused marked increase in tissue conductance, short-circuit current, and permeability to mannitol; these changes were associated with histologic damage. Again, coincubation with 5 mM ascorbic acid protected against these changes. Additional studies indicated that the effects of HOCl and the protective effects of ascorbic acid were not mediated through changes in pH. CONCLUSIONS: HOCl in low concentrations is capable or increasing the short-circuit current in equine colon, possibly by increasing secretions; however, higher concentrations can cause tissue damage. The addition of 5 mM ascorbic acid blocks these changes. CLINICAL RELEVANCE: The concentration of HOCl produced by activated neutrophils could damage equine colonic mucosa and potentially contribute to or cause reperfusion injury. The ability of ascorbic acid to ameliorate this injury in an in vitro setting offers a potential method for pharmacologic evaluation of this injury and for treatment.

Animals↗

PubMed1994

Iron bioavailability studied in infants: the influence of phytic acid and ascorbic acid in infant formulas based on soy isolate.

The influence of phytic acid and ascorbic acid content of soy formula on iron (Fe) bioavailability was investigated in infants by analysis of the incorporation of stable isotopes of Fe into red blood cells 14 d after administration using a double stable isotope technique. Paired comparisons were made with each infant acting as his or her own control. The geometric mean fractional Fe incorporation into red blood cells increased from 5.5 to 6.8% (p < 0.05) when soy formula with the native content of phytic acid was compared with a 83% dephytinized formula. A more pronounced effect was shown with soy formula containing no phytic acid; the mean fractional Fe incorporation increased from 3.9 (native phytic acid) to 8.7% (zero phytic acid; p < 0.001). A significant (p < 0.01) effect was also demonstrated when the Fe:ascorbic acid molar ratio in the native phytate-containing formula was increased from 1:2.1 to 1:4.2; mean fractional Fe incorporation increased from 5.9 to 9.6%. These results demonstrate that the Fe bioavailability from soy-based infant formulas can be similarly increased by either removing phytic acid or increasing the ascorbic acid content.

Ascorbic Acid↗

PubMed2004

Evaluation of the hepatic reduction of a nitroxide radical in rats receiving ascorbic acid, glutathione or ascorbic acid oxidase by in vivo electron spin resonance study.

BACKGROUND: A nitroxide radical, 4-hydroxyl-2,2,6,6-tetramethylpiperidin-1-oxyl (TEMPOL), is directly reduced to hydroxylamine by ascorbic acid (AsA). Ascorbic acid is oxidized to dehydroascorbic acid (DHA) by ascorbic acid oxidase (AAOx), and DHA is reduced to AsA by glutathione (GSH). In the present study, in vivo and ex vivo reduction of TEMPOL in the rat liver under various conditions of AsA supply was investigated using an electron spin resonance (ESR) spectrometer equipped with a surface coil-type resonator. METHODS: To investigate in vivo hepatic reduction of TEMPOL, an ESR study of the liver of living rats which orally received AsA or intravenously received GSH or AAOx was made. To investigate direct interactions between TEMPOL and GSH or AAOx, an in vitro ESR study was conducted. To investigate TEMPOL reduction in the hepatic homogenate, an ex vivo ESR study was performed. RESULTS: Ascorbic acid and GSH administration increased the in vivo hepatic reducing ability of TEMPOL. In contrast, AAOx administration decreased the reducing ability. In vitro TEMPOL was not reduced by GSH and hydroxylamine was not oxidized by AAOx. Reducing ability in the hepatic homogenate of AAOx-treated rats decreased, but that for GSH-treated rats was unchanged. CONCLUSION: Ascorbic acid administration directly increases hepatic reducing ability. Ascorbic acid, which increased in the plasma due to GSH administration, entered the liver and enhanced the hepatic reducing ability. Administration of AAOx impaired the hepatic reducing ability by oxidizing AsA in the plasma and/or the liver.

Animals↗

PubMed1976

Interaction of erythorbic acid with ascorbic acid catabolism.

After a vitamin C depletion period of 12 days supplementing erythorbic acid (50 mg/day/kg bodyweight) over 16 days significantly accelerated the catabolism of a newly ingested tracer dose of (1-14C) ascorbic aicd in guinea pigs in comparison to animals supplemented with ascorbic acid (5 mg/day/kg bodyweight), but this effect of erythorbic acid could not be normalized by additional supplementation with ascorbic acid. Half-lives for (1-14C) ascorbic acid (50% of the dose excreted) were drastically reduced from 97 h to 50 h and 59 h, respectively. Also figures on the retention of radioactivity showed the availability of ascorbic acid to be reduced. This is in accordance with the significant reduction in size of ascorbic acid bodypool, and in weight gain in the groups receiving erythorbic acid, or erythorbic and ascorbic acids. The bioavailability was calculated to be strongly depressed to nearly 50% of the total ingested biologically active material (ascorbic plus erythorbic acids), assuming erythorbic acid to have only one-twentieth of the biological activity of ascorbic acid.

Animals↗

PubMedDate not supplied

Fluid-bed microencapsulation of ascorbic acid.

Ascorbic acid has been fluidized and microencapsulated with three different hydrophobic coating materials by the top-spray method. The experiments were conducted with polymethacrylate coating material formulated as a water dispersion, and ethyl-cellulose and waxy coating material both formulated as organic solutions. Characteristics of the fluidized bed procedure in conical geometry have been determined by estimation of two parameters: bed porosity and total pressure drop. A satisfactory agreement between experimental and calculated values has been reached. The following properties of the microencapsulated ascorbic acid have been determined: core content, bulk and tapped density, crystal size distribution prior and after microencapsulation, surface morphology and release profile. The comparison and evaluation of different hydrophobic coating materials have been performed on the basis of these findings.

Ascorbic Acid↗

PubMed1990

Absorption of ascorbic acid and ascorbic sulfate and ascorbate metabolism in common carp (Cyprinus carpio L.).

Ascorbate metabolism was analyzed in fasted common carp and carp offered diets lacking ascorbic acid or supplemented with ascorbic acid (AA) or ascorbic sulfate (AS). Ascorbic acid and ascorbic sulfate were analyzed in the contents collected from various parts of the digestive tract. The major site of the dietary ascorbate absorption was located in the first 20% of the anterior intestine region (58.7 +/- 10.2%), whereas absorption increased to 94.3 +/- 1.9% (in the whole gut). Considerable secretion of ascorbate into the initial part of the intestine was found (71 micrograms AA.g-1 dry food) in fish offered the diet lacking ascorbate, but this amount was completely reabsorbed in the following portions of the intestine. AS was concentrated in the contents of the digestive tract and the external marker method revealed no absorption of AS from the intestine. In fish fed the AA-supplemented diet, the concentration of ascorbate in plasma, hepatopancreas, kidney, intestine, spleen, and brain was significantly (P less than 0.01) higher than in similar tissues from the other groups, suggesting that ascorbic sulfate hydrolysis was ineffective. Small amounts of AS were found in the intestine and spleen of fish fed a diet supplemented with AS. Ascorbate analysis in the whole fish allowed the estimate of the catabolic rate of fasting and scorbutic-diet-fed fish, which amounted to 0.7% and 1.46% daily of the ascorbate body pool, respectively. There was no indication that ascorbic sulfate sulfohydrolase activity was induced in hepatic, kidney, or intestinal tissue of fish offered a diet with AS in comparison to other groups. It seems unlikely that cyprinid fish are able to utilize ascorbic sulfate as a vitamin C source, and thus resemble scurvy-prone mammals in this respect.

Animals↗

PubMed1983

Influence of erythorbic acid on ascorbic acid retention and elimination in the mouse.

Large quantities of ascorbic acid or erythorbic acid were administered to Swiss mice over a period of seven months. Urinary ascorbic acid and erythorbic acid were determined two weeks before termination of the experiment. At the end of the experiment, ascorbic acid and erythorbic acid contents in plasma, liver and brain tissues were measured. In the ascorbic acid-treated mice, there was a marked elevation in plasma and urine ascorbate levels, and there was a 38% increase of ascorbate level in the liver but there was no substantial increase in ascorbate levels in the four brain regions studied, namely the cerebrum, cerebellum, medulla and brain stem, upon large intake of ascorbic acid. In the erythorbic acid-treated mice, erythorbic acid is well absorbed by the gastrointestinal tract, enters the blood stream, and is rapidly excreted in the urine. The results show that erythorbic acid is able to replace 45% of ascorbic acid in the liver and 28-39% of ascorbic acid in the brain tissues. Although erythorbic acid appears in the blood at significantly high level, it does not lower blood ascorbate levels.

Animals↗

PubMed1989

Applications of a simultaneous assay of ascorbic acid, dehydroascorbic acid and ascorbic sulphate in biological materials.

A modified spectrophotometric assay for ascorbic acid and its derivatives based on their reaction with 2,4-dinitrophenylhydrazine (DNPH) is described. Using standard ascorbic acid or ascorbic sulphate solutions, together with animal tissue or compound diet extracts, the conditions for ascorbic acid degradation were determined. For the differential measurement of reduced ascorbic acid (AA), dehydroascorbic acid (dAA) and ascorbic sulphate (AS), five series of simultaneous determinations were performed. These included the use of (1) KBrO3 for the hydrolysis of AS, (2) 2,6-dichlorophenolindophenol as an oxidant, (3) DNPH to form a hydrazone derivative with dAA and (4 and 5) two blanks (where ascorbate was degraded) to correct for interfering substances. A variety of vertebrate and invertebrate tissues were examined for their ascorbate content, and the advantages of the modified procedure over currently available assays are discussed. The results suggest that the Artemia cyst is a unique material in which ascorbic sulphate is present in large amounts whereas fish tissues do not contain this form of vitamin C.

Animals↗

PubMed1979

[The excretion of hippuric acid and ascorbic acid in the urine of liver-damaged rats (author's transl].

The authors investigated the effects of the administration of thioacetamide, carbon tetrachloride and aminophenazone on the excretion of ascorbic acid and hippuric acid in adult male and female Wistar rats. After a single application of thioacetamide and aminophenazone, the ascorbic acid content in the urine showed a dose-dependent increase, whereas that in the liver had decreased. This increase in the urinary ascorbic acid might be due to a release of stored ascorbic acid from the liver cells. When thioacetamide was given for a prolonged period, the ascorbic acid content in the urine increased at the beginning; later one, at the end of three weeks, it was slightly inferior to the control value. Both single and repeated applications of thioacetamide led to a decrease in the excretion of hippuric acid in the urine, which is attributed to an impairment of the mitochondrial hippuric acid synthesis. Long-term treatment with aminophenazone resulted in an increase of ascorbic acid in the urine, which is indicative of an induction effect, whereas the ascorbic acid content in the liver remained unchanged. There was no effect on the excretion of hippuric acid. In regard to their use in the toxicological evaluation of drugs, these two metabolic effects offer no decisive advantage over current liver function tests.

Aminopyrine↗

PubMed1990

Kinetic studies on the reaction of compound II of myeloperoxidase with ascorbic acid. Role of ascorbic acid in myeloperoxidase function.

Ascorbic acid is known to stimulate leukocyte functions. In a recent publication it was suggested that the role of ascorbic acid is to reduce compound II of myeloperoxidase back to the native enzyme (Bolscher, B. G. J. M., Zoutberg, G. R., Cuperus, R. A., and Wever, R. (1984) Biochim. Biophys. Acta 784, 189-191). In this paper we report rapid spectral scan and transient state kinetic results on the reaction of three myeloperoxidase compounds II, namely, human neutrophil myeloperoxidase, canine myeloperoxidase, and bovine spleen heme protein with ascorbate. We show by rapid scan spectra that compound II does not pass through any other intermediate when ascorbic acid reduces it back to native form. We also show that the reactions of all three compounds II involve a simple binding interaction before enzyme reduction with an apparent dissociation constant of 6.3 +/- 0.9 x 10(-4) to 2.0 +/- 0.3 x 10(-3)M and a first-order rate constant for reduction of 12.6 +/- 0.6 to 18.8 +/- 1.3 s-1. The optimum pH is 4.5, and at this pH the activation energy for the reaction is 13.2 kJ mol-1. Results of this work lend further evidence that the spleen green heme protein is very similar if not identical to leukocyte myeloperoxidase based on a comparison of spectral scans, pH-rate profiles, and kinetic parameters. We demonstrate that chloride cannot reduce compound II whereas iodide reduces compound II to native enzyme at a rate comparable to that of ascorbate. This explains why ascorbate accelerates chlorination but inhibits iodination. Formation of compound II is a dead end for the generation of hypochlorous acid; ascorbate regenerates more native enzyme to enhance the chlorination reaction namely: myeloperoxidase + peroxide----compound I followed by compound I + chloride----HOCl. On the other hand, ascorbate is a competitor with iodide for both compounds I and II and so inhibits iodination.

Animals↗

PubMed1999

Rapid on-line microdialysis hyphenated technique for the dynamic monitoring of extracellular pyruvate, lactic acid and ascorbic acid during cerebral ischemia.

Rapid on-line microdialysis coupled with liquid chromatography was developed for the continuous monitoring of brain neurochemicals during cerebral ischemia. Isocratic separation of these analytes was achieved within 3 min, hence, over 80 analyses could be performed in a 4-h experiment. The dead volume of the microdialysis system was estimated to be less than 10 microl. The detection limits of the present assay, at a signal-to-noise ratio of five, were 2.0, 0.2 and 0.5 microM, for lactic acid, pyruvate and ascorbic acid, respectively. To validate this assay, a transient ischemia was produced by occlusion of two common carotid arteries for 10 min in an anesthetized gerbil. A microdialysis probe was inserted into the striatum of the gerbil to simultaneously monitor pyruvate, lactic acid and ascorbic acid during cerebral ischemia. Significant and dynamic changes in these analytes could be resolved in 3-min intervals. This rapid assay can be used as a tool to study dynamic changes in neurochemicals of the brain, such as during cerebral ischemia.

Animals↗

PubMed2001

Beneficial effects of alpha-lipoic acid and ascorbic acid on endothelium-dependent, nitric oxide-mediated vasodilation in diabetic patients: relation to parameters of oxidative stress.

The impairment of nitric oxide (NO)-mediated vasodilation in diabetes has been attributed to increased vascular oxidative stress. Lipoic acid has been shown to have substantial antioxidative properties. The aim of this study was to assess the effect of lipoic acid on NO-mediated vasodilation in diabetic patients in comparison with the well-recognized effect of ascorbic acid. Using venous occlusion plethysmography, we examined the effects of lipoic acid (0.2 mM) and ascorbic acid (1 and 10 mM) on forearm blood flow responses to acetylcholine, sodium nitroprusside and concomitant infusion of the NO-inhibitor, N(G)-monomethyl-L-arginine, in 39 diabetic patients and 11 control subjects. Plasma levels of antioxidants and parameters of lipid peroxidation were measured and correlated to endothelial function tests. Lipoic acid improved NO-mediated vasodilation in diabetic patients, but not in controls. NO-mediated vasodilation was improved by ascorbic acid at 10 mM, but not 1 mM. Improvements of endothelial function by ascorbic acid and lipoic acid were closely related. The beneficial effects of lipoic acid were positively related to plasma levels of malondialdehyde and inversely related to levels of ubiquinol-10. These findings support the concept that oxidative stress contributes to endothelial dysfunction and suggest a therapeutic potential of lipoic acid particularly in patients with imbalance between increased oxidative stress and depleted antioxidant defense.

Acetylcholine↗

PubMed1986

Dehydroascorbic acid and ascorbic acid transport systems in the guinea pig ileum.

The transport properties of dehydroascorbic acid and ascorbic acid in membrane vesicle preparations of guinea pig ileum were evaluated. Na-dependent transport of ascorbic acid in the brush-border membrane was confirmed, and an Na-independent mechanism was found in the basolateral membrane. The electrically neutral oxidized form of vitamin C is transported by an Na-independent mechanism at both cell surfaces. Transport of each substrate is saturable and exhibits cis-inhibition and trans-stimulation in the presence of structural analogues. Additional studies on ascorbate metabolism will be necessary to support a comprehensive model of intestinal handling of vitamin C.

Animals↗

PubMed1995

Proposed role for a combination of citric acid and ascorbic acid in the production of dietary iron overload: a fundamental cause of disease.

This paper presents a review of the significant body of literature liking dietary iron overload, not only to heart disease, but also to cancer, diabetes, osteoporosis, arthritis, and possibly other disorders. Following an analysis of our understanding of the mechanistic role iron plays in oxidative damage, an interpretation of the fact that plasma concentrations of several antioxidants are decreased in the presence of disease is offered. Evaluation of (1) age-related dietary trends over time and (2) factors involved in iron absorption leads to the hypothesis that the combination of citric acid and ascorbic acid (a synergistic pair of strong enhancers) is instrumental in causing a deleterious increase in iron load in aging populations. Iron overload may be the most important common etiologic factor in the development of the diseases mentioned; therefore, the synergistic combination of citric and ascorbic acids may play a major role in our worsening disease statistics. Evidence to support this hypothesis and possible experiments to test it are included. This combination needs further study, particularly because the iron overload produced may be correctable.

Aging↗

PubMed1998

Enhancing effect of 2-O-alpha-D-glucopyranosyl-L-ascorbic acid, a stable ascorbic acid derivative, on collagen synthesis.

The objective of the present study was to compare 2-O-alpha-D-glucopyranosyl-L-ascorbic acid (AA-2G) with ascorbic acid (AA) and ascorbic acid 2-phosphate (AA-2P) concerning the promotion of collagen production in human skin fibroblasts. Though AA-2G was still observed to be promoting collagen synthesis at the same level on the 8th day of the culture, collagen synthesis was seen to decrease on the fifth day of culturing with AA and AA-2P. This sustained collagen synthesis-promoting action is considered to be a major feature of the novel vitamin C derivative, AA-2G by conducting an experiment in which an alpha-glucosidase inhibitor was present, it was shown that AA-2G exerts its collagen synthesis-promoting action after being decomposed to AA by alpha-glucosidase. Further, we observed that for AA-2G, even on the 8th day of the culture, the amount of AA in the fibroblasts was virtually unchanged from the beginning of the experiment, whereas, in the case of adding AA and AA-2P, virtually no AA was detectable in the culture medium on the fifth day. These findings suggests that AA-2G is decomposed to AA by alpha-glucosidase in the cells. This AA promotes collagen synthesis, which is prolonged through AA-2G's sustained decomposition.

Ascorbic Acid↗