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PubMed1996

Long term administration of ascorbic acid does not improve a decreased bone weight and mineral content in rats with neonatally induced streptozotocin diabetes.

Adult female rats which were neonatally made diabetic with streptozotocin showed evidence of a pronounced decrease of dry weight, ash weight, calcium, phosphorus and ascorbic acid content in the femur, as compared with control rats. However, such diabetic rats receiving large doses of ascorbic acid (100 mg/kg/day) for 85 days did not show any improvement of the above measures in spite of normalization of bone ascorbic acid content. Thus, additional ascorbic acid given to diabetic rats with osteopenia restored bone ascorbic acid content but did not improve the bone loss resulting from chronic diabetes mellitus. Additional ascorbic acid given to intact rats did not show any additional effect on the increase of bone mass and mineral content.

Journal Article↗
PubMed1997

Flow injection fluorimetric determination of ascorbic acid based on its photooxidation by thionine blue.

The photooxidation of ascorbic acid sensitized by Thionine Blue was studied. The Leucothionine Blue formed during the reaction is highly fluorescent. A flow injection method using merging zones is proposed for the determination of ascorbic acid over a concentration range from 8 x 10(-7) to 5 x 10(-5) mol l-1 with a throughout of 80 samples per h. The method was used for the simple and rapid determination of ascorbic acid in pharmaceuticals, fruit juices and soft drinks.

Ascorbic Acid↗
PubMed1991

Ascorbic acid and the eye.

In this report literature on transport and function of ascorbic acid in ocular tissues is reviewed. The role of ascorbic acid in various regions of the eye is not well understood. It appears one important function of this compound is protection against oxidative damage, particularly photoinduced damage. In contrast, data are also reviewed that suggest ascorbic acid may participate in the oxidative modification of lens proteins seen with aging.

Aging↗
PubMed2002

[Ascorbic acid enhances the apoptosis of U937 cells induced by arsenic trioxide in combination with DMNQ and its mechanism].

OBJECTIVE: To investigate whether ascorbic acid could enhance the efficacy of arsenic trioxide (As(2)O(3)) combined with 2, 3-dimethoxy-1, 4-naphthoquinone (DMNQ) in inducing the apoptosis of leukemia cell line U937 and its possible mechanism. METHODS: Flow cytometry and electron microscopy were applied to detect apoptosis of U937 cells after treatment with various combinations of As(2)O(3), DMNQ and ascorbic acid for 24 hours. RESULTS: As(2)O(3) and DMNQ induced-apoptosis of U937 cells was enhanced (35.24%-->61.20%) upon cotreatment with ascorbic acid. Catalase could reverse this effect of DMNQ. Ascorbic acid had no effect on DMNQ-induced apoptosis of U937 cells. CONCLUSION: Ascorbic acid enhanced the apoptosis of U937 cells via reactive oxygen species-dependent pathway in the presence of As(2)O(3).

Apoptosis↗
PubMed2006

Direct effects of quercetin on impaired reactivity of spontaneously hypertensive rat aortae: comparative study with ascorbic acid.

1. There is a growing interest in the anti-oxidant characteristics and use of flavonoids in the management of cardiovascular diseases. The cardiovascular mechanism of action of these plant derivatives remains controversial. This study compared the effects of the flavonoid quercetin with those of the anti-oxidant vitamin ascorbic acid (vitamin C) on the reactivity of aortic rings from spontaneously hypertensive rats (SHR). 2. The phenylephrine (PE)-induced contractile and the endothelium-dependent and independent relaxant responses of aortic rings from 21 to 22 week old SHR and age-matched normotensive Wistar (WKY) rats were observed in the presence of quercetin or ascorbic acid. All the experiments were performed in the presence of the cyclooxygenase inhibitor, indomethacin (10 micromol/L). 3. The endothelium-dependent and independent relaxations to acetylcholine (ACh) and sodium nitroprusside (SNP), respectively, were significantly lesser in the SHR compared to the WKY tissues whereas the contractile responses to PE were similar in both tissues. Pretreatment of WKY rings with quercetin or ascorbic acid had no effect on the responses to ACh or PE. In the SHR tissues, however, quercetin or ascorbic acid significantly improved the relaxation responses to ACh and reduced the contractions to PE with greater potency for quercetin. Both compounds lacked any effects on the responses to SNP in either aortic ring types. N(omega)-nitro-L-arginine methyl ester (l-NAME, 10 micromol/L) significantly attenuated the vasodepressor effects of quercetin and ascorbic acid, raising the responses to PE to a level similar to that observed in the control SHR tissues. In l-NAME pretreated aortic rings, quercetin and ascorbic acid inhibited the contractile responses to PE with the same magnitude in WKY and SHR tissues. 4. The present results suggest that acute exposure to quercetin improves endothelium-dependent relaxation and reduces the contractile responses of hypertensive aortae with a greater potency than ascorbic acid. This suggests a better vascular protection with this flavonoid than ascorbic acid in the SHR model of hypertension and possibly in human cardiovascular diseases.

Acetylcholine↗
PubMed2001

Mechanisms of ascorbic acid recycling in human erythrocytes.

Vitamin C, or ascorbic acid, is efficiently recycled from its oxidized forms by human erythrocytes. In this work the dependence of this recycling on reduced glutathione (GSH) was evaluated with regard to activation of the pentose cycle and to changes in pyridine nucleotide concentrations. The two-electron-oxidized form of ascorbic acid, dehydroascorbic acid (DHA) was rapidly taken up by erythrocytes and reduced to ascorbate, which reached intracellular concentrations as high as 2 mM. In the absence of D-glucose, DHA caused dose-dependent decreases in erythrocyte GSH, NADPH, and NADH concentrations. In the presence of 5 mM D-glucose, GSH and NADH concentrations were maintained, but those of NADPH decreased. Reduction of extracellular ferricyanide by erythrocytes, which reflects intracellular ascorbate recycling, was also enhanced by D-glucose, and ferricyanide activated the pentose cycle. Diethylmaleate at concentrations up to 1 mM was found to specifically deplete erythrocyte GSH by 75-90% without causing oxidant stress in the cells. Such GSH-depleted erythrocytes showed parallel decreases in their ability to take up and reduce DHA to ascorbate, and to reduce extracellular ferricyanide. These results show that DHA reduction involves GSH-dependent activation of D-glucose metabolism in the pentose cycle, but that in the absence of D-glucose DHA reduction can also utilize NADH.

Ascorbic Acid↗
PubMed2004

Alpha-tocopherol and ascorbic acid decrease the production of beta-apo-carotenals and increase the formation of retinoids from beta-carotene in the lung tissues of cigarette smoke-exposed ferrets in vitro.

Previously, we found that exposing ferrets to cigarette smoke enhanced oxidative excentric cleavage of beta-carotene. In the present study, we examined whether alpha-tocopherol, ascorbic acid, or the two combined can prevent smoke-altered beta-carotene metabolism. In vitro incubation of beta-carotene (10 micro mol/L) with lung postnuclear fractions from ferrets exposed to cigarette smoke was carried out in the absence or presence of alpha-tocopherol (50 micro mol/L), ascorbic acid (10 or 50 micro mol/L), or both vitamins to evaluate their effects on the production of beta-apo-carotenals and retinoids from beta-carotene. The oxidative cleavage metabolites of beta-carotene, beta-apo-carotenals (beta-apo-14', beta-apo-12', beta-apo-10', and beta-apo-8'), retinoic acid (RA), and retinal were analyzed by HPLC. We found that the smoke-enhanced production of individual beta-apo-carotenals was significantly decreased by 36-77% when alpha-tocopherol (50 micro mol/L) and ascorbic acid (50 micro mol/L) were added together to the incubation mixture. alpha-Tocopherol alone had a modest effect. Ascorbic acid in the presence of alpha-tocopherol inhibited the production of beta-apo-carotenals in a dose-dependent manner, although ascorbic acid alone had no effect. In contrast, the production of RA and retinal among smoke-exposed ferrets was substantially increased ( approximately 3-fold, P < 0.05) when both alpha-tocopherol and ascorbic acid were added to the incubation mixtures. However, when ascorbic acid or alpha-tocopherol alone was added, the production of RA among smoke-exposed ferrets increased only modestly (80%, P < 0.05) and did not differ from the RA levels in control ferrets. In conclusion, these data indicate that alpha-tocopherol and ascorbic acid may act synergistically in preventing the enhanced oxidative excentric cleavage of beta-carotene induced by smoking exposure, thereby facilitating the conversion of beta-carotene into RA and retinal.

Analysis of Variance↗
PubMed1993

Ascorbic acid accumulation and transport in human fibroblasts.

As the initial step in the use of fibroblasts as a model system for 'in situ kinetics', ascorbic acid (vitamin C) accumulation in normal human fibroblasts was investigated for the first time. Ascorbic acid was transported into fibroblasts and accumulated against a concentration gradient up to 20-fold, as measured by h.p.l.c. with coulometric electrochemical detection. Ascorbic acid accumulation was mediated by two concentration-dependent transport activities. The first was a high-affinity activity with an apparent Km of 6 microM and an apparent Vmax. of 203 microM/h, and the second was a low-affinity activity with an apparent Km of 5 mM and an apparent Vmax. of 1.8 mM/h. Both activities were inhibited by metabolic inhibitors and inhibitors of ascorbic acid transport in human neutrophils. The low-affinity transporter could not be accounted for by diffusion. Although the high-affinity transport activity was comparable with that described for human neutrophils, the low-affinity transporter was different. These data provide the first evidence that two-component ascorbic acid transport may be a generalized mechanism for accumulation of this vitamin in humans.

2,4-Dinitrophenol↗
PubMed1983

The effect of ascorbic acid on plasma sulfate conjugated catecholamines after eating bananas.

The effects of eating bananas, a rich source of biogenic amines, on the plasma concentration of free and sulfate conjugated norepinephrine (NE) and dopamine (DA), and free epinephrine (E), were examined in normal male subjects before and after treatment with ascorbic acid, 2 g daily for 7 days. There were no significant changes in the levels of free NE or E in any subjects after eating a banana, either before or after ascorbic acid. Plasma free DA became detectable in some subjects, but the overall changes were not significant. Sulfate conjugated DA and NE increased markedly after banana ingestion, as previously demonstrated in our laboratory. After ascorbic acid treatment the rise in sulfate conjugated NE was attenuated, presumably because ascorbic acid acts as a competitive inhibitor of sulfate conjugation. In contrast, the rise in conjugated DA was potentiated after ascorbic acid treatment. This may be indicative of the higher affinity of DA for phenolsulfotransferase, an inhibitory effect of ascorbic acid on dopamine-receptor coupling or of ascorbic acid protecting DA from oxidation in the gut.

Adult↗
PubMed1981

Ineffectiveness of intravenous ascorbic acid as an acidifying agent in man.

The acidifying effect of intravenous (IV) ascorbic acid was studied in seven healthy adult volunteers. After obtaining baseline urine and blood samples, 2-g IV doses of ascorbic acid were administered to each subject during a 20-minute period. Venous blood samples were obtained at times 0.5, 1, and 2 hours, and urine was collected at times 0.5, 1, 2, and 3 hours. Our results show that venous blood pH, plasma bicarbonate concentration, urine PCO2, and urine bicarbonate excretion did not change significantly during the study period. Urinary titratable acidity, ammonium excretion, and net hydrogen ion excretion decreased, and urinary pH actually showed a significant rise at two hours. We therefore conclude that IV ascorbic acid administered in recommended doses does not effectively acidify urine.

Acid-Base Equilibrium↗
PubMed1979

[Effect of dibasol and ascorbic acid on the antiviral activity of human interferon in cell culture].

The antiviral effect of human lymphocytic interferon was studied in the primary culture of human embryonic fibroblasts in the presence of dibazol and ascorbic acid. It was found that dibazol and ascorbic acid in concentrations of 5 and 10 gamma/ml respectively were capable of increasing the antiviral effect of human interferon in homological cells. The assays of 13 lots of interferon showed that its average titer in the experiments with ascorbic acid was 2.5 times higher than that in the control. The assays of 21 lots of interferon showed that its average titer in the experiments with dibazol was 3 times higher than that in the control. It is suggested that an increase in the protective properties of interferon in the presence of dibazol and ascorbic acid is connected with their capacity for stimulating the intracellular production of DNA and protein. The data obtained indicate that dibazol and ascorbic acid may be recommended in the complex of therapy and prophylaxis of antiviral infections.

Antiviral Agents↗
PubMed1999

Effect of topical ascorbic acid on free radical tissue damage and inflammatory cell influx in the cornea after excimer laser corneal surgery.

OBJECTIVE: To evaluate the effect of topical ascorbic acid on oxygen free radical tissue damage and the inflammatory cell influx in the cornea after excimer laser keratectomy. METHODS: Five New Zealand white rabbits underwent bilateral phototherapeutic keratectomy with the 193-nm argon fluoride excimer laser. Following treatment, the right eye of each rabbit was treated with 10% ascorbic acid every 3 hours for 24 hours. The left eyes served as controls. After 24 hours, all animals were killed and their corneas were trephined and processed. Sections were stained with fast blue B and with hematoxylin-eosin. Oxidative tissue damage in the form of lipid peroxidation was detected by fluorescent peroxidized carbonyl compounds using a confocal laser scanning microscope. The quantity of these compounds was determined using the National Institutes of Health digital image analysis system. Statistical comparisons of lipid peroxidation and polymorphonuclear cell count between the ascorbic acid groups and the controls were performed using the Student t test. RESULTS: Lipid peroxidation and polymorphonuclear cell counts were significantly decreased in the superficial cornea of ascorbic acid-treated eyes compared with control eyes (P <.03 and <.02, respectively). CONCLUSIONS: Topical ascorbic acid application decreased oxygen radical tissue damage following excimer keratectomy; moreover, topical application of ascorbic acid was shown to reduce the acute inflammatory reaction efficiently. This suggests that topical ascorbic acid could be considered a complementary treatment in the pharmacological modulation after excimer laser corneal surgery. CLINICAL RELEVANCE: Corneal opacity may complicate excimer keratectomy. The use of an antioxidant to reduce tissue damage could help minimize postoperative stromal opacification.

Administration, Topical↗
PubMed1981

Ascorbic acid treatment in nephropathic cystinosis in identical twins.

Metabolic studies were performed on two HLA identical 9 1/2-year-old twins with nephropathic cystinosis during 14 months' participation in a double-blind study to evaluate ascorbic acid treatment for cystinosis. Replacement therapy was identical in both children throughout the study except for the use of ascorbic acid. Leukocyte cystine content was markedly abnormal and elevated in both children prior to, during, and after the ascorbic acid study. We postulate that the lack of improvement in growth or chemical parameters in the twin treated with ascorbic acid was due to the ineffectiveness of ascorbic acid in decreasing intracellular cystine content.

Amino Acids↗
PubMed1993

Ascorbic acid and collagen synthesis: rethinking a role for lipid peroxidation.

Ascorbic acid positively affects the synthesis of collagen, the most abundant extracellular protein. The mechanism by which ascorbate mediates the increased synthesis is debated. One recent hypothesis suggests that ascorbic acid induces an increase in lipid peroxidation and that this increase, in some manner, up-regulates collagen gene expression. Evidence is presented that indicate increases in lipid peroxidation [thiobarbituric acid (TBA)-reactive material] is coincidental to collagen increases in ascorbate-treated cells, not a causal factor. Thus, cell impermeable iron chelators totally abolish ascorbate-mediated lipid peroxidation but do not affect collagen synthesis in the least. Decreases in TBA-reactive products seen at higher ascorbate levels (indicative of the well known pro- to antioxidant conversion of ascorbate in vitro) are paralleled by decreases in collagen synthesis. The decrease seen in collagen is completely reversed by treatment of the cell cultures with superoxide dismutase and catalase while the measure of lipid peroxidation is unaffected by coincubation with these antioxidant enzymes. Additionally, incubation conditions used to measure ascorbate induction of TBA-reactive material (buffers vs media, adherent vs detached cells) were found to be very important and results support the thesis that lipid peroxidation and collagen synthesis can be dissociated. While these results do not rule out a role for lipid mediators in regulating collagen synthesis at some level, they suggest this mechanism need not be involved for collagen increases seen in ascorbic acid-treated cells.

Ascorbic Acid↗
PubMed1982

Effect of large doses of ascorbic acid on the mixed function oxidase system in guinea pig liver.

Reports of the beneficial effects of large doses of ascorbic acid have stressed its water solubility and non-toxic properties. In this study male guinea pigs, dosed with 150 mg twice daily, ascorbic acid, demonstrated no differences in effect on liver weight, body weight or hepatic total protein when compared with controls. The activities of NADPH-dependent cytochrome c reductase, N-demethylase (Type I) and O-de-ethylase enzymes (Type II) remained unaffected, but the activity of the Type I hydroxylating enzyme, biphenyl-4-hydroxylase, and the amounts of cytochromes P-450 and b5 were significantly reduced. Total microsomal haem proteins were reduced and mirrored the effects in cytochromes P-450 and b5. The rate-limiting enzyme in haem synthesis, delta-amino-laevulinic acid synthetase, rose in the ascorbic acid group and this was associated with a fall in activity of the haem degrading enzyme, microsomal haem oxygenase. Thus, large amounts of ascorbic acid have similar effects to those found in scorbutic animals and appear to interfere with the construction of the cytochrome P-450 molecule.

Animals↗
PubMed2003

Ascorbic acid does not improve endothelium-dependent flow-mediated dilatation of the brachial artery in patients with Raynaud's phenomenon secondary to systemic sclerosis.

Previous studies have shown that patients with Raynaud's phenomenon secondary to systemic sclerosis present abnormal endothelial function; the mechanisms responsible for the endothelial dysfunction are unknown but increased vascular oxidative stress could be a possible cause. The hypothesis that a potent water-soluble antioxidant can reverse endothelial dysfunction in these patients was tested in the present study. We examined 11 female patients with Raynaud's phenomenon secondary to systemic sclerosis and ten healthy control women by ultrasound imaging of the brachial artery to assess flow-mediated (endothelium-dependent) and nitrate-induced (endothelium-independent) vasodilatation. Flow-mediated dilatation and nitrate-induced dilatation were significantly reduced in patients with Raynaud's phenomenon, indicating abnormal endothelial and smooth muscle cell function. Patients with Raynaud's phenomenon entered a double-blind, randomized, crossover placebo-controlled trial and received orally 2 g of ascorbic acid or placebo; vascular studies were repeated two hours after ascorbic acid or placebo administration. Flow-mediated dilatation did not improve after ascorbic acid (1.6 +/- 2.2% to 2.2 +/- 2.5%, ns) or placebo administration (1.2 +/- 1.9% to 1.7 +/- 1.4%, ns); also nitrate-induced dilatation was similar after ascorbic acid or placebo (16 +/- 7.4% vs 17 +/- 8%, ns), suggesting no effect of ascorbic acid on endothelial and vascular smooth muscle function. In conclusion, ascorbic acid does not reverse endothelial vasomotor dysfunction in the brachial circulation of patients with Raynaud's phenomenon secondary to systemic sclerosis. The use of different antioxidants or different dosing of ascorbic acid may be required to show a beneficial effect on endothelial vasodilator function.

Administration, Oral↗
PubMed1996

Effects of morphine treatment and withdrawal on striatal and limbic monoaminergic activity and ascorbic acid oxidation in the rat.

Since ascorbic acid (AA) reportedly suppresses tolerance to and dependence on morphine in humans and rodents, levels of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 3-methoxytyramine (3-MT), 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), AA, dehydroascorbic acid (DHAA), uric acid, xanthine, hypoxanthine, glutamate and gamma-aminobutyric acid (GABA) were determined by high-pressure liquid chromatography (HPLC) in the striatum and in the limbic forebrain of the rat following morphine treatment (single or repeated) and withdrawal. Single morphine administration (20 mg/kg s.c.) increased DOPAC + HVA/DA, 5-HIAA/5-HT and DHAA/AA ratios, uric acid levels, and decreased xanthine, hypoxanthine, glutamate and GABA levels in both regions. 3-MT levels were decreased in the striatum and increased in the limbic forebrain. After 7 days of morphine treatment, striatal DOPAC + HVA/DA and DHAA/AA ratios and uric acid levels were still higher and striatal and limbic xanthine levels still lower than in controls, while all other parameters were in the range of control values in both regions. Morphine treatment also increased the glutamate/GABA ratio in the striatum. In all morphine-treated rats, individual striatal DOPAC + HVA/DA and DHAA/AA ratio values were directly correlated. After a 48 h withdrawal period, both striatal AA oxidation and glutamate/GABA ratio further increased; limbic 3-MT levels further decreased, while all other parameters did not differ from control values. We conclude that: (i) tolerance to morphine-induced increase in hypoxanthine, xanthine and AA oxidation develops in the limbic forebrain faster than in the striatum; (ii) the morphine-induced increase in striatal and limbic AA oxidation may be considered a consequence of increased formation of reactive oxygen species due to increased DA, hypoxanthine and xanthine oxidative metabolism; (iii) a striatal excitotoxic imbalance characterizes the withdrawal state and may be taken into account to explain the further increase in striatal AA oxidation.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Ascorbic acid requirements for smokers: analysis of a population survey.

The recommended dietary allowance (RDA) of ascorbic acid for smokers was recently increased from 60 to 100 mg. To determine whether this new RDA for smokers is sufficient to reduce the risk of low serum ascorbic acid (AA) concentrations (LoC) to the same concentration as nonsmokers, we analyzed the dietary intakes and serum concentrations of AA in 11,582 adult respondents in the National Health and Nutrition Examination Survey (1976-1980). Serum AA concentrations and the risk of LoC (serum ascorbic acid levels less than 23 mumol/L) for smokers consuming different amounts of AA were compared with those for nonsmokers whose AA intake exceeded the RDA (60 mg). Serum AA concentrations were reduced, and risk of LoC increased, in smokers maintaining AA intakes greater than 60, 100, and 150 mg. Only smokers consuming greater than 200 mg AA/d had serum ascorbate concentrations and risk of LoC equivalent to nonsmokers meeting the RDA.

Adult↗