SEARCH · Search PubMed

Results for “ASCORBIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 829 records · Page 46Linked to original sources

PubMed2003

Detection of in vivo genotoxicity of endogenously formed N-nitroso compounds and suppression by ascorbic acid, teas and fruit juices.

The genotoxicity of endogenously formed N-nitrosamines from secondary amines and sodium nitrite (NaNO(2)) was evaluated in multiple organs of mice, using comet assay. Groups of four male mice were orally given dimethylamine, proline, and morpholine simultaneously with NaNO(2). The stomach, colon, liver, kidney, urinary bladder, lung, brain, and bone marrow were sampled 3 and 24 h after these compounds had been ingested. Although secondary amines and the NaNO(2) tested did not yield DNA damage in any of the organs tested, DNA damage was observed mainly in the liver following simultaneous oral ingestion of these compounds. The administration within a 60 min interval also yielded hepatic DNA damage. It is considered that DNA damage induced in mouse organs with the coexistence of amines and nitrite in the acidic stomach is due to endogenously formed nitrosamines. Ascorbic acid reduced the liver DNA damage induced by morpholine and NaNO(2). Reductions in hepatic genotoxicity of endogenously formed N-nitrosomorpholine by tea polyphenols, such as catechins and theaflavins, and fresh apple, grape, and orange juices were more effective than was by ascorbic acid. In contrast with the antimutagenicity of ascorbic acid in the liver, ascorbic acid yielded stomach DNA damage in the presence of NaNO(2) (in the presence and absence of morpholine). Even if ascorbic acid acts as an antimutagen in the liver, nitric oxide (NO) formed from the reduction of NaNO(2) by ascorbic acid damaged stomach DNA.

Animals↗

PubMed2000

Inhibition of purified soluble guanylyl cyclase by L-ascorbic acid.

OBJECTIVE: L-Ascorbic acid has been described to exert multiple beneficial effects in cardiovascular disorders associated with impaired nitric oxide (NO)/cGMP signalling. The aim of the present study was to investigate the effect of vitamin C on the most prominent physiological target of endogenous and exogenous NO, i.e. soluble guanylyl cyclase (sGC). METHODS: To address this issue we used a highly purified enzyme preparation from bovine lung (from the slaughterhouse). Enzymic activity was measured by a standard assay based on the conversion of [alpha-32P]GTP to [32P]cGMP and the subsequent quantification of the radiolabelled product. NO was quantified using a commercially available Clark-type electrode. RESULTS: Stimulation of sGC by the NO donor 2, 2-diethyl-1-nitroso-oxyhydrazine was inhibited by ascorbate with an IC(50) of approximately 2 microM. Maximal enzyme inhibition ( approximately 70%) was observed at 0.1-1 mM vitamin C. Stimulation of sGC by the NO-independent activator protoporphyrin-IX was also inhibited with similar potency. The effect of ascorbate on sGC was largely antagonised by reduced glutathione (1 mM) and the specific iron chelator diethylenetriaminepentaacetic acid (0.1 mM). Electrochemical experiments revealed that NO is potently scavenged by vitamin C. Consumption of NO by ascorbate was prevented by reduced glutathione (1 mM), diethylenetriaminepentaacetic acid (0.1 mM) and superoxide dismutase (500 units/ml) whereas up to 5000 units/ml superoxide dismutase failed to restore sGC activity. CONCLUSIONS: Our results suggest that physiological concentrations of L-ascorbic acid diminish cGMP accumulation via both scavenging of NO and direct inhibition of sGC.

Animals↗

PubMed2005

Variation in ascorbic acid and oxalate levels in the fruit of Actinidia chinensis tissues and genotypes.

Ascorbic acid and total oxalate were measured in fruit from six genotypes of Actinidia chinensis. Ascorbic acid was separated from oxalate in fruit extracts by HPLC and quantified from absorbance at 245 nm, whereas oxalate was measured enzymatically in the HPLC eluate. Levels of whole fruit mean ascorbic acid in the different genotypes ranged from 98 to 163 mg/100 g of fresh weight (FW), whereas mean oxalate varied between 18 and 45 mg/100 g of FW. Ascorbic acid was highest in the inner and outer pericarp, whereas oxalate was concentrated in the skin, inner pericarp, and seed. Essentially no ascorbic acid was found in the seed. Each tissue clustered separately when the tissue ascorbic acid and oxalate data were normalized to the whole fruit level of ascorbic acid and oxalate in that genotype and plotted against each other, suggesting that oxalate is not a sink for excess ascorbic acid but that oxalate formation is regulated.

Actinidia↗

PubMed1976

Compatibility of penicillin and ascorbic acid injection.

The stability of Potassium Penicillin G, USP, when mixed with Ascorbic Acid Injection, USP, in 5% Dextrose Injection, USP, was studied. The change in concentration over an eight-hour period of potassium penicillin G in the admixture was determined by the hydroxylamine colorimetric assay method and the microbiological assay method. The stability of penicillin was not adversely affected by the presence of sodium ascorbate. Reports of incompatibilities between penicillin and ascorbic acid are a function of pH rather than a characteristic of the ascorbate ion. Articles reporting studies involving ascorbic acid should specify whether the work refers to the use of ascorbic acid or Ascorbic Acid Injection, USP. Confusion in the literature could be reduced by changing the official title from Ascorbic Acid Injection to Sodium Ascorbate Injection.

Ascorbic Acid↗

PubMed1983

Lack of effect of experimental ascorbic acid deficiency on bile acid metabolism, sterol balance, and biliary lipid composition in man.

Extensive studies in animal models indicate that subclinical ascorbic acid deficiency impairs the conversion of cholesterol to bile acid, elevates plasma cholesterol levels, and predisposes to development of cholesterol cholelithiasis. The present study was designed to see if this is also true in man. Five normal volunteers were hospitalized in a metabolic ward and placed on a controlled diet containing 3-4 mg of ascorbic acid each day. Ascorbic acid supplementation was given as follows: control period I (days 1-33), 75 mg/day; deficient period (days 34-96), 0 mg/day; and repletion period (days 97-101), 1000 mg/day. In addition, three of the subjects were studied during a second control period (days 102-139) during which they were given 75 mg/day of ascorbic acid. Ascorbate levels at the end of both control periods were 0.87-1.34 mg/dl in plasma and 19.4-29.5 micrograms/10(8) cells in leukocytes. At the end of the deficient period these levels were 0.09-0.15 mg/dl in plasma and 6.2-10.0 micrograms/10(8) cells in leukocytes, levels approaching those seen in scurvy. There was no effect of ascorbic acid deficiency on plasma cholesterol and triglycerides; plasma cholesterol in high, very low, and low density lipoprotein fractions; biliary lipid composition and saturation index of gallbladder bile; synthesis, fractional turnover, or pool size of either cholic or chenodeoxycholic acids; output of fecal acid or neutral sterols; and fecal sterol balance. Total bile acid pool size calculated by the one-sample technique was reduced 11% in the deficient period compared to control period I (P less than 0.005), and increased to 98.7% of the baseline levels in control period II. However, total bile acid pool calculated by the Lindstedt method did not change during deficiency. These data demonstrate that short-term subclinical ascorbic acid deficiency near the scorbutic range has no significant effect on bile acid and cholesterol metabolism in man.

Adult↗

PubMed1997

The mechanism of the relaxing effect of ascorbic acid in guinea pig isolated tracheal muscle.

1. The effect of ascorbic acid was studied in the guinea pig isolated tracheal muscle. 2. Ascorbic acid with relatively higher concentrations produced a dose-dependent relaxation in tracheal muscle submaximally precontracted with KCl, histamine, and carbachol. 3. Removing the epithelium did not significantly alter the relaxing effect of ascorbic acid in histamine- and KCl-precontracted strips. 4. The relaxing effect of ascorbic acid is stronger in carbachol-precontracted epithelium-denuded strips than in epithelium-intact strips. 5. Indomethacin, but not L-NAME, partially inhibited the relaxing effect of ascorbic acid. 6. These results indicate that the relaxation induced by ascorbic acid in guinea pig isolated tracheal muscle does not fully depend on the presence of epithelium but is partially mediated by the production of prostanoids from smooth muscle.

Animals↗

PubMed1987

Effect of ascorbic acid on brain amphetamine concentrations in the rat.

Ascorbic acid is reported to have antiamphetamine effects in rodents. The effect of ascorbic acid (1 g/kg ip) on the half-life of amphetamine (10 mg/kg) in rat brain using 3H-amphetamine and on amphetamine-induced stereotyped behaviour was investigated. Ascorbic acid had no effect on amphetamine-induced stereotyped behaviour or on the half-life of amphetamine in brain. If ascorbic acid antagonizes amphetamine-induced behavioural responses this is unlikely to be a result of altering the pharmacokinetics of amphetamine.

Amphetamine↗

PubMed1976

Effects of L-lysine administration on certain aspects of ascorbic acid metabolism.

The effects of administration of L-lysine on total ascorbic acid level of various tissues and plasma of rats were studied. The biosynthesis of L-ascorbic acid by the liver tissue was also followed. L-lysine was administered at a dose of 88.3 mg day-1 (20% of LD50) for each 100 g body weight for 14 days. L-lysine administration at the present dose elevated the total ascorbic acid level of liver, kidney, testes, spleen and brain tissues. The plasma total ascorbic acid level was also elevated. The synthesis of L-ascorbic acid from both D-glucuronolactone and L-gulonolactone by the liver was, however, reduced after L-lysine administration. It has been suggested that L-lysine administration at the present dose altered the plasma amino acid pattern which in turn impaired the in vivo synthesis of tissue proteins and, consequently, the synthesis of apoproteins of ascorbic acid-synthesizing enzymes, the D-glucuronoreductase and L-gulonooxidase, were reduced. The elevation in the total ascorbic acid level of extra-hepatic tissues and plasma after L-lysine administration was ascribed to the reduced catabolism and diminished urinary excretion of ascorbic acid.

Animals↗

PubMed2003

Ascorbic acid concentrations in dimethylnitrosamine-induced hepatic fibrosis in rats.

BACKGROUND: Ascorbic acid is a potent antioxidant and is involved in many metabolic activities including collagen biosynthesis. In the present investigation, ascorbic acid and lipid peroxides were monitored in the blood and liver samples during the progression of experimentally induced hepatic fibrosis. METHODS: Liver injury was induced by intraperitoneal injections of dimethylnitrosamine (DMN) on three consecutive days of every week over a period of 21 days. The progression of fibrosis was assessed by histopathological examination and by monitoring of the collagen content of the liver tissue. Ascorbic acid and lipid peroxides were monitored in both blood and liver samples on days 0, 7, 14, and 21 after the start of DMN administration. The liver total protein was also measured during the investigation. RESULTS: Histopathological examination demonstrated centrilobular necrosis, fibrosis, and early cirrhosis during DMN treatment. The collagen content increased four-fold on the 21st day of investigation. Lipid peroxides were elevated significantly in both blood and liver specimens on days 7, 14, and 21. A drastic decrease was observed in the ascorbic acid concentrations in both liver and blood samples on all days after the start of DMN administration. Liver total protein concentrations were significantly reduced during DMN administration. CONCLUSIONS: The exact mechanism of the decrease of ascorbic acid during DMN-induced hepatic fibrosis is not clear. The most probable reason for the decreased blood and liver ascorbic acid during DMN-induced hepatic fibrosis is the increased utilization of ascorbic acid for free radical scavenging in order to reduce the highly elevated oxidative stress.

Animals↗

PubMed1999

Inhibition by ascorbic acid of apoptosis induced by oxidative stress in HL-60 myeloid leukemia cells.

The human myeloid leukemia cell line HL-60 transports the oxidized form of ascorbic acid, dehydroascorbic acid (DHA), and accumulates reduced ascorbic acid. We studied the effect of ascorbic acid loading on apoptosis induced by serum- and glucose-free culture and by oxidative stress induced by H2O2. Uptake accumulation studies indicated that incubation of HL-60 cells with DHA resulted in the accumulation of intracellular ascorbic acid which decreased with time when cells were incubated in DHA-free medium. Exposure of HL-60 cells to increasing concentrations of H2O2 resulted in dose-dependent intracellular accumulation of peroxides, as determined by the use of the oxidation-sensitive fluorescent probe 2',7'-dichlorofluorescin-diacetate (DCFH-DA), which was accompanied by a decrease in intracellular ascorbic acid and an increase in apoptosis. A dramatic decrease in intracellular ascorbic acid was noted when preloaded HL-60 cells were exposed to 150 microM H2O2 (the concentration dropped from 5.2 +/- 0.6 mM to 3.6 +/- 0.1 mM in cells preincubated with 150 microM DHA). A dose-dependent protective effect of DHA was observed. Ascorbic acid loading also provided strong protection from apoptosis associated with serum- and glucose-free culture. Flow cytometry studies showed that exposure of HL-60 cells to 150 microM H2O2 resulted in decreased Bcl-2 expression that was associated with enhanced apoptosis (up to 33.6 +/- 2.6%). No significant variation of Bcl-2 expression was measured following exposure of HL-60 cells, loaded with ascorbic acid, to 150 microM H2O2 and only a slight increase (up to 10.1 +/- 3.1%) in apoptosis. These findings indicate that ascorbic acid can inhibit apoptosis induced by oxidative stress in HL-60 cells.

Antioxidants↗

PubMed2001

beta-Carotene: interactions with alpha-tocopherol and ascorbic acid in microsomal lipid peroxidation.

beta-Carotene, alpha-tocopherol, and ascorbic acid were tested for their ability to inhibit, enhance, or react synergistically with O(2) (15, 150, 760 torr) and, 2,2'-azobis (2-amidino-propane) dihydrochloride (AAPH) or 1,1'-azobis (cyclohexane-carbonitrile) (ACCN) in isolated rat liver microsomes. beta-Carotene did not protect against lipid peroxidation, i.e., malondialdehyde (MDA) formation, in microsomal samples incubated at 37 degrees C with aqueous soluble AAPH at all added beta-carotene concentrations and oxygen tensions. More MDA (16%, p < 0.001) was produced at 15 torr of O(2,) and 160 nmol/mg protein of beta-carotene compared to respective vehicle control. Individually, alpha-tocopherol and ascorbic acid exhibited antioxidant protection (ascorbic acid &z.Gt; alpha-tocopherol); however, a mixture of both compounds was no more protective than ascorbic acid alone. beta-Carotene demonstrated a concentration-dependent antioxidant affect at 15 torr O(2) (p < 0.01); but a prooxidant effect at higher O(2) at 150 and 760 torr (>57%, p < 0.001) by lipid-soluble ACCN. alpha-Tocopherol exhibited concentration-dependent inhibitory effects on microsomal MDA formation at all oxygen tensions, but was most effective under 150 torr. Ascorbic acid demonstrated a concentration-dependent antioxidant effect only at 150 torr. ACCN-induced lipid peroxidation was no greater for the combination of the three compounds than ascorbic acid added alone. Thus, antioxidant or prooxidant activities for beta-carotene, alpha-tocopherol, and ascorbic acid in microsomal suspensions are related to O(2) tension, solubility, antioxidant concentrations and are governed by complex interactions. Differences between AAPH- and ACCN-induced lipid peroxidation are related to differences in lipid solubility.

Journal Article↗

PubMed2002

Stability of ascorbic acid in serum and plasma prior to analysis.

INTRODUCTION: The stability of ascorbic acid in serum and plasma prior to analysis was studied. METHODS: Blood samples were collected from ten healthy subjects into Vacutainer tubes containing either dipotassium EDTA, lithium-heparin or no additive. Ascorbic acid was analysed following immediate separation and preservation of samples, following delayed separation for 2 h and after delayed deproteinization and preservation for 2, 5 and 8 h. Deproteinization and preservation were achieved using a solution containing perchloric acid, EDTA and dithiothreitol. Ascorbic acid was analysed by high-performance liquid chromatography. RESULTS: Blood collected into EDTA and separated, deproteinized and preserved immediately gave the highest yield of ascorbic acid. Loss of analyte after delayed separation was least for EDTA tubes (median 7%, range 4-13%), followed by lithium-heparin (median 18%, range 10-32%) and serum (median 26%, range 14-50%). Immediate separation of samples but delayed deproteinization and preservation also resulted in substantial losses of ascorbic acid. CONCLUSION: Minimum loss of ascorbic acid is achieved if blood is collected into tubes containing dipotassium EDTA and separated within 2 h, followed by immediate deproteinization and preservation.

Analysis of Variance↗

PubMed1980

Ascorbic acid in intestinal tissues.

About a fifth of the ascorbic acid is readily lost from intestinal tissue during handling procedures such as washing with saline and blotting. Further losses occur during incubation in Krebs-phosphate saline; after 10 min strips of intestine retained 80% of their original ascorbic acid content and chopped tissue only 50%. This suggests that some of the intestinal ascorbic acid is very loosely held in the tissue. The small intestine is capable to accumulating double the normal amount of ascorbic acid when animals are dosed intramuscularly and retains some ascorbic acid (0.7 to 5 microgram/mg DNA) even when the animals' body stores are depleted.

Animals↗

PubMed1989

Ascorbic acid and erythorbic acid metabolism in nonpregnant women.

Ascorbic acid (AA) metabolism and requirements were studied in 11 adult nonpregnant women maintained in a metabolic unit and fed a formula diet devoid of AA for 54 d. After depletion for 24 d, the subjects received increasing supplements of AA in the presence or absence of 600 mg/d of erythorbic acid (EA). Various analytical procedures were used to measure AA concentrations in blood components. The depletion period resulted in a marked decrease in AA in all blood indices. During the study scorbutic signs developed in some of the subjects. AA supplements of 30 mg/d for 10 d failed to increase plasma ascorbate concentrations; 60 mg/d for 10 d produced a small increase; 90 mg/d resulted in a mean AA concentration of 29 mumol/L. EA did not present any adverse effects, but rather had a small sparing effect. Vitamin C requirements for adult nonsmoking, nonpregnant women would be marginally met by an intake of 60 mg/d of AA whereas 90 mg/d would provide an allowance for body storage.

Adult↗

PubMed1980

Stability of vitamin B12 in the presence of ascorbic acid in food and serum: restoration by cyanide of apparent loss.

Ascorbic acid in varying amounts was added to food and serum samples and heated at 37 C. Vitamin B12 was then measured by radioimmunoassay and microbiologically using several extraction methods. B12 values in a cottage cheese meal were lower than controls when concentrations of ascorbic acid greater than but not equal or less than 0.5 mg/ml were added and if KCN was not used during extraction, but when 70 micrograms/ml KCN was added after ascorbic acid exposure B12 was quantitatively recovered. Serum B12 was variably decreased by lesser concentrations of ascorbic acid but was also quantitatively restored by increasing KCN concentration during extraction. In the absence of KCN in the extraction step some loss of B12 at 100 C was observed; the loss was greater with added ascorbic acid. Our results indicate that previous reports on B12 loss in the presence of ascorbic acid are artifacts of the methods used. In view of these in vitro findings B12 destruction by ascorbic acid in vivo seems highly improbable.

Ascorbic Acid↗

PubMed1990

Microbial processes for ascorbic acid biosynthesis: a review.

L-Ascorbic acid is an important product currently made using the Reichstein process, which is mainly chemical. Recently, bacteria have been identified that are able to transform in a very efficient way glucose to 2,5-keto-D-gluconic acid and this product to 2-keto-L-idonic acid, precursor of L-ascorbic acid. When the corresponding strains are used together, it is possible to get 2-keto-L-idonic acid directly from glucose. Moreover, new strains have been constructed by introducing a gene from a strain responsible for the second step into a strain responsible for the first step. By using one of the new strains, the transformation can be performed in a single step with only one strain. However, the classical process still remains the most competitive.

Acetobacter↗

PubMed2007

Dose-dependent modulation of the T cell proteome by ascorbic acid.

To investigate the hypothesis that the micronutrient ascorbic acid can modulate the functional genome, T cells (CCRF-HSB2) were treated with ascorbic acid (up to 150 microM) for up to 24 h. Protein expression changes were assessed by two-dimensional electrophoresis. Forty-one protein spots which showed greater than two-fold expression changes were subject to identification by matrix-assisted laser desorption ionisation time of flight MS. The confirmed protein identifications were clustered into five groups; proteins were associated with signalling, carbohydrate metabolism, apoptosis, transcription and immune function. The increased expression of phosphatidylinositol transfer protein (promotes intracellular signalling) within 5 min of ascorbic acid treatment was confirmed by Western blotting. Together, these observations suggest that ascorbic acid modulates the T cell proteome in a time- and dose-dependent manner and identify molecular targets for study following antioxidant supplementation in vivo.

Ascorbic Acid↗

PubMed1977

[On the mechanism of ascorbic acid induced methemoglobin reduction of human erythrocytes (author's transl)].

Ascorbic acid and dehydroascorbic acid penetrate the human erythrocyte membrane. In vitro methemoglobin is reduced nonenzymatically by both substances in concentrations of 10(-2) M to 10(-3) M. Dehydroascorbic acid is reduced nonenzymatically to ascorbic acid by GSH, even with low GSH-content of erythrocytes. Under physiological conditions ascorbic acid induced methemoglobin reduction is far less important than reduction by the NADH dependent methemoglobin reductase system. In methemoglobinemic conditions caused by toxic effects or by congenital methemoglobin reductase deficiency treatment with ascorbic acid is possible. However, critically increased methemoglobin content of the blood higher than 30% makes therapy with methylene blue necessary.

Ascorbic Acid↗