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PubMed1983

A relationship between ascorbic acid and threonic acid in guinea-pigs.

Threonic acid is a major breakdown product of ascorbic acid used as a food additive. When administered orally to guinea-pigs (100 mg/kg body weight) for periods of 4 or 28 days, it produced a significant fall in the ascorbic acid concentration of certain organs but was without effect on other physiological and biochemical characteristics. The lifespan of scorbutic guinea-pigs was significantly reduced by dietary threonic acid (100 mg/kg body weight). The results indicate that threonic acid may modify the metabolism of ascorbic acid in guinea-pigs.

Animals↗
PubMed1976

Ascorbic acid-2-sulfate sulfhohydrolase activity of human arylsulfatase A.

Pure human arylsulfatase A (EC 3.1.6.1) was found to hydrolyze ascorbic acid 2-sulfate to ascorbic acid and inorganic sulfate at rates from 200 to 2000 mumol/mg per h depending on the method of assay. This rate was lower than that observed with the synthetic substrate 4-nitrocatechol sulfate, but higher than that seen with the physiological substrate cerebroside sulfate. Extracts of cultured fibroblasts from normal subjects were also shown to hydrolyze ascorbic acid 2-sulfate; extracts of fibroblasts from patients with metachromatic leukodystrophy, known to be deficient in arylsulfatase A, did not. Similarly, hydrolysis of ascorbic acid 2-sulfate was not observed when a partially purified preparation of human arylsulfatase B was tested under a variety of conditions. Thus, in the human, arylsulfatase A appears to be the major, if not the only, ascorbic acid-2-sulfate sulfohydrolase.

Ascorbic Acid↗
PubMed1977

Effect of histones on the intracellular metabolism of ascorbic acid.

Basic proteins are able to control the intracellular metabolism of ascorbic acid in human erythrocytes. The stimulating effect of ascorbic acid expressed by means of cellular peroxidase reactions of intact erythrocytes depends on the ascorbic acid and basic protein concentrations as well as on the structure of the histone molecule. Leukocyte and calf thymus histones can stimulate the intracellular metabolism of ascorbic acid in human erythrocytes, in contrast to the protamines which show an inhibitory effect in the above mentioned intracellular peroxidase metabolic system.

Ascorbic Acid↗
PubMed1977

Effects of plasma ascorbic acid levels on heat acclimatization in man.

Thirteen male volunteers were heat acclimatized for 4 h/day for 10 consecutive days. Three to four hours before each heat exposure, four of the subjects received an oral dose of 250 ascorbic acid, five received 500 mg ascorbic acid, and the remaining four a placebo. Rectal temperature, heart rate, and sweat rate were measured hourly during exposure. Venous blood samples were collected before each administration of drug or placebo. On days 1, 2, 3, 5, 8, and 10, blood samples were also collected just prior to heat exposure and after two and four hours of exposure. In the subjects receiving ascorbic acid, total circulating plasma ascorbic acid increased over the first three or four days to a plateau level some fourfold higher than in the subjects receiving the placebo. The plateau level was the same in the subjects receiving 250 mg and 500 mg ascorbic acid. The increased ascorbic acid concentration was shown to be associated with a reduction in total sweat output, independent of rectal temperature, and a reduction in rectal temperature, independent of total sweat output. The results indicate that ascorbic acid may be effective in reducing heat strain in unacclimatized individuals.

Acclimatization↗
PubMed1999

[Mechanism of combined oxidation of ascorbic acid and hydroquinone in the presence of horseradish peroxidase].

A steady-state kinetics of peroxidase cooxidation of ascorbic acid and hydroquinone catalyzed by horseradish peroxidase was studied. Ascorbic acid and hydroquinone were shown to be oxidized successively, and hydroquinone promoted the oxidation of ascorbic acid. Excess ascorbic acid inhibited peroxidase in the cooxidation of the substrates at pH 5-7. The values of catalytic constants, (kcat, K(m), and Ka) were determined. A possible activation mechanism of the peroxidation of ascorbic acid in the presence of hydroquinone was suggested, and its biological significance was considered.

Ascorbic Acid↗
PubMed2005

Orthomolecular oncology review: ascorbic acid and cancer 25 years later.

The effect of ascorbic acid on cancer has been a subject of great controversy. This is a follow-up review of the 1979 article by Cameron, Pauling, and Leibovitz published in Cancer Research. In this updated version, the authors address general aspects of ascorbic acid and cancer that have been presented before, while reviewing, analyzing, and updating new existing literature on the subject. In addition, they present and discuss their own mechanistic hypothesis on the effect of ascorbic acid on the cancer cell. The objective of this review is to provide an updated scientific basis for the use of ascorbic acid, especially intravenously as adjuvant treatment in pharmacological nutritional oncology.

Antioxidants↗
PubMed2000

Use of an amino acid in the mobile phase for the determination of ascorbic acid in food by high-performance liquid chromatography with electrochemical detection.

The possibility of using monosodium L-glutamate (MSG) (20 mM MSG, pH 2.1) in the mobile phase for the determination of ascorbic acid (AA) in foods by high-performance liquid chromatography (HPLC) with electrochemical detection was examined. The hydrodynamic voltammogram of AA and the background current were also examined. The applied potential was set at 400 mV versus an Ag/AgCl reference electrode. It was demonstrated that MSG was a useful mobile phase for the determination of AA in foods. This paper also examines the stability of AA under various conditions in order to optimize HPLC conditions and the pre-run sample stabilization. The proposed method is simple, rapid (analysis time: approximately 6 min), sensitive (detection limit: approximately 0.1 ng per injection (5 microl) at a signal-to-noise ratio of 3), highly selective and reproducible (relative standard deviation: approximately 2.5%, n=7). The calibration graph of AA was linear in the range 0.1-50 ng per injection (5 microl). Recovery of AA was over 90% by the standard addition method.

Amino Acids↗
PubMed1986

The effect of controlled ascorbic acid depletion and supplementation on periodontal health.

To determine if systemic levels of vitamin C influence periodontal health, changes in plaque accumulation, gingival health and periodontal probing depth were measured in healthy subjects housed for 3 months in a nutrition suite that provided controlled periods of ascorbic acid depletion and supplementation. Eleven healthy, nonsmoking men, aged 19 to 28 years, ate a rotating 7-day diet adequate in all nutrients except ascorbic acid. This basal diet, which contained less than 5 mg/day ascorbic acid, was supplemented with 60 mg/day ascorbic acid for 2 weeks, 0 mg/day ascorbic acid for 4 weeks, 600 mg/day ascorbic acid for 3 weeks and 0 mg/day ascorbic acid for 4 weeks. Plasma, urine and leukocyte ascorbate levels, Plaque Index, Gingival Index, Bleeding Index and probing depths were monitored throughout the study. A uniform oral hygiene program was maintained in which oral hygiene instructions were reinforced bi-weekly. Ascorbate concentrations in body fluids and leukocytes responded rapidly to changes in ascorbic acid intake. No mucosal pathoses or changes in plaque accumulation or probing depths were noted during any of the periods of depletion or supplementation. However, measures of gingival inflammation were directly related to the ascorbic acid status. The results suggest that ascorbic acid may influence early stages of gingivitis, particularly crevicular bleeding.

Adult↗
PubMed1995

Effects of intestinal resection, cholecalciferol and ascorbic acid on iron metabolism in rats.

The effect of dietary supplementation with ascorbic acid or cholecalciferol on Fe utilization was studied using the metabolic balance technique, in rats in which 50% of the distal small intestine was removed, or in which the mid small intestine was transected and reanastomosed (controls). Three different diets were used. The first (basal diet) contained (g/kg dry wt): protein (casein + 50 mg D,L-methionine/g) 120 and fat (medium-chain triacylglycerols, olive oil and sunflower oil, in equal parts) 40. The other diets were obtained by adding ascorbic acid (150 mg/kg diet) or cholecalciferol (0.4 mg/kg diet) to the basal diet. Apparent digestibility coefficient (ADC) and Fe retention were significantly lower in resected animals than in their respective control groups (transected rats). However, the addition of ascorbic acid or cholecalciferol to the basal diet increased the ADC and Fe retention in both transected and resected rats. Five weeks after surgery, resection also resulted in a reduced concentration of Fe in the sternum, but did not reduce the concentration of haemoglobin or serum Fe total Fe-binding capacity or the concentration of Fe in liver, testes, femur or muscle (longissimus dorsi). Supplementation with ascorbic acid increased serum Fe concentration, while the concentration of Fe in muscle was reduced by supplementation with both ascorbic acid and cholecalciferol. Neither supplementation had any effect on the Fe concentration in other tissues, on haemoglobin concentration or plasma total Fe-binding capacity. Thus, supplementation with ascorbic acid or with cholecalciferol increased Fe absorption and reduced the concentration of Fe in muscle.

Animals↗
PubMedDate not supplied

Ascorbic acid, dehydroascorbic acid and glutathione in liver disease.

Controlled studies were conducted to find out the plasma values of ascorbic acid, dehydroascorbic acid (DHA), urinary excretion of ascorbic acid and blood levels of glutathione in patients with viral hepatitis, alcoholic hepatitis, cirrhosis of liver and carcinoma of liver. Leucocyte ascorbic acid and DHA/AA index were also determined in order to assess the ascorbic acid status of these patients. It was observed that the plasma and leucocytes contents of ascorbic acid were significantly subnormal with markedly decreased urinary excretion in these patients. Decreased level of glutathione and significantly higher level of DHA reflect an over all reducing status of the body is markedly deranged in these conditions. Further it was observed that the DHA/AA ratios were significantly altered in these groups of patients.

Ascorbic Acid↗
PubMed2003

Microencapsulated ascorbic acid for milk fortification.

The present study was designed to develop a microencapsulated L-ascorbic acid and iron that could be used to fortify milk and to determine the sensory properties of milk fortified with microencapuslation. Coating material was medium-chain triacylglycerol (MCT), and selected core material was ferric ammonium sulfate and L-ascorbic acid. The highest efficiency of microencapsulation was 95.0% in the ratio of 15:1 as coating to core material. Ascorbic acid release was increased sharply up to 5 d storage as 6.5%. TBA value was the lowest when both capsulated iron and ascorbic acid were added during 12 d storage, compared with other treatments. In sensory analysis, most aspects were not significantly different between control and capsulated ascorbic acid fortified milk at 5 d storage. The present study indicated that the use of microencapsulated ascorbic acid with MCT is effective for fortifying milk. In addition, these results suggest that acceptable milk products can be prepared with microencapsulated ascorbic acid and iron.

Animals↗
PubMed1992

Collagen synthesis in human skin fibroblasts is stimulated by a stable form of ascorbate, 2-O-alpha-D-glucopyranosyl-L-ascorbic acid.

We evaluated the effect of 2-O-alpha-D-glucopyranosyl-L-ascorbic acid (AA-2G) on collagen synthesis in cultured human skin fibroblasts and on proliferation of fibroblasts. At concentrations of 0.1-0.5 mmol/L, AA-2G effectively stimulated collagen synthesis with an effectiveness comparable to that of L-ascorbic acid. On the other hand, 6-O-alpha-D-glucopyranosyl-L-ascorbic acid showed a weak effect. The stimulation of collagen synthesis by AA-2G was attenuated by the addition of a collagen synthesis inhibitor, L-azetidine 2-carboxylic acid, in a dose-dependent manner. In addition, AA-2G-induced stimulation of collagen synthesis could be completely inhibited by the addition of castanospermine, an inhibitor of neutral alpha-glucosidase. Relatively high alpha-glucosidase activity, which would contribute to release of ascorbic acid from AA-2G, could be detected in the lysate of cultured fibroblasts. The stimulatory activity of AA-2G on collagen synthesis was observed after 5 d in culture, whereas L-ascorbic acid tended to lose its stimulatory activity. Continuous supplementation of AA-2G (0.25 mmol/L) to culture medium for 24 d enhanced the cell growth four times that of the control. These results indicate that AA-2G is gradually cleaved by the cellular alpha-glucosidase to release L-ascorbic acid, which adequately stimulates collagen synthesis and proliferation of human skin fibroblasts.

Alkaline Phosphatase↗
PubMed1987

Inhibition of 12-O-tetradecanoylphorbol-13-acetate induction of ornithine decarboxylase activity, DNA synthesis, and tumor promotion in mouse skin by ascorbic acid and ascorbyl palmitate.

The effects of topically applied 12-O-tetradecanoylphorbol-13-acetate (TPA) on the level of ascorbic acid in the epidermis and the effects of topically applied ascorbic acid, ascorbyl palmitate (a synthetic lipophilic derivative of ascorbic acid), palmitic acid and sorbitan monopalmitate on TPA-induced epidermal ornithine decarboxylase activity, epidermal DNA synthesis, and the promotion of skin tumors were evaluated in female CD-1 mice. Topical application of 5 or 16 nmol of TPA resulted in a 45-50% decrease in the amount of ascorbic acid per mg protein in mouse epidermis at 5 h after TPA application. Large topical doses of ascorbic acid inhibited TPA-induced tumor promotion in mouse epidermis, but smaller doses were inactive. The topical application of relatively small doses of ascorbyl palmitate had a marked inhibitory effect on TPA-induced ornithine decarboxylase activity, DNA synthesis, and tumor promotion in mouse epidermis. Ascorbic acid, palmitic acid, and sorbitan monopalmitate were less effective than ascorbyl palmitate as inhibitors of tumor promotion. The topical application of 4 mumol of ascorbyl palmitate inhibited by 60-76% the induction of epidermal ornithine decarboxylase activity and DNA synthesis that occurred after a single topical application of 2 nmol of TPA whereas similar doses of ascorbic acid had no inhibitory effect. The topical application of 4 mumol of ascorbyl palmitate together with 5 nmol of TPA twice weekly for 20 weeks to previously initiated mice inhibited by 91% the number of tumors per mouse.

Administration, Topical↗
PubMed1980

Regional brain ascorbic acid distribution: its functional relationship to appetite and leptazol-induced convulsions in guinea-pigs.

The distribution of ascorbic acid has been compared in the fore-, mid- and hind-brains of guinea-pigs maintained on a scorbutogenic diet alone, or the diet with supplementary Vitamin C, or the supplemented diet and a terminal convulsant dose of leptazol after 27 days. At the beginning of the investigation, mid-brain ascorbic acid concentrations were similar in both sexes and highest in the mid-brain. After 27 days on the supplemented diet, levels of ascorbic acid were raised in all three brain sections and were still highest in the mid-brains. In the scorbutic group, ascorbic acid concentrations had not changed from control levels in the mid-brain, but had fallen in the other two sections. In a dose-range of 40-60 mg/kg, leptazol caused an increase in convulsive index, and progressive depletion of brain ascorbic acid. No change occurred in fore-brain ascorbic acid, a reduction took place in the hindbrain, and the greatest fall occurred in the mid-brain. It is concluded that ascorbic acid plays an essential role in mid-brain metabolism, and that the convulsant effect of leptazol is influenced by an interaction with brain ascorbic acid.

Animals↗
PubMed1990

Ascorbic acid stimulates production of glycosaminoglycans in cultured fibroblasts.

The effect of ascorbic acid on collagen synthesis is well characterized. Proteoglycans and their attached glycosaminoglycans are components of the extracellular matrix closely associated with collagen fibers. We examined whether ascorbic acid also plays a role in glycosaminoglycan production. Synthesis and deposition of glycosaminoglycans into the extracellular matrix and secretion into the media were followed in human skin fibroblasts cultured in the presence and absence of ascorbic acid. Specific glycosaminoglycans were identified and quantitated by differential enzyme digestion, ion-exchange column chromatography, and cellulose-acetate electrophoresis. No major qualitative changes in glycosaminoglycans were observed. However, quantitatively, synthesis of glycosaminoglycans increased 30 to 90%, and deposition into the extracellular matrix increased 80% in the presence of ascorbic acid. This effect was only in part secondary to decreased levels of collagen, and the diminished capacity of underhydroxylated collagen to bind proteoglycans. The effect of ascorbic acid on extracellular macromolecules is thus more pervasive than previously assumed.

Ascorbic Acid↗
PubMed1980

Effects of high ascorbic acid intake on the metabolism of catecholamines in the rat.

The effect of high dietary ascorbic acid intake on the homeostasis of ascorbic acid and on the metabolism of catecholamine was studied in rats. In order to eliminate changes in serum levels due to stress, blood was obtained without anesthesia through implanted cannulas. Rats with a high intake of ascorbic acid (20 g/kg diet, for 7-9 weeks) had significantly higher levels of ascorbic acid in serum (83%), liver (28%), kidney (47%) and superior cervical ganglia (43%). The values were slightly, but not significantly higher in adrenal gland, brain and interscapular brown adipose tissue. However, no significant differences were observed in the levels of noradrenalin, adrenalin and dopamine in any of the tissues analyzed. Dopamine beta-hydroxylase activity was also unchanged. There was thus no evidence of an effect of high dietary intakes of ascorbic acid on the metabolism of catecholamines in the intact rat.

Adipose Tissue, Brown↗
PubMed1996

Ascorbic acid protects against male infertility in a teleost fish.

An animal unable to synthesize ascorbic acid uniquely mimicks human and non-human primates. Therefore, in this study we used the rainbow trout, a teleost fish, as the model animal to study the importance of dietary ascorbic acid on the fertilizing ability of sperm. A high concentration of ascorbic acid in semen plays a key role in maintaining the genetic integrity of sperm cells, by preventing oxidative damage to sperm DNA. This study will show that the concentration of ascorbic acid in seminal plasma reflects the dietary intake of vitamin C. The concentration of ascorbic acid in seminal plasma of fish declined significantly in groups fed either an ascorbate-free diet (from 4.74 +/- 0.9 to 0.16 +/- 0.08 microgram ml-1) or an ascorbate-rich diet (from 37.9 +/- 4.7 to 17.7 +/- 3.2 microgram ml-1) during the spermiation season. The relationship between ascorbate status and fertility was studied in six groups of fish fed graded levels of ascorbic acid, which spermiated over a 150-day-period. Sperm from individual males was used to fertilize several batches of eggs. When the seminal plasma ascorbate concentration decreased to 7.3 microgram ml-1 a significant decrease of fertilization rate and the hatching rate of embryos resulted. This is the first evidence that dietary ascorbate level directly affected sperm quality and influenced male fertility in a scurvy-prone vertebrate.

Animals↗
PubMedDate not supplied

Pretreatment with intravenous ascorbic acid preserves endothelial function during acute hyperglycaemia (R1).

1. Acute hyperglycaemia may impair endothelial function. Ascorbic acid (AA), administered intra-arterially, has been reported to improve endothelium-dependent vasodilatation during a forearm hyperglycaemic clamp. Using a randomized, double-blind, placebo-controlled, cross-over study, we investigated the potential for intravenous ascorbic acid to modify the endothelial response to acute systemic hyperglycaemia in humans. 2. Nine healthy male volunteers were recruited from the hospital staff. Endothelial function was determined by measuring the forearm blood flow responses to intrabrachial infusions of endothelium-dependent (ED) and endothelium-independent (EID) vasodilators. The endothelial function index (EFI) was derived from the ratio of ED and EID vasodilatation. Haemodynamic and endothelial function measurements were performed at baseline and then repeated 2 h after a systemic hyperglycaemic clamp (14 mmol/L). The subjects, studied on two separate occasions, were randomized to placebo or 2 g intravenous ascorbic acid prior to the initiation of hyperglycaemia. 3. After systemic hyperglycaemia with placebo pretreatment, the EFI fell from 1.08 +/- 0.21 to 0.74 +/- 0.13 (difference (95% confidence interval): 0.34 (0.20, 0.47); P < 0.001). When subjects were pretreated with ascorbic acid, the EFI was not affected by hyperglycaemia (1.11 +/- 0.21 to 1.12 +/- 0.17; P = 0.938). This difference between placebo and ascorbic acid was significant (P < 0.001). Plasma ascorbate concentrations decreased during hyperglycaemia and correlated directly with the reduction in the EFI (r = 0.798; P < 0.001). 4. Pretreatment with an intravenous bolus of ascorbic acid can prevent endothelial dysfunction during acute systemic hyperglycaemia. Therefore, ascorbic acid may have potential therapeutic use in clinical situations where acute hyperglycaemia may be a complication.

Acute Disease↗