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PubMed1992

Determination of ascorbic acid in elemental diet by high-performance liquid chromatography with electrochemical detection.

Determination of ascorbic acid in a multi-component elemental diet was performed by high-performance liquid chromatography with electrochemical detection. This method is suitable for the routine determination of ascorbic acid in elemental diet because it is simple, rapid, sensitive, highly selective and reproducible. The calibration graph of ascorbic acid was linear in the range 0-1.0 micrograms. The recovery of ascorbic acid was over 95% by the standard addition method. There was good agreement between the concentrations of ascorbic acid stated and found.

Ascorbic Acid↗
PubMedDate not supplied

Ex vivo cutaneous absorption assessmentof a stabilized ascorbic acid formulation using a microdialysis system.

BACKGROUND: Reactive oxygen species generated by ultraviolet light result in photocarcinogenic and photoaging changes in the skin. Antioxidants protect the skin from these insults. OBJECTIVE: The aim of this study was to determine the ex vivo ascorbic acid penetration and its degradation in the skin after its topical application from an 8% new formulation. METHOD: Ascorbic acid was applied to human skin fragments. Ascorbic acid and its metabolites were collected by microdialysis and assessed by gas chromatography mass spectrometry. RESULTS: After topical application of the new formulation, the ascorbic acid level achieved was 8.5% higher than [corrected] times the normal tissue value. This high ascorbic acid dermal concentration remained constant if a topical application was made every 8 h. No degradation of ascorbic acid was detected. CONCLUSION: Ascorbic acid penetrates rapidly after its topical application. The persistent reservoir of ascorbic acid provides an important and attractive photoprotection strategy.

Administration, Topical↗
PubMed1988

The effect of ascorbic acid deficiency on leukocyte phagocytosis and killing of actinomyces viscosus.

The ascorbic acid content of guinea pig leukocytes is reduced by a factor of 16:1 between normal and scorbutic guinea pigs. Ascorbic acid deficiencies do not appear to affect phagocytic activity but do change leukocyte morphology. A deficiency of this vitamin appears to significantly interfere with the in vitro bactericidal effectiveness of circulating leukocytes against ingested, cell-associated, and extracellular bacterial cells of the oral pathogen, Actinomyces viscosus. Leukocytes from scorbutic guinea pigs killed 13% of ingested and cell-associated Actinomyces viscosus compared to 83% killed by normal leukocytes by both acridine orange staining and viable count. Degranulation resulted in extracellular killing in normal but not scorbutic leukocytes. This decreased bactericidal activity can be reversed by adding supplements of the vitamin to the diet of scorbutic animals. Chemotactic responses were much lower in vivo and absent in vitro in scorbutic leukocytes. The acridine orange staining technique is an excellent indicator of leukocyte health. This study supports the important role for ascorbic acid in leukocyte function and also discusses its probable protective and bactericidal activities related to oral pathogens.

Actinomyces↗
PubMed1996

Iron absorption from a traditional Sri Lankan weaning food and the enhancing effect of ascorbic acid in adult male volunteers.

OBJECTIVE: To study absorption of iron from Centella gruel and the enhancing effect of ascorbic acid in young adult males. DESIGN: An in vivo absorption study. SETTING: Faculty of Medicine, Galle. METHODS: The percentage of iron absorbed from the Centella gruel was measured using a double isotope technique with 55Fe and 59Fe on 10 healthy male volunteers. OUTCOME MEASURE: Percentage of iron absorption from the gruel with and without ascorbic acid. RESULTS: The mean iron absorption from each meal of Centella gruel was 2.2% (SEM 0.8). This increased to 5% (SEM 1.6) by addition of 50 mg ascorbic acid. When ingested with ascorbic acid, the bioavailable nutrient density (BND) of the weaning food was increased from 0.23 to 0.53 mg iron/1,000 kcal. To satisfy the daily physiological requirements of iron in infants and toddlers, it was calculated that apart from ascorbic acid supplementation, the total iron content also needs to be increased from 2.05 mg to 4.0 mg/meal. CONCLUSION: Centella gruel cannot provide the amount of iron to meet the BND for iron required by infants and toddlers, unless supplemented with an enhancer of iron absorption such as ascorbic acid and its total iron content is increased.

Adult↗
PubMedDate not supplied

Activity of ascorbic acid in inhibiting the multiplication of M. leprae in the mouse foot pad.

Ascorbic acid was fed to mice in concentrations of 0.05%, 0.15%, and 0.45% w/w in the diet. Six months after inoculation of M. leprae into the foot pads, there were significantly fewer acid-fast bacilli harvested from animals receiving 0.15% and 0.45% w/w ascorbic acid than from control mice. On the other hand, M. leprae did multiply in mice fed ascorbic acid while no multiplication at all was observed in animals fed dapsone, clofazimine or rifampin. No toxic effects of ascorbic acid were noted in these mice.

Administration, Oral↗
PubMedDate not supplied

Structure of ascorbic acid and its biological function: V. Transport of ascorbate and isoascorbate across artificial membranes as studied by the spin label technique.

It could be shown by the reduction of the spin label (1,14) located within DPPC vesicles, that Na-ascorbate and K-isoascorbate can permeate membranes. At physiologic pH value, these two compounds exist as electroneutral radicals with a cyclic side chain structure. Ascorbic acid and isoascorbic acid, on the contrary, can hardly permeate such an artificial membrane. Since the radical will cause lipid peroxidation, it must be modified prior to permeation. This can be done by GSH which changes the radical state but maintains the electroneutral bicyclic configuration.

Ascorbic Acid↗
PubMed1970

Ascorbic acid deficiency and pituitary adrenocortical activity in the guinea-pig.

1. Guinea-pigs kept on a diet deficient in ascorbic acid lost weight and became moribund in about 24 days.2. The adrenal ascorbic acid concentration fell rapidly during the first 2 weeks, and the plasma corticosteroid concentration and 17-oxogenic steroid excretion rose sharply in the third week of ascorbic acid deficiency.3. Both histamine and corticotrophin increased the plasma corticosteroid concentration when injected during the second week but failed to change the pre-existing high concentration of the steroid in the third week of ascorbic acid deficiency.4. The observations confirm that ascorbic acid is not involved in corticoidogenesis and that scurvy is a severe stress which increases adrenocortical activity to such an extent that the rate of synthesis of corticosteroids is incapable of matching the rate of their release.

Adrenal Cortex Hormones↗
PubMed1998

Structures of the N-linked carbohydrate of ascorbic acid oxidase from zucchini.

The N-glycan moiety of ascorbic acid oxidase from zucchini (Cucurbita pepo) has been described to be a core-pentasaccharide with a xylose [D'Andrea et al. (1988) Glycoconjugate J 5:151-7]. Ascorbic acid oxidase is sometimes used to characterize antibodies directed against carbohydrate determinants on plant glycoproteins. To prevent misinterpretations of immunological data, the structure of the N-glycan of ascorbic acid oxidase has been reinvestigated. The oligosaccharides were released by almond N-glycosidase and analysed as their pyridylamino derivatives by 2D-HPLC and exoglycosidase digestions. The main structure resembled the typical complex plant N-glycan consisting of a core-pentasaccharide decorated with xylose and 3-linked fucose. The other abundant species lacked the fucose residue. Small amounts of these glycans carried a GlcNAc residue on the 6-arm. Therefore, ascorbic acid oxidase will not only react with antibodies directed against the xylosylated region but also with those binding to N-glycans with 3-linked fucose.

Ascorbate Oxidase↗
PubMed1990

Ascorbic acid potentiates the inhibitory effect of dopamine on prolactin release: a putative supplementary agent for PIF.

Dopamine has a catechol group which can be easily oxidized by mild oxidizing agents. Ascorbic acid has been routinely added to a dopamine solution in order to protect it from oxidation. We have examined the effect of ascorbic acid on dopaminergic inhibition of prolactin release. Male rat pituitary cells were dispersed using trypsin and cultured for 5-7 days before experiments. Ascorbic acid did not stimulate nor inhibit prolactin release in both static monolayer culture and dynamic perifusion systems, but potentiated by approximately 100 times the inhibitory effect of dopamine on prolactin release. In order to differentiate chemical protection from potentiation, we tested the potentiation effect of isoascorbic acid which is an epimer of biologically active L-ascorbic acid but is biologically less active. Our results indicated that isoascorbic acid caused less potentiation of the dopaminergic effect on prolactin release than did ascorbic acid. In a perifusion system, a high concentration of dopamine (100 nmol/l) was unable to inhibit prolactin release for a 1 h experimental period, but a low concentration of dopamine (10 nmol/l) plus ascorbic acid (10 mumol/l) inhibited prolactin release for the entire 1 h perifusion period. There is a strong possibility that ascorbic acid may be a physiological supplementary agent for the prolactin-release inhibiting factor (PIF) since the blood concentration of ascorbic acid is rather high (23-85 mumol/l).

Animals↗
PubMed1995

[Ascorbic acid concentrations in ruminal fluid and in blood of cattle and sheep].

Plasma and ruminal fluid ascorbic acid levels were determined in Holstein calves aged four months and in ruminal fluid of merino rams aged 2,5 years under in vitro conditions. Ascorbic acid values decreased in plasma until 6th month. The highest Ascorbic acid value in ruminal fluid was found in 5th month. Under in vitro conditions shown ascorbic acid concentrations in ruminal fluid with time upward tendency. For analysis of ascorbic acid concentrations the acid phosphotungstate method were used for each samples.

Aging↗
PubMed1981

Oxidation of 1-14C-ascorbic acid in the guinea pig: effect of the route of administration.

Twenty-four hours after the administration of (1-14C)-ascorbic acid to guinea pigs by oral, intraperitoneal or intracardiac routes, 14CO2 expired levels were 22.6 plus or minus 1.8, 17.6 plus or minus 1.4 and 14.4 plus or minus 0.6 percent, respectively, of the administered radioactive doses. Whole blood concentrations of ascorbic acid were 80.2 plus or minus 2 micrograms per ml and, in general they were inversely related to expired 14CO2 production, which in turn reflects the degree of ascorbic acid catabolism in ascorbic acid adequate animals. Regardless of the route of (1-14C)-ascorbic acid administration, there was a biphasic pattern of 14CO2 evolution; the first peak occurs at two hours and the second peak at five hours after administration of the doses. Thin layer chromatography analysis of (1-14C)-ascorbic acid verified the reagent's purity. In vitro isolated stomach content and intestinal content experiments illustrated that at least 1-2% of the expired 14CO2 might also result from enterohepatic circulation of the label.

Administration, Oral↗
PubMed1983

Hyperglycemia-induced intracellular depletion of ascorbic acid in human mononuclear leukocytes.

It has recently been reported that glucose and its analogues inhibit in vitro ascorbic acid transport across the cell membrane of polymorphonuclear leukocytes and fibroblasts. We have studied the effect of in vivo hyperglycemia on the intracellular ascorbic acid level of mononuclear leukocytes in normal and diabetic human subjects. Administration of an intravenous glucose load resulted in a prompt decrease of mononuclear leukocyte ascorbic acid level in the normal subjects. The rate of its decline correlated closely with the rate of change of plasma glucose. Among the NIDDM subjects in the fasting state, the plasma glucose was high and the leukocyte ascorbic acid level was low when compared with that of the normal subjects. The decrease in the leukocyte ascorbic acid level during disposition of the i.v. glucose load was not statistically significant in the diabetics. The hyperglycemia-induced intracellular depletion of ascorbic acid could be clinically important and requires further evaluation.

Adult↗
PubMed1997

Microplate assay of ascorbic acid in aqueous humor with bicinchoninic acid.

An inexpensive microplate assay method was developed to determine ascorbic acid in human aqueous humor samples. The method is based on the selective oxidation of ascorbic acid at alkaline pH and determination of ascorbic acid and other reducing substances in samples with bicinchoninic acid/CuSO4 before and after the alkaline treatment. The two-point measurement eliminates the effect of interfering substances, such as glucose, uric acid and glutathione, which are stable at alkaline pH. The advantages of the method are that it requires small sample volumes and allows handling of a large number of samples simultaneously.

Aqueous Humor↗
PubMed1986

Ascorbic acid stimulates collagen production without altering intracellular degradation in cultured human skin fibroblasts.

The influence of ascorbic acid on intracellular degradation of collagen synthesized by cultured human-skin fibroblasts was examined. In confluent cells maintained in 0.5% serum-supplemented medium, ascorbic acid had no significant effect on collagen degradation measured with hydroxyproline as the marker. Similar results were obtained when collagen degradation was measured with the marker hydroxylysine, the cellular synthesis of which is independent of ascorbic acid. The stimulatory effects of ascorbic acid on collagen production therefore cannot be explained by a change in the rate of degradation. Ascorbic acid acts at some as yet undetermined level to increase the rate of collagen synthesis.

Ascorbic Acid↗
PubMed1986

Antioxidants in sickle cell disease: the in vitro effects of ascorbic acid.

The authors examined the ability of antioxidants to prevent in vitro oxidant damage to the sickle red blood cell (RBC). One millimolar ascorbic acid and alpha-mercaptopropionylglycine significantly (p less than 0.005) protected against RBC Heinz body formation during incubation with acetylphenylhydrazine, while cysteine, cysteamine, and methionine did not. The effect of ascorbic acid was concentration dependent with concentrations as low as 0.1 mM having significant antioxidant effects. Ascorbic acid protected the RBC against hydrogen peroxide induced hemolysis as well (p less than 0.05). Ascorbic acid had a significant stimulatory effect on the rate of glucose oxidation by the pentose phosphate shunt (PPS), especially in the sickle RBC. Ascorbic acid did not protect the RBC from a patient with chronic hemolytic anemia due to G6PDTorrance from Heinz body formation, suggesting that an intact PPS is necessary for ascorbic acid to express its antioxidant properties. These data suggest that clinical trials should be undertaken to examine the efficacy of ascorbic acid in the treatment of SCD.

Adult↗
PubMed1984

The failure of ascorbic acid therapy to alter the induction or remission of murine amyloidosis.

It has been claimed that ascorbic acid enhances the in vitro degradation of AA amyloid fibrils. This raises the possibility that ascorbic acid may be of benefit in systemic AA amyloidosis, a condition with serious morbidity and mortality for which there is as yet no specific treatment. The effect was therefore tested of oral or injected supplements of ascorbic acid on the induction of AA amyloidosis in mice. Amyloid was induced either by repeated injections of casein or by injection of 'amyloid enhancing factor' and silver nitrate. Mice with established amyloidosis were also treated with additional ascorbic acid. Despite the fact that plasma ascorbic acid levels were significantly higher in orally supplemented mice than in controls there was no demonstrable effect on the induction, the extent and distribution or the progression of amyloidosis.

Amyloid↗
PubMed1985

The influence of ascorbic acid on the occurrence of tibial dyschondroplasia in young broiler chickens.

Two distinctly different basal diets were used to test the influence of supplementary ascorbic acid on the occurrence of tibial dyschondroplasia. Addition of either .1 or .25% ascorbic acid to these diets did not alter the occurrence of tibial dyschondroplasia in 25-day-old broiler chickens. However, supplementary ascorbic acid did increase the amounts of ascorbic acid present in blood plasma. Also, individual differences in circulating ascorbic acid were not associated with this disease. Furthermore, two strains of chickens selected for high or low incidence of tibial dyschondroplasia had similar amounts of this vitamin in blood plasma. In contrast to the results reported for the Willow Ptarmigan, ascorbic acid does not appear to be involved in the development of tibial dyschondroplasia in the young broiler chicken.

Animals↗
PubMed2002

[The role of L-ascorbic acid in free radical reactions].

L-ascorbic acid is one of the basic vitamins, necessary to the normal growth and behaviour of organisms. The primary of this review is to present the chemical characteristics of this substance and to discuss its relation to various biological functions of vitamin C, mainly as an antioxidant barrier (we analysed product of reaction between phenothiazine derivative and L-ascorbic acid).

Antioxidants↗