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At least 1,063 records · Page 59Linked to original sources
PubMed2000

Ascorbic acid concentration and total antioxidant activity of human tear fluid measured using the FRASC assay.

PURPOSE: To evaluate a novel method (FRASC) for total ferric reducing (antioxidant) activity and ascorbic acid concentration applied to human tears, to investigate the stability of ascorbic acid, and to determine the antioxidant status of human reflex tears. METHODS: Linearity, sensitivity, and precision of FRASC and ascorbic acid loss during 7 days' storage were assessed; total antioxidant activity and ascorbic acid and uric acid concentrations of reflex tears from 47 healthy subjects were measured. RESULTS: FRASC has good precision, linearity, and sensitivity. Ascorbic acid is stable for at least 7 days at moderately acidic pH (pH 3.6) and low temperature. Total antioxidant activity and ascorbic acid and uric acid concentrations (mean +/- SD) in reflex tears were 409 +/- 162, 23 +/- 9.6, and 68 +/- 46 microM, respectively. Ascorbic acid and uric acid constituted around half the total antioxidant activity measured. There was a significant correlation between uric acid and total antioxidant activity (r = 0.754; P: < 0.0001). Men had significantly (P: = 0.0045) higher tear ascorbic acid concentrations than women. CONCLUSIONS: FRASC is suitable for measuring total antioxidant activity and ascorbic acid in human tears. Further clinical study is needed to investigate the male-female difference seen, to characterize the remaining 50% antioxidant activity, and to investigate the effects of environmental conditions, antioxidant supplementation, age, and ocular disease on tear antioxidant status.

Adult↗
PubMed1992

Effect of ascorbic acid supplementation on the sperm quality of smokers.

OBJECTIVE: To determine the effect of ascorbic acid supplementation on the sperm quality of heavy smokers. DESIGN: Microscopic examination of semen for 1 month during supplementation with placebo or ascorbic acid at dose levels of 200 or 1,000 mg/d. SETTING: Department of Obstetrics and Gynecology, The University of Texas Medical Branch. PARTICIPANTS: Seventy-five men (20 to 35 years old) randomly divided into one of three supplementation groups: placebo, 200 mg and 1,000 mg of ascorbic acid. MAIN OUTCOME: Improvement in sperm quality as compared with presupplementation levels and between the three treatment groups. RESULTS: The placebo group showed no improvement in sperm quality. The groups receiving ascorbic acid showed improvement in sperm quality with most improvement in the 1,000-mg group. Pearson's correlation showed statistically significant relationships between the weekly group means of serum and seminal plasma ascorbic acid levels and sperm qualities. CONCLUSIONS: Ascorbic acid supplementation of heavy smokers in excess of 200 mg/d results in improved sperm quality.

Adult↗
PubMed1996

Total vitamin C, ascorbic acid, and dehydroascorbic acid concentrations in plasma of critically ill patients.

Plasma concentrations of the antioxidant vitamin ascorbic acid were measured by high-performance liquid chromatography in critically ill patients in whom the excessive generation of reactive oxygen species could compromise antioxidant defense mechanisms. Median concentrations of both total vitamin C (ascorbic acid and dehydroascorbic acid) and ascorbic acid in these patients were < 25% (P < 0.001) of the values found in healthy control subjects and in subjects in two other disease groups (diabetes, gastritis) in which reactive oxygen species are reported to be increased. The low values could not be explained by age, sex, intake, or treatment differences, but were associated with the severity of the illness and were not prevented by the use of parenteral nutrition containing ascorbic acid. In addition, the vitamin was less stable in blood samples taken from critically ill patients than in similar samples from subjects in the other groups. The findings indicate that antioxidant defenses could be considerably compromised in these very sick patients. If this reduces the patient's capacity to scavenge reactive species, then the potential of these species to damage DNA and lipid membranes could be increased and compromise recovery.

Adult↗
PubMed1982

The distribution of ascorbic acid between various cellular components of blood, in normal individuals, and its relation to the plasma concentration.

1. A study was undertaken to investigate the distribution of ascorbic acid between various cellular components of blood, in normal individuals, and its relation to the plasma concentration. Forty-one unsupplemented individuals and sixteen supplemented (2 g/d for 5 d) individuals were studied. 2. Granulocytes, mononuclear leucocytes, platelets and erythrocytes were separated by differential sedimentation and centrifugation. Ascorbic acid contents were measured by the dinitrophenylhydrazine method. 3. Ascorbic acid content per cell was higher in mononuclear leucocytes and granulocytes than in platelets and erythrocytes. Intracellular ascorbic acid concentrations, calculated from published values for cell volumes, when compared with the plasma concentration showed a marked ability to concentrate ascorbic acid in mononuclear leucocytes (80 times), platelets (40 times) and granulocytes (25 times). 4. Erythrocytes showed little ability to concentrate ascorbic acid over the normal range of plasma concentration but because of their relative numbers they and the plasma fraction accounted for most of the blood-borne ascorbic acid (greater than 70%). 5. The ascorbic acid content of granulocytes, platelets and erythrocytes showed a significant positive correlation with the plasma concentration and supplementation with ascorbic acid significantly increased the content of these cell types. Mononuclear leucocytes in contrast did not show any such relationship. 6. The ability of the mononuclear leucocytes to maintain the highest levels of ascorbic acid in the cell types studied, despite variation in plasma availability, warrants further study, particularly in view of the importance of these cells in immunocompetence.

Adolescent↗
PubMed1991

Additional antilipoperoxidant activities of alpha-tocopherol and ascorbic acid on membrane-like systems are potentiated by rutin.

The effects of alpha-tocopherol, ascorbic acid and rutin on peroxidative processes were studied in xanthine-xanthine oxidase system, linoleic acid ufasomes and human erythrocyte membranes. In these three systems, tested compounds scavenge superoxide anion radicals or inhibit lipid peroxidation in a concentration-dependent manner, and it was shown that rutin was the most potent radical scavenger, followed by ascorbic acid and alpha-tocopherol. An important antilipoperoxidant activity was observed when these compounds were tested in combination, demonstrating that a dose-dependent interaction occurs. Water-soluble (rutin and ascorbic acid) as well as lipid-soluble (tocopherol) antioxidants are involved in the protection of polyunsaturated fatty acids constituting the ufasome or erythrocyte ghosts. When these compounds are used in combination, an additive effect is observed with alpha-tocopherol and ascorbic acid or rutin, while a supra-additive effect (synergism) is noted with ascorbic acid and rutin. Results obtained with the triple combination alpha-tocopherol-ascorbic acid-rutin show that an increase in superoxide radical scavenging activities or in lipid peroxidation inhibition is possible after the addition of a third antioxidant, as compared with the protective effects produced by the double combination of these compounds. This interaction takes place not only in homogeneous aqueous solutions, but also in ufasome or erythrocyte ghost preparations. It is suggested that ascorbic acid and rutin interacts with tocopherol at the surface of or the interface with the membrane, and that rutin simultaneously interacts with ascorbic acid.

Antioxidants↗
PubMed1981

Transport mechanisms for ascorbic acid in the human placenta.

The mechanisms for ascorbic acid transport were investigated in samples of human placenta obtained from normal term pregnancies. Results suggest that at very high ascorbic acid concentrations this vitamin may cross the placenta by simple diffusion. However, at lower ascorbic acid concentrations the predominant form of transport is carrier mediated and energy dependent. The energy used in the transport process can be derived from either glycolysis or oxidative phosphorylation. In addition, the transport system also requires the presence of sodium and of Na+-K+-dependent ATPase activity.

2,4-Dinitrophenol↗
PubMed1975

Effect of ascorbic acid on histamine metabolism in scorbutic guinea-pigs.

1. In guinea-pigs fed an ascorbic-acid-free diet, as the ascorbic acid levels decreased the histamine levels in blood and urine rose steadily to maxima in about 10-12 days. The elevated histamine levels persisted in the blood and urine of scorbutic guinea-pigs and the histamine levels in lung, gastric mucosa and spleen also increased. The increased histamine content of the urine, blood and other tissues in the ascorbic-acid-depleted condition could be brought back to normal levels by administration of a single dose of ascorbic acid 5 mg/100 g body wt. guinea-pig. 3. The drop in the elevated histamine level was not due to an indirect effect of ascorbic acid on histamine forming capacity, histaminase activity or histamine release.

Amine Oxidase (Copper-Containing)↗
PubMed2003

Ascorbic acid modifies the surface of asbestos: possible implications in the molecular mechanisms of toxicity.

Ascorbic acid is one of the major components of the antioxidants defenses of the lung lining layer where inhaled asbestos fibers are deposited. Crocidolite fibers were incubated at 37 degrees C in a 0.01 M aqueous solution of ascorbic acid for 25 days in order to investigate modifications in surface reactivity. Iron (820 nmol/mg) and monomeric silica (470 nmol/mg) were released in the supernatant, while ascorbic acid was consumed. The amount of iron and silicon released, respectively, 17 and 6% (in atoms) of the total fiber content, exceeded what was expected at the surface, suggesting a partial disgregation of crocidolite promoted by ascorbic acid. In the absence of ascorbic acid but at the same pH, the release of iron and monomeric silica was minimal. At time intervals, aliquots of fibers were withdrawn to evidence chemical modifications progressively taking place. Three families of Fe(II) centers, differing in coordinative unsaturation and progressively removed during incubation, have been evidenced from the FTIR spectra of NO adsorbed onto the fibers. The most uncoordinated ones are removed first. New highly uncoordinated iron sites are exposed at the fiber surface as a consequence of the erosion of the outmost layers while hydration of silica tetrahedra yields new silanol groups. The activity in the Fenton-like reaction (*OH from H(2)O(2)) decreases following surface iron depauperation. Conversely, the homolytic cleavage of the C-H bond (CO(2)*-) from the formate ion) appears related to the small fraction of iron ions always present but easily quenched by the adsorption of ascorbic acid or its oxidation products.

Adsorption↗
PubMedDate not supplied

Pro-oxidative vs antioxidative properties of ascorbic acid in chromium(VI)-induced damage: an in vivo and in vitro approach.

The effect of antioxidant ascorbic acid (vitamin C) pretreatment on chromium(VI)-induced damage was investigated using the yeast Saccharomyces cerevisiae as a model organism. The objective of this study was to pretreat yeast cells with the antioxidant ascorbic acid in an effort to increase cell tolerance against reactive chromium intermediates and reactive oxygen species formed during chromium(VI) reduction. Intracellular oxidation was estimated using the fluorescence indicators dihidro-2,7-dichlorofluorescein, dihydroethidium and dihydrorhodamine 123. The role of ascorbic acid pretreatment on chromium(VI) toxicity was determined by measuring mitotic gene conversion, reverse mutations, 8-OHdG, hydroxyl radical, superoxide anion and chromium(V) formation. The chromium content in the biomass was determined by flame atomic absorption spectrometry. In the absence of chromium, ascorbic acid effectively protected the cells against endogenous reactive oxygen species formed during normal cellular metabolism. In vitro measurements employing EPR and the results of supercoiled DNA cleavage revealed that the pro-oxidative action of ascorbic acid during Cr(VI) reduction was concentration-dependent and that harmful hydroxyl radical and Cr(V) had formed following Cr(VI) reduction. However, the in vivo results highlighted the important role of increased cytosol reduction capacity related to modification of Cr(V) formation, increased chromium accumulation, better scavenging ability of superoxide anions and hydrogen peroxide, and consequently decreased cytotoxicity and genotoxicity in ascorbic acid pretreated cells. Ascorbic acid influenced Cr(VI) toxicity both as a reducing agent, by decreasing Cr(V) persistence, and as an antioxidant, by decreasing intracellular superoxide anion and hydrogen peroxide formation and by quenching free radicals formed during Cr(VI) to Cr(III) reduction. Increased 8-OHdG and decreased reduced glutathione in ascorbic acid-treated cells might induce an endogenous antioxidant defense system and thus increase cell tolerance against subsequent Cr-induced stress.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1980

Ascorbic acid levels of trematode parasites of fish and mammalian hosts.

Ascorbic acid levels of seven species of digenetic trematodes, living under different environmental conditions in fish and mammals were determined colorimetrically. Ascorbic acid levels ranged from 0.312 mg/100 g fresh weight in Gastrothylax crumenifer to 5.070 mg/100 g fresh weight in Fasciola indica. Low levels of ascorbic acid were detected in the rumen parasites and in Isoparorchis hypselobagri. In contrast the liver parasites were found to have relatively high ascorbic acid levels.

Animals↗
PubMed1985

Biosynthesis of ascorbic acid in chick embryos.

Biosynthesis of ascorbic acid was found in the kidneys (mesonephros and metanephros) of the chick embryo as well as in the yolk sac membrane. The activity of L-gulonolactone oxidase in the yolk sac membrane suggested that it was the major source of ascorbic acid in the chick embryo.

Age Factors↗
PubMed1991

Ascorbic acid concentration in amniotic fluid in late pregnancy.

Amniotic fluid and venous blood specimens were obtained from 34 pregnant women and analyzed for the ascorbic acid concentration. The mean amniotic ascorbic acid concentration of smoking pregnant women was less than 50% of that of non-smoking women. Pregnant women who smoked had a significantly lower serum and amniotic fluid ascorbic acid concentration than those who did not smoke. No differences were observed between the groups with or without premature rupture of the fetal membrane. The results suggest that ascorbic acid in the amniotic fluid reflects the ascorbic acid status in the blood of pregnant women and smoking had a greater effect in decreasing the ascorbic acid concentration in amniotic fluid than in serum.

Adult↗
PubMed1986

Potentiation of haloperidol-induced catalepsy by ascorbic acid in rats and nonhuman primates.

Ascorbic acid was examined for potentiative effects on the catalepsy induced by haloperidol in rats and squirrel monkeys. In both animal species pretreatment with ascorbic acid (1000 mg/kg) markedly potentiated catalepsy induced by haloperidol. It is suggested that vitamin binds to, and inactivates, some brain dopamine receptors and in so doing potentiates an otherwise minimally cataleptogenic dose of haloperidol.

Animals↗
PubMed1968

Sporicidal action of auto-oxidized ascorbic acid for Clostridium.

Neutralized ascorbic acid (AA), buffered or unbuffered and autoclaved or filter-sterilized, was sporicidal for Clostridium. A 0.2% concentration of AA was generally employed, and spore counts were made in a soft-agar modification of Wynne's medium in Prickett tubes. Spores of Clostridium botulinum 115B were less susceptible than those of C. sporogenes PA 3679, whereas C. bifermentans spores were by far the most sensitive. At 75 C, spores of PA 3679 were killed at a rate of about 9% at 0 min (warm-up) to 99+% at 100 min. The lower the temperature, the longer the time needed for a given lethality. The percentage of killing increased with increasing concentrations of AA, and the rate of killing was lower at a higher concentration of spores. At least two mechanisms were operative: a major mechanism involving a product(s) of AA auto-oxidation, and a minor mechanism involving copper-ascorbate toxicity. AA reduced in natural gas was not sporicidal after 18.5 hr at 25 C, whereas 92% of the spores were killed by oxidized AA. Although H(2)O(2) per se was sporicidal, catalase did not reverse lethality of fresh or oxidized AA. Dehydroascorbate was as sporicidal as any AA preparation. Added copper (0.00001%) increased the rate of lethality of freshly prepared AA from 66 to 83% but was not effective with thoroughly oxidized AA. Ethylenediaminetetraacetic acid, NH(4) (+), and phosphate partially reversed AA toxicity, deionized water had no effect, and complex media, as well as thioglycolate, eliminated AA lethality. Since the percentage of killing was affected by spore concentration, AA did not seem to stimulate "lethal germination."

Ascorbic Acid↗
PubMed1982

Interference by ascorbic acid in test systems involving peroxidase. I. Reversible indicators and the effects of copper, iron, and mercury.

I describe the mechanism whereby ascorbic acid can hamper test systems involving a peroxide-generating system, peroxidase, and a benzidine-type indicator. In test media such as urines, abnormally high concentrations of ascorbic acid may give rise to false negatives in the determination of analytes such as glucose. Absorbance measurements in solution or reflectance measurements on commercially available paper reagent strips demonstrate either inhibition of visible activity by ascorbic acid or a lag time in the development of oxidized indicator color. The duration of the lag time is proportional to the ascorbic acid concentration, is inversely proportional to the enzyme concentration, and is also affected by concentrations of hydrogen peroxide and o-tolidine indicator. The same results were seen in both citrate buffer pH 5 and phosphate buffer pH 7. Because the complete system (o-tolidine indicator, hydrogen peroxide, and peroxidase) must be present if the ascorbate is to be oxidized rapidly, this indicates that ascorbic acid inhibits color development by re-reducing oxidized indicator as fast as it is formed; the o-tolidine then acts catalytically in oxidizing ascorbic acid. Added Cu2+ and Fe3+, both known to react with ascorbic acid, had measurable but small effects on the system. In contrast, Hg2+ abolished the ascorbic acid-elicited lag time, even when present in near-stoichiometric concentration. Hg2+ showed little inhibitory effect on the activity of either glucose oxidase or peroxidase. Presumably it rapidly oxidizes ascorbic acid to dehydroascorbate. The reaction of mercuric ion with ascorbate was measured by reflectance measurements of paper reagent strips in addition to absorbance measurements of solution assays; equivalent results were obtained. Incorporation of Hg2+ into reagent strips can thus render both strips and solution diagnostic tests insensitive to interfering substances such as ascorbic acid.

Ascorbic Acid↗
PubMed1983

Effect of ascorbic acid on response to methacholine challenge in asthmatic subjects.

We studied the effect of ascorbic acid in 14 mild asthmatic subjects. The effect of ascorbic acid (1.0 g orally) was assessed by the changes in concentration of methacholine required to decrease the specific airway conductance by 40% (pD40). Ascorbic acid increased pD40 from control values of 9.38 +/- 1.97 mg/ml (mean +/- SEM) to 12.59 mg/ml +/- 2.52 (p less than 0.05). Administration of 50 mg of indomethacin, orally, reversed the effect of ascorbic acid. Indomethacin alone had no effect on the mean pD40. The results suggest that ascorbic acid exerts its effect via alteration of arachidonic acid metabolism.

Adult↗