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PubMed2006

A cerebroprotective dose of intravenous citrate/sorbitol-stabilized dehydroascorbic acid is correlated with increased cerebral ascorbic acid and inhibited lipid peroxidation after murine reperfused stroke.

OBJECTIVE: Oxidative damage has been implicated in the pathogenesis of cerebral ischemia. We previously demonstrated that exogenously supplied dehydroascorbic acid (DHA), an oxidized, blood-brain barrier transportable form of the antioxidant ascorbic acid (AA), improves outcome after experimental stroke. METHODS: To investigate the neuroprotective effect of DHA therapy, we measured cerebral AA levels using a novel assay, quantified markers of lipid peroxidation, and evaluated infarct volume after reperfused stroke in a murine model. All experiments were performed using a new citrate/sorbitol-stabilized DHA formulation to improve the stability of the compound. RESULTS: Intraparenchymal AA levels declined after cerebral ischemia/reperfusion and were repleted in a dose-dependent fashion by postischemic administration of intravenous DHA (P < 0.01). Repletion of these levels was associated with reductions in cerebral malondialdehyde levels (P < 0.05), which were also elevated after reperfused stroke. DHA repletion of interstitial AA levels and reduction in cerebral lipid peroxidation was associated with dose-dependent reductions in infarct volume (P < 0.05). CONCLUSION: Together, these results indicate that an intravenous cerebroprotective dose of citrate/sorbitol-stabilized DHA is correlated with increased brain ascorbate levels and a suppression of excessive oxidative metabolism.

Animals↗
PubMed1991

Ascorbic acid stimulation of collagen biosynthesis independent of hydroxylation.

Ascorbic acid stimulates collagen gene expression in cultured fibroblasts but mechanisms responsible for this effect are poorly understood. In the presence of the transitional metal iron, ascorbic acid could induce lipid peroxidation with the formation of reactive aldehydes. Because another aldehyde, acetaldehyde, the first metabolite of ethanol, also stimulates collagen transcription in cultured fibroblasts, we investigated whether ascorbic acid induces lipid peroxidation in cultured cells and if this is the mechanism by which ascorbic acid stimulates collagen gene expression. Ascorbic acid (0.2 mmol/L) induced lipid peroxidation and stimulated collagen alpha 1(I) gene transcription in cultured human fibroblasts. Inhibition of the ascorbic acid-induced lipid peroxidation in cultured human fibroblasts with alpha-tocopherol (50 mumol/L) or methylene blue (10 mumol/L) prevented the stimulation of collagen gene expression. Addition of malondialdehyde (200 mumol/L), a product of lipid peroxidation, to cultured human fibroblasts also increased two- to threefold collagen production and procollagen alpha 1(I) mRNA levels. Thus, ascorbic acid induces lipid peroxidation and reactive aldehydes, and this step may be necessary for stimulation of collagen gene expression by ascorbic acid in cultured human fibroblasts.

Ascorbic Acid↗
PubMed1991

Ascorbic acid in human neutrophils.

The uptake and distribution of ascorbic acid and the effect of extracellular glucose on ascorbic acid transport were investigated in human neutrophils. Freshly isolated neutrophils contained 1.0-1.4 mmol ascorbic acid/L, at least 94% of which was present unbound in the cytosol. Intracellular ascorbic acid was found only in the reduced form. The presence of physiologic amounts of ascorbic acid in the extracellular buffer led to the accumulation of millimolar concentrations of ascorbic acid intracellularly. Accumulation was mediated by a high- and a low-affinity transport activity. The high-affinity transport activity had an apparent Km of 2-5 mumol/L whereas the low-affinity transport activity had an apparent Km of 6-7 mmol/L. Glucose inhibited the uptake and accumulation of ascorbic acid by both transport activities in a concentration-dependent fashion. Glucose-induced inhibition of both ascorbic acid transport activities was completely reversible.

Ascorbic Acid↗
PubMed2004

The influence of sex hormones and vitamin E on ascorbic acid concentration in rat tissues.

Ascorbic acid concentration in a living body undergoes alterations continually. The changes in homeostasis of this important antioxidant may be induced by the effect of sex hormones for example. Based on this, the aim of our work was to estimate the influence of sex hormones administration and vitamin E supplementation on tissue ascorbic acid concentration in female and male rats. It has been showed that estrogen administration to females resulted in vitamin C loss, while testosterone administration to males elevated this level in all the tested tissues. However, the supplementation of vitamin E during sex hormones administration had beneficial effects on the tissue ascorbic acid concentration.

Animals↗
PubMed1984

Gamma-aminobutyric acid stimulates the release of endogenous ascorbic acid from rat striatal tissue.

Gamma-aminobutyric acid (GABA) was found to induce the release of ascorbic acid from rat striatal homogenates and minces. This release was studied with the use of a rapid superfusion system with an on-line amperometric detector that monitors for the presence of easily oxidized substances (i.e., ascorbate, 3,4-dihydroxyphenylethylamine). The release was found to be calcium-independent and depolarization-dependent. This releasable pool of ascorbate could be replenished through nonstereospecific uptake. The releasing action of GABA was mimicked by the GABA agonist, muscimol, and was completely inhibited by the GABA antagonist, picrotoxin. The structural analogues of GABA, beta-alanine and gamma-hydroxybutyric acid, had no effect. These data indicate that ascorbate release is GABA-receptor mediated and synaptically localized.

Animals↗
PubMed1986

Ascorbic acid promotes prostanoid release in human lung parenchyma.

Ascorbic acid reduces airway reactivity to inhaled bronchoconstrictor agents in man and guinea pigs. The precise mechanism(s) responsible for this effect are unknown, but in both species an acute indomethacin treatment reverses the action of the ascorbic acid. To determine if ascorbic acid promotes prostanoid synthesis and/or inhibits degradation, human lung parenchymal slices (100-200 mg) were incubated for 60 minutes in oxygenated Tyrode's solution alone or with sodium ascorbate (0.001 M-1 M) and/or methacholine (1 microM-100 microM) and/or indomethacin (0.17 microM-17 microM). Aliquots of the incubation medium were assayed by radioimmunoassay for PGE2, PGF2 alpha, thromboxane B2 and 6-keto-PGF1 alpha. Ascorbic acid increased the accumulation of all four prostanoids in the incubation medium, especially thromboxane B2 and 6-keto-PGF1 alpha. This stimulatory effect of ascorbic acid was concentration-dependent and was inhibited by indomethacin. We conclude that ascorbic acid can alter prostanoid generation by human lung tissue and this effect may, in part, explain its antibronchoconstrictor activity in man.

Ascorbic Acid↗
PubMed1990

[Mechanism of ascorbic acid transport in the aqueous humor].

The concentration of ascorbic acid in the aqueous humor in many species (including humans and oxen) is several times higher than the plasma concentration. The role of ascorbic acid as a protective mechanism in the intraocular tissues against light-induced damage is discussed. We have performed uptake studies using 14C-labeled ascorbic acid in cultured bovine pigmented ciliary epithelial cells in order to study the mechanisms for ascorbic acid transport from the ciliary body to the aqueous humor. We found that intracellular accumulation of ascorbic acid was Na(+)-dependent. Data from kinetic experiments suggest the presence of a co-transport system for 2 Na+ and 1 ascorbate. The oxidized form of the vitamin (dehydro-ascorbic acid, DHA) was taken up in the cell by a Na(+)-independent mechanism. Using thin-layer chromatographic assay, we found intracellularly only ascorbic acid after incubation with extracellular DHA, indicating the presence of DHA reductase activity in ciliary body epithelial cells. Thus, these cells possess two mechanisms for intracellular accumulation of ascorbic acid: (1) co-transport for 2 Na+ and 1 ascorbate and (2) a Na(+)-independent DHA transport in cooperation with intracellular DHA reductase. These mechanisms could be involved in the transport of ascorbic acid from the stroma to the aqueous humor.

Animals↗
PubMed2005

Metabolic clearance of the antioxidant ascorbic acid in surgical patients.

BACKGROUND: A reduction of plasma ascorbic acid concentration in the post-operative period has been well documented and is associated with an increase in post-operative complications. The underlying reason for the decreased concentration of ascorbic acid in the plasma is not clear. However, only an increased post-operative requirement for ascorbic acid would justify a substitution. Therefore, we investigated the pre-operative and post-operative metabolic clearance of ascorbic acid. MATERIALS AND METHODS: We calculated the metabolic clearance subsequent to intravenous bolus injection of 6 mg ascorbic acid/kg body weight in 15 patients before and after they underwent major maxillofacial surgery. Blood samples were taken before and 5, 15, 30, 45, 60, 90, 120, and 240 min after administration of ascorbic acid before and after the operation. Urine was collected. Ascorbic acid in plasma and urine was analyzed using a high performance liquid chromatographic technique. RESULTS: The pre-operative metabolic clearance was 7.6 +/- 2.22 l/h (mean +/- SD), increasing significantly to 12.1 +/- 4.87 l/h on the first post-operative day (P < 0.001). Doses of approximately 1150 mg ascorbic acid would be necessary to compensate for the observed loss and to raise plasma ascorbic acid to high normal values. CONCLUSIONS: There is a significantly increased post-operative metabolic clearance of ascorbic acid that might be considered when framing future dose recommendations in post-operative patients.

Adult↗
PubMedDate not supplied

Plasma vitamin C (ascorbic acid) levels in asthmatic children.

Plasma concentration of ascorbic acid was determined in fifty-one asthmatic children and a group of matched controls. The mean ascorbic acid level of 0.54 mg/100 ml among the asthmatics was significantly lower than a mean of 0.84 mg/100 ml for controls (P less than 0.001). Ascorbic acid level was directly related to the socio-economic class (SC) since asthmatic children from SC I, II and II had significantly higher ascorbic acid levels than those from SC IV and V. There was however, no relationship between the plasma ascorbic acid level and atopy, frequency of asthmatic attacks over the previous 12 months and the duration of asthma. It is postulated that if plasma ascorbic acid level was related to the susceptibility to viral respiratory tract infections, the observed low level of the vitamin in the asthmatics would make them more liable to such infections which are capable of precipitating acute asthmatic attacks. Confirmation of our results would indicate the need for regular ascorbic acid supplement in some children with bronchial asthma.

Adolescent↗
PubMed2005

Development and application of a novel UV method for the analysis of ascorbic acid.

A UV method for the analysis of ascorbic acid with methanol as solvent to prepare a sample has been developed and applied. The effect of copper(II) concentrations on the oxidation of ascorbic acid in aqueous solution has been studied in detail, and the regularities of ascorbic acid oxidation in methanol, USP phosphate buffer (pH 2.50) and de-ionized water have been found. Upon experiments ascorbic acid has been found to dissolve in methanol, and its solubility in it has been measured to be 81.0mg/ml at room temperature (22 degrees C). The ascorbic acid bulk material from a manufacturer has been assayed to be 89.34% with this method, in good agreement with the assay value (89.58%) from the titration method. The ascorbic acid granule and tablet content uniformity also has been tested using this method. This method is simple, rapid, accurate and reliable, and can be adopted for the routine determination of ascorbic acid in its granule and tablet formulations.

Ascorbic Acid↗
PubMed1990

Enhancement of hydroperoxide-dependent lipid peroxidation in rat liver microsomes by ascorbic acid.

Simultaneous addition of ascorbic acid and organic hydroperoxides to rat liver microsomes resulted in enhanced lipid peroxidation (approximately threefold) relative to incubation of organic hydroperoxides with microsomes alone. No lipid peroxidation was evident in incubations of ascorbate alone with microsomes. The stimulatory effect of ascorbate on linoleic acid hydroperoxide (LAHP)-dependent peroxidation was evident at all times whereas stimulation of cumene hydroperoxide (CHP)-dependent peroxidation occurred after a lag phase of up to 20 min. EDTA did not inhibit CHP-dependent lipid peroxidation but completely abolished ascorbate enhancement of lipid peroxidation. Likewise, EDTA did not significantly inhibit peroxidation by LAHP but dramatically reduced ascorbate enhancement of lipid peroxidation. The results reveal a synergistic prooxidant effect of ascorbic acid on hydroperoxide-dependent lipid peroxidation. The inhibitory effect of EDTA on enhanced peroxidation suggests a possible role for endogenous metals mobilized by hydroperoxide-dependent oxidations of microsomal components.

Animals↗
PubMed2004

Ascorbic acid and melatonin reduce heat-induced performance inhibition and oxidative stress in Japanese quails.

1. The effects of ascorbic acid (L-ascorbic acid) and melatonin supplementation on performance, carcase characteristics, malondialdehyde (MDA) as lipid peroxidation indicator, ascorbic acid, retinol, tocopherol and mineral status in the Japanese quail (Coturnix coturnix japonica) exposed to high ambient temperature were evaluated. 2. Two hundred and forty Japanese quails (10 d old) were randomly assigned to 8 treatment groups consisting of 10 replicates of three birds each. The birds were kept in a temperature-controlled room at 22 degrees C (Thermoneutral, TN groups) or 34 degrees C (for 8 h/d; 09:00 to 17:00 h; Heat stress, HS groups). Birds in both TN and HS were fed either a basal (control) diet or the basal diet supplemented with 250 mg of L-ascorbic acid/kg of diet (Ascorbic acid group), 40 mg of melatonin/kg of diet (Melatonin group) or both (Ascorbic acid + Melatonin group). 3. Supplementing heat-stressed quails with ascorbic acid and melatonin improved performance compared with the control group. Effects generally were greatest in quails supplemented with both ascorbic acid and melatonin. 4. Although supplementation did not consistently restore the concentrations of serum ascorbic acid, retinol and tocopherol to those of TN groups, these concentrations increased significantly with supplementation. Furthermore, serum and liver MDA and serum cholesterol and glucose concentrations were lower in the supplemented groups than in the heat-stressed controls. 5. Within each environment, excretion of Ca, P, Mg, Zn, Fe and Cr were lowest in the combination group and, in all cases, highest in the HS group. Interactions between diet and temperature were detected for live weight gain, cold carcase weight, MDA, ascorbic acid, tocopherol concentrations and excretion of zinc. 6. The results of the study indicate that ascorbic acid and melatonin supplementation attenuate the decline in performance and antioxidant and mineral status caused by heat stress and such supplementation may offer protection against heat-stress-related depression in performance of Japanese quails.

Animals↗
PubMed1988

Effects of ascorbic acid on trabecular meshwork cells in culture.

We examined the effects of ascorbic acid on trabecular meshwork cells in culture. Bovine trabecular meshwork cells were plated for 6 days and were exposed to media containing either no ascorbic acid or ascorbic acid in the following concentrations for 24 hr: 50-, 100-, 500-, and 750 micrograms ml-1. Fresh media were then added and incubation was continued for an additional 24 hr. The cell number was subsequently determined for the effects of the various concentrations of ascorbic acid on cell growth. In a parallel experiment, cells were labeled with [35S] sulfate (50 microCi ml-1) and [3H]glucosamine (15 microCi ml-1) for 24 hr with or without ascorbic acid for glycosaminoglycan studies. Results indicated that ascorbic acid stimulated the trabecular cell growth in culture at concentrations of 50-, 100-, and 250 micrograms ml-1. However, at 750 micrograms ml-1, cell growth was inhibited. In addition, cells exposed to 100 micrograms ml-1 of ascorbic acid demonstrated increased incorporation of [3H]glucosamine and [35S]sulfate; enhancement of incorporation of [35S]sulfate was also noted at 250 micrograms ml-1. Incorporation of labels was otherwise either unchanged or retarded at other concentrations. These data suggest that the ascorbic acid level in the aqueous humour may influence trabecular meshwork cell metabolism.

Animals↗
PubMed1980

Absorption of large, single, oral intakes of ascorbic acid.

A male non-smoking volunteer increased his daily intake of ascorbic acid continuously by ingesting in a single, oral dose 1, 2, 3, 4 and 5 g crystalline ascorbic acid. The dose was always kept constant for 2 days and was taken with breakfast. During the regimen of ascorbic acid ingestion blood samples were taken and all urine was collected. Then, with a 5 g dose of ascorbic acid 8.17 micro Ci (170 microgram) (1-14C)ascorbic acid was ingested. Following the labelled dose radioactivity was determined in plasma, urine, and faeces. Daily ingestion of 5 g ascorbic acid was continued for 10 days. During the whole experiment the ascorbic acid concentrations in plasma and in urine were determined. The urinary excretion of unmetabolized unlabelled ascorbic acid per day was taken as index for the absorption of ascorbic acid. It decreased from 75% (1 g), 44.0% (2 g), 39%, (3g), 28% (4 g) to 20% (5 g) of the ingested ascorbic acid. The linearisation of the relationship between ingested dose and the excreted amount in urine yielded a maximum amount of 1160 mg ascorbic acid which can be absorbed in 24 h under the conditions of the experiment. The experiment with (1-14C)ascorbic acid revealed that a single oral dose of 5 g ascorbic acid is absorbed to 22.2%, in the faeces collected up to 117 h following ingestion of label only 2.8% of the radioactivity could be recovered. Several possibilities are discussed regarding the fate of the remaining unabsorbed (1-14C)ascorbic acid.

Adult↗
PubMed2002

Blood pressure, hematologic and erythrocyte fragility changes in children suffering from sickle cell anemia following ascorbic acid supplementation.

The effect of ascorbic acid supplementation (100 mg/day for 6 weeks) on blood pressure, packed cell volume, irreversibly sickled cells, per cent fetal hemoglobin, hemoglobin concentration, and erythrocyte osmotic fragility was assessed in children suffering from sickle cell anemia. Fifteen children whose ages ranged from 4 to 11 years (7.5 +/- 0.75 years) were studied. Ascorbic acid supplementation reduced systolic blood pressure by 10.9 +/- 3.4 mmHg (p < 0.01), diastolic blood pressure by 7.3 +/- 2.0 mmHg (p < 0.01) and mean arterial pressure by 9.4 +/- 2.6 mmHg (p < 0.01). It significantly increased packed cell volume (p < 0.001), hemoglobin concentration (p < 0.001) and per cent fetal hemoglobin (p < 0.001), but reduced per cent irreversibly sickled cells (p < 0.001). Ascorbic acid supplementation also abolished the long tail of the erythrocyte osmotic fragiligram and increased the resistance of the cells to lysis.

Anemia, Sickle Cell↗
PubMed2000

Reduction of resuscitation fluid volumes in severely burned patients using ascorbic acid administration: a randomized, prospective study.

HYPOTHESIS: High-dose ascorbic acid (vitamin C) therapy (66 mg/kg per hour) attenuates postburn lipid peroxidation, resuscitation fluid volume requirements, and edema generation in severely burned patients. STUDY DESIGN AND SETTING: A prospective, randomized study at a university trauma and critical care center in Japan. SUBJECTS AND METHODS: Thirty-seven patients with burns over more than 30% of their total body surface area (TBSA) hospitalized within 2 hours after injury were randomly divided into ascorbic acid and control groups. Fluid resuscitation was performed using Ringer lactate solution to maintain stable hemodynamic measurements and adequate urine output (0.5-1.0 ml/kg per hour). In the ascorbic acid group (n = 19; mean burn size, 63% +/- 26% TBSA; mean burn index, 57 +/- 26; inhalation injury, 15/ 19), ascorbic acid was infused during the initial 24-hour study period. In the control group (n = 18; mean burn size, 53% +/- 17% TBSA; mean burn index, 47 +/- 13; inhalation injury, 12/18), no ascorbic acid was infused. We compared hemodynamic and respiratory measurements, lipid peroxidation, and fluid balance for 96 hours after injury. Two-way analysis of variance and Tukey test were used to analyze the data. RESULTS: Heart rate, mean arterial pressure, central venous pressure, arterial pH, base deficit, and urine outputs were equivalent in both groups. The 24-hour total fluid infusion volumes in the control and ascorbic acid groups were 5.5 +/- 3.1 and 3.0 +/- 1.7 mL/kg per percentage of burn area, respectively (P<.01). In the first 24 hours, the ascorbic acid group gained 9.2% +/- 8.2% of pretreatment weight; controls, 17.8% +/- 6.9%. Burned tissue water content was 6.1 +/- 1.8 vs 2.6 +/- 1.7 mL/g of dry weight in the control and ascorbic acid groups, respectively (P<.01). Fluid retention in the second 24 hours was also significantly reduced in the ascorbic acid group. In the control group, the ratio of PaO2 to fraction of inspired oxygen at 18, 24, 36, 48, and 72 hours after injury was less than that of the ascorbic acid group (P<.01). The length of mechanical ventilation in the control and ascorbic acid groups was 21.3 +/- 15.6 and 12.1 +/- 8.8 days, respectively (P<.05). Serum malondialdehyde levels were lower in the ascorbic acid group at 18, 24, and 36 hours after injury (P<.05). CONCLUSIONS: Adjuvant administration of high-dose ascorbic acid during the first 24 hours after thermal injury significantly reduces resuscitation fluid volume requirements, body weight gain, and wound edema. A reduction in the severity of respiratory dysfunction was also apparent in these patients.

Adolescent↗
PubMed1982

Human T-cell function in experimental ascorbic acid deficiency and spontaneous scurvy.

Studies in animal models suggest that ascorbic deficiency impairs T-cell-mediated immunity. We studied five normal volunteers hospitalized on a metabolic unit and consuming a strictly controlled diet deficient in ascorbic acid I) after a 5-wk control period of ascorbic acid supplementation (75 mg/day) and 2) after a 9-wk period of no supplementation. Three of the subjects were restudied after a 5-wk period of ascorbic acid supplementation after the deficient period. At the end of both control periods ascorbic acid levels in plasma ranged from 0.9 to 1.3 mg/dl and in leukocytes from 19 to 30 microgram/10(8) cells. At the end of the deficient period levels of ascorbic acid in plasma ranged from 0.09 to 0.15 mg/dl and in leukocytes from 6.2 to 10 microgram/10(8) cells, levels at or below those frequently found in frank scurvy. None of the T-cell parameters tested including mitogen responsiveness to phytohemagglutinin and percentage of T-cells bearing receptors for IgM (helper cells) and IgG (suppressor cells) was different in the deficient period compared to the control periods. One patient with spontaneous scurvy (plasma ascorbic acid 0.07 mg/dl, leukocytic ascorbic acid 4.9 microgram/10(8) cells) was studied at the time of admission and after vigorous ascorbic acid repletion. All T-cell parameters after repletion were unchanged from admission. We conclude that in man ascorbic acid deficiency, even at the scorbutic level, does not alter T-cell numbers or impair in vitro T-cell function.

Adult↗
PubMed1990

Ascorbic acid accumulation in plated human neutrophils.

Ascorbic acid uptake was investigated in isolated, plated human neutrophils using high-performance liquid chromatography with coulometric electrochemical detection. Freshly isolated neutrophils contained 1.3 mM ascorbic acid and accumulated significantly greater amounts when physiologic concentrations of the vitamin were present in the extracellular buffer. In several different buffers uptake was dependent on the presence of calcium and magnesium. Under these conditions, scintillation spectrometry of [14C]ascorbic acid in conjunction with high-performance liquid chromatography was suited for measuring ascorbic acid transport.

Ascorbic Acid↗