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PubMed1983

Rapid diagnostic tests for glucosuria are still influenced by ascorbic acid.

The influence of ascorbic acid on commercial rapid diagnostic tests for glucosuria is demonstrated in vitro. Although much work has been done to stabilize the tests against such interference, and although manufacturers of tests trips declare their products now to be fairly stable against ascorbic acid 'at higher glucose levels', all the investigated commercial rapid diagnostic tests for glucose at the lower pathological range of glucosuria were substantially influenced by ascorbic acid at potentially physiological concentrations.

Ascorbic Acid↗
PubMed1992

Inhibition of key enzymes of carbohydrate metabolism in regenerating mouse liver by ascorbic acid.

The effect of ascorbic acid on the key enzymes of carbohydrate metabolism e.g. hexokinases, phosphofructokinase, pyruvate kinase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase and malic enzyme was determined in regenerating mouse liver. All the enzymes showed a significant increase in the activity during regeneration. Ascorbic acid reduced the activities of the enzymes in regenerating liver. A decrease in liver weight in ascorbic acid treated animals may be correlated with its effect on these enzymes as glycolytic pathway is the main source of energy required by the dividing cells.

Animals↗
PubMed1983

Bicyclic ring formation is not necessary for the (auto)oxidation of ascorbic acid.

The oxidation rates of ascorbic acid and several of its derivatives have been examined in order to delineate the role of bicyclic ring formation in the autooxidation of ascorbic acid. The compounds evaluated and their respective oxidation rates at pH 7.4 are in uM X min-1: ascorbate, 0.70; 5 methyl 3,4 dihydroxytetrone, 0.65; D-iso ascorbate, 0.73; and ascorbyl palmitate, 0.64. These data do not support the contention that bicyclic ring formation is required for the oxidation of ascorbic acid because both 5 methyl 3,4 dihydroxytetrone and ascorbyl palmitate, neither of which can form the bicyclic intermediate, have oxidation rates similar to that of ascorbate. Furthermore, evidence is presented which suggests that ionization of the oxygen on C3 of ascorbic acid is an obligatory initial step in ascorbic acid autooxidation.

Ascorbic Acid↗
PubMed2005

Reaction of 5-aminosalicylic acid with peroxyl radicals: protection and recovery by ascorbic acid and amino acids.

PURPOSE: The aims of the study are to analyze the interaction between 5-aminosalicylic acid (5-ASA) and peroxyl radicals and to evaluate the effect of some endogenous compounds such as ascorbic acid and amino acids on the oxidation of 5-ASA induced by 2,2'-azo-bis(2-amidinopropane) dihydrochloride. METHODS: The consumption and/or the recovery of 5-ASA (7.6 microM) exposed to a peroxyl radical source [2,2'-azo-bis(2-amidinopropane)] was followed by techniques such as spectrofluorescence, high-performance liquid chromatography, and differential pulse voltammetry. RESULTS: 5-Aminosalicylic acid was found to readily react with peroxyl radicals at micromolar concentrations and to protect c-Phycocyanin in a very similar fashion to that shown by Trolox. Exposure of 5-ASA to peroxyl radicals led to its oxidation into the corresponding quinone-imine. Disappearance of 5-ASA was prevented by tryptophan, cysteine, glutathione, and ascorbic acid. Furthermore, some of these compounds induced the partial (cysteine and glutathione) or total (ascorbic acid) recovery of 5-ASA when added after its almost total consumption. CONCLUSIONS: 5-Aminosalicylic acid is a very efficient peroxyl radical scavenger. The 5-ASA oxidation by peroxyl radicals was prevented by ascorbic acid, cysteine, and glutathione. In addition, 5-ASA can be regenerated by these endogenous compounds, which would be a valuable mechanism to preserve 5-ASA in tissues undergoing oxidative stress conditions.

Amidines↗
PubMed2003

Increase in tartrate-resistant acid phosphatase of bone at the early stage of ascorbic acid deficiency in the ascorbate-requiring Osteogenic Disorder Shionogi (ODS) rat.

The effect of ascorbic acid deficiency on bone metabolism was evaluated using the ascorbate-requiring Osteogenic Disorder Shionogi (ODS) rat model. Ascorbic acid (Asc)-deficient rats gained body weight in a manner similar to Asc-supplemented rats (control) during 3 weeks, but began to lose weight during the 4th week of Asc deficiency. The tartrate-resistant acid phosphatase (TRAP) activity in serum increased to about 2-fold the control value in the rats fed the Asc-free diet for 2, 3, and 4 weeks (AscD2, AscD3, and AscD4), while a decrease in the alkaline phosphatase (ALP) activity was observed only in AscD4 rats. The serum pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP) level significantly increased to 1.3-, 1.4-, and 1.9-fold of that in the controls in AscD2, D3, and D4, respectively. The ALP activity in the distal femur was unchanged in AscD1, D2, and D3, but decreased to 50% of the control level in AscD4 rats. The TRAP activity in the distal femur increased to about 2-fold of that in the controls in the AscD2 and D3 and decreased to the control level in the AscD4 rats. The amount of hydroxyproline in the distal femur significantly decreased to about 80%, 70%, and 60% of the control in AscD2, D3, and D4 rats, respectively. These decreases were associated with a similar reduction in the calcium content of the distal femur. Histochemical analysis of the distal femur showed an increase in TRAP-positive cells in AscD2 and AscD3 rats and a decrease in the trabecular bone in AscD2, D3, and D4 rats. These results suggested that a deficiency of Asc stimulated bone resorption at an early stage, followed by a decrease in bone formation in mature ODS rats which already had a well-developed collagen matrix and fully differentiated osteoblasts.

Acid Phosphatase↗
PubMed1983

Tissue concentrations and proliferative effects of massive doses of ascorbic acid in the mouse.

The effect of ascorbic acid supplementation on CF1 mice fed ascorbic acid for approximately six months at dose levels of 1%, 5%, and 10% of diet was investigated by analysis of tissue ascorbic acid concentration in the liver, kidney, stomach, small intestine, and large bowel. The effect on epithelial cell proliferation was also examined in the small and large bowel but only at the 5% level. In the control animals, ascorbic acid concentration was lowest in the liver (0.406 +/- 0.07 mg/g) and highest in the small bowel (0.754 +/- 0.16 mg/g). Dietary intake of 5% and 10% ascorbic acid significantly elevated levels in the liver (0.741 +/- 0.13; p less than 0.05), and all doses of ascorbic acid significantly raised tissue concentrations in the kidney and colon. No difference was observed in the percentage of DNA-synthesizing cells in the jejunum of controls or animals fed 5% ascorbic acid at 1 or 24 hours after 3HTdR injection. However, at 1 hour a significantly decreased level of proliferation was observed in the distal colon of ascorbic-acid-treated mice compared with controls (labeling index [L.I.] = 7.3 +/- 0.28 vs. 10.1 +/- 1.15; p less than 0.05), and an even greater suppression of DNA synthesis was achieved by 24 hours (L.I. = 11.4 +/- 1.06 vs. 18.6 +/- 1.61; p less than 0.01). None of the doses of ascorbic acid employed was toxic to the experimental mice.

Animals↗
PubMed2006

The use of microorganisms in L-ascorbic acid production.

L-Ascorbic acid has been industrially produced for around 70 years. Over the past two decades, several innovative bioconversion systems have been proposed in order to simplify the long time market-dominating Reichstein method, a largely chemical synthesis by which still a considerable part of L-ascorbic acid is produced. Here, we describe the current state of biotechnological alternatives using bacteria, yeasts, and microalgae. We also discuss the potential for direct production of l-ascorbic acid exploiting novel bacterial pathways. The advantages of these novel approaches competing with current chemical and biotechnological processes are outlined.

Ascorbic Acid↗
PubMed1985

Interaction between ascorbic acid and acetylsalicylic acid and their effects on nutritional status in man.

Healthy adults were given four diets, each one for one week: Low ascorbic acid diet, low ascorbic acid diet plus acetylsalicylic acid (3 g/d), high ascorbic acid diet (1 g/d) and high ascorbic acid diet plus acetylsalicylic acid. At low ascorbic acid intake, acetylsalicylic acid increased urinary ascorbic acid, but at high ascorbic acid intake, acetylsalicylic acid instead decreased urinary ascorbic acid. The latter effect was probably due to an inhibited intestinal absorbtion of ascorbic acid, and the former effect may reflect decreased protein binding and tissue uptake of ascorbic acid caused by acetylsalicylic acid. In no instance, acetylsalicylic acid affected plasma ascorbic acid. The effect of ascorbic acid on substances related to lipid peroxidation was investigated. The high ascorbic acid diets decreased plasma lipoperoxide and retinol binding protein. No change was observed in serum tocopherol, iron status, erythrocyte lipid fluorescence, plasma ceruloplasmin, urinary and plasma selenium and glutathione peroxidase activity. Thus, one-week supplementation of ascorbic acid seems to have only marginal effects on lipid peroxidation and antioxidant status.

Adult↗
PubMed1983

Variation in prolyl hydroxylase activity of keloid-derived and normal human fibroblasts in response to hydrocortisone and ascorbic acid.

The effects of ascorbic acid and hydrocortisone on activity of prolyl hydroxylase in fibroblasts from keloid and normal human dermis were investigated and compared to the effects of these agents on collagen synthesis. Prolyl hydroxylase activity in normal fibroblasts grown to confluency in 1.5 microM hydrocortisone was approximately half that of cells grown without the steroid. The concentration of hydrocortisone effective in reducing enzyme activity was the same as that for reducing the rate of collagen synthesis; a half-maximal effect on both parameters was achieved at 10(-7) M. Hydrocortisone lowered enzyme activity through most of the culture cycle. Fibroblasts derived from keloids were significantly less subject to hydrocortisone-mediated reduction of prolyl hydroxylase activity and rate of collagen synthesis. This difference between keloid and normal cells was dependent on the simultaneous presence of ascorbic acid and hydrocortisone. These data suggest that the defect in wound healing that results in keloid formation is associated with a change in a regulatory mechanism that controls the rate of collagen synthesis and is sensitive to physiological levels of hydrocortisone. Continuous culture of fibroblasts in medium supplemented with ascorbic acid also lowered prolyl hydroxylase activity. Unlike the effect of hydrocortisone, growth in ascorbate increased the rate of collagen synthesis and affected keloid and normal strains equally.

Ascorbic Acid↗
PubMed1978

Characterization of intermediate hemoglobin produced during methemoglobin reduction by ascorbic acid.

Methemoglobin reduction by ascorbic acid was found apparently to cease halfway without further reduction. Studies by isoelectric focusing on Ampholine plate gel revealed that the solutions of the halfway reduced methemoglobin are composed of about 6% oxyhemoglobin, 59% intermediate hemoglobin, and 35% methemoglobin. The intermediate hemoglobin was isolated by CM Sephadex C-50 column chromatography and identified as alpha3+beta2+ valency hybrid by studies using the pattern of isoelectric focusing of p-chloromercuribenzoate-treated intermediate hemoglobin on Ampholine plate gel, absorption spectra, and difference spectra induced by the addition of inositol hexaphosphate in comparison with the reconstituted valency hybrids, alpha3+beta2+ and alpha2+beta3+. Essentially no alpha2+beta3+ valency hybrid was included in the intermediate hemoglobin solutions. These results suggest that methemoglobin reduction by ascorbic acid is mainly initiated by the attack of beta-methemoglobin chains accompanied by the following scheme. Methemoglobin leads to alpha3+beta2+ valency hybrid leads to oxyhemoglobin. The course of methemoglobin reduction by ascorbic acid through alpha2+beta3+ is likely to be small.

Ascorbic Acid↗
PubMed2006

An efficient synthesis of tetramic acid derivatives with extended conjugation from L-ascorbic acid.

BACKGROUND: Tetramic acids with polyenyl substituents are an important class of compounds in medicinal chemistry. Both solid and solution phase syntheses of such molecules have been reported recently. Thiolactomycin, a clinical candidate for treatment of tuberculosis has led to further explorations in this class. We have recently developed an efficient synthesis of tetramic acids derivatives from L-ascorbic acid. In continuation of this work, we have synthesised dienyl tetramic acid derivatives. RESULTS: 5,6-O-isopropylidene-ascorbic acid on reaction with DBU led to the formation of tetronolactonyl allyl alcohol, which on oxidation with pyridinium chlorochromate gave the respective tetranolactonyl allylic aldehydes. Wittig olefination followed by reaction of the resulting tetranolactonyl dienyl esters with different amines resulted in the respective 5-hydroxy lactams. Subsequent dehydration of the hydroxy lactams with p-toluene sulphonic acid afforded the dienyl tetramic acid derivatives. All reactions were performed at ambient temperature and the yields are good. CONCLUSION: An efficient and practical method for the synthesis of dienyl tetramic acid derivatives from inexpensive and easily accessible ascorbic acid has been developed. The compounds bear structural similarities to the tetramic acid based polyenic antibiotics and thus this method offers a new and short route for the synthesis of tetramic acid derivatives of biological significance.

Journal Article↗
PubMed1990

Bioavailability of ascorbic acid in horses.

The bioavailability of ascorbic acid administered to thoroughbreds by intramuscular injection was investigated. For intramuscular injection two preparations were studied, and the percentage bioavailability up to 24 h of 10 g of ascorbic acid was 95% +/- 22 in four horses and 60% in two horses with preparations A and B, respectively. Bioavailability at 24 h in three horses injected subcutaneously with 10 g of preparation B was 82%. Intramuscular injection of both preparations was apparently well tolerated while subcutaneous injection of preparation B (pH 6.0) was associated with marked irritancy. In a cross-over trial in seven thoroughbreds the effect of 13 or 15 days of oral administration of crystalline ascorbic acid (20 g) or ascorbyl palmitate (47 g) on plasma ascorbic-acid concentrations was investigated. Marked differences occurred between individuals. There was a greater increase in plasma ascorbic-acid concentration with ascorbyl palmitate compared to ascorbic acid at 6 and 24 h following administration. In two horses there was no increase in plasma ascorbic acid at 6 h following either oral preparation. The finding of lowered plasma ascorbic-acid concentrations following a period of supplementation warrants further investigation to assess its significance.

Administration, Oral↗
PubMed1990

[Comparison of presence of ascorbic acid and the appearance of ascorbate peroxidase activity in embryos of Avena sativa L].

Avena sativa L. grains are devoid of ascorbic acid (AA) and of oxidative enzymes (AA oxidase and AA peroxidase), while both reducing enzymes (AFR reductase and DHA reductase) are present. AA biosynthesis in the embryos starts after 12-14 hours of germination and at the same time AA peroxidase activity is detectable. During the following 14 hours the AA peroxidase activity rises up to 28 nmoles/AA oxidated/min/mg/prot. Incubation of Avena embryos with GL (the last precursor of AA according to the Isherwood biosynthetic pathway), results in both earlier AA biosynthesis and enhanced AA peroxidase activity. A 4 hour treatment is enough to induce AA synthesis and AA peroxidase elicitation. These data suggest that the development of AA peroxidase activity is controlled by AA, but they are not sufficient to clarify how that happens. Probably AA induces the synthesis of specific m-RNAs or activates enzymic precursors present in the embryos but still not working.

Ascorbate Peroxidases↗
PubMed1991

[Cadmium-induced changes in the activity of the dopaminergic and purinergic systems and in ascorbic acid catabolism in the rat striatum].

Levels of dopamine (DA), 3-4-dihydroxyphenylacetic acid (DOPAC), ascorbic acid (AA), dehydroascorbic acid (DHAA), uric acid (UA) and adenosine (ADO), were determined by HPLC in the striatum of male Wistar rats treated with repeated injections of cadmium (as sulfate) 3 mg/kg/day s.c. for 10 consecutive days. Cadmium treatment significantly reduced DOPAC levels with consequent decrease of the DOPAC/DA ratio; AA levels were significantly reduced, while DHAA levels were significantly increased, with consequent increase of DHAA/AA ratio: levels of UA and ADO were both significantly increased. It is concluded that cadmium, given systemically, reduces dopaminergic system activity in the rat striatum; such impairment occurs together with an increase of AA oxidation and of markers of purinergic system activity. The inhibition of striatal dopaminergic activity could be considered the neurochemical basis of behavioral changes induced by cadmium, while the increase of AA oxidation and of purinergic system activity could be considered an antitoxic metabolic response.

Adenosine↗
PubMed1991

Investigations into the relationship between the dopaminergic system and ascorbic acid in rat striatum.

Levels of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), ascorbic acid (AA) and dehydroascorbic acid (DHAA) were determined by HPLC in the striatum of male Wistar rats after single or repeated injections of apomorphine (1 mg/kg/day s.c.) and/or haloperidol (1 mg/kg/day i.p.), and 24 h after the last drug administration. Apomorphine significantly reduced the DOPAC/DA ratio and increased the DHAA/AA ratio; these ratio changes were significantly correlated (r = -0.9969, P less than 0.0005). Haloperidol greatly increased the DOPAC/DA ratio; the DHAA/AA ratio was also slightly increased, but there was no significant correlation. When apomorphine was associated with haloperidol, the resulting DOPAC/DA ratio was significantly lower than after haloperidol alone; the DHAA/AA ratio was also significantly reduced in contrast to the effect of apomorphine alone. It is concluded that a non-selective DA receptor activation mediates, in a correlated way, both the inhibition of DA turnover and the increase of AA oxidation in the rat striatum.

Animals↗
PubMed2003

Concomitant alterations in intragastric pH and ascorbic acid concentration in patients with Helicobacter pylori gastritis and associated iron deficiency anaemia.

BACKGROUND: Seroepidemiological and clinical studies suggest that Helicobacter pylori may cause iron deficiency anaemia (IDA) in the absence of peptic lesions by undefined mechanisms, which still remain to be fully elucidated. Gastric acidity and ascorbic acid (AA) promote iron absorption. AA is lowered in the presence of H pylori infection. H pylori can cause atrophic body gastritis with achlorhydria, decreased iron absorption, and consequent IDA. Whether alterations in intragastric acidity and AA concentrations play a role in IDA developing in patients with H pylori gastritis remains to be determined. AIM: To evaluate gastric juice pH and gastric juice and plasma AA in patients with H pylori infection and unexplained IDA, compared with controls with IDA and a healthy stomach or with controls with H pylori infection and no IDA. RESULTS: Patients with IDA and H pylori gastritis were characterised by concomitant increased intragastric pH (median value 7) and decreased intragastric AA (median value 4.4 micro g/ml) compared with controls with a healthy stomach (median pH 2; median intragastric AA 17.5 micro g/ml) and with H pylori positive controls without IDA (median pH 2.1; median intragastric AA 7.06 micro g/ml). Intragastric AA was inversely related to pH (r=-0.40, p=0.0059) and corporal degree of gastritis (r=-0.53, p=0.0039). Plasma AA concentrations were lower in all infected groups than in healthy controls. CONCLUSIONS: Patients with unexplained IDA and H pylori gastritis present concomitant changes in intragastric pH and AA that may justify impaired alimentary iron absorption and consequent IDA.

Adult↗
PubMed1986

Selective effects of ascorbic acid on acetylcholine receptor number and distribution.

Ascorbic acid in soluble extracts of neural tissue can account for the increase in surface acetylcholine receptors (AChR's) seen on L5 myogenic cells treated with crude brain extract (Knaack, D., and T. R. Podleski, 1985, Proc. Natl. Acad. Sci. USA., 82:575-579). The present study further elucidates the nature of the response of L5 cells to ascorbic acid. Light autoradiography showed that ascorbic acid treatment affects both the number and distribution of surface AChR's. Ascorbic acid, like crude brain extracts, caused a three- to fourfold increase in average AChR site density. However, the number of AChR clusters induced by ascorbic acid was only one-fifth that observed with crude brain extract. The rate constant for degradation of AChR in ascorbic acid-treated cells of 0.037 +/- 0.006 h-1 (t1/2 = 19 h) was not significantly different from that in untreated controls of 0.050 +/- 0.001 h-1 (t1/2 = 14 h). The increase in AChR site density is primarily due to a 2.8-fold increase in the average rate of AChR incorporation. Ascorbic acid also stimulates thymidine incorporation and increases the total number of nuclei per culture. However, cellular proliferation is not responsible for the increase in AChR's since 10 microM cytosine arabinofuranoside blocks the mitogenic effect without affecting the AChR increase. The specificity of ascorbic acid on AChR expression was established by showing that (a) ascorbic acid produced only a slight increase in total protein, which can be accounted for by the mitogenic effect, and (b) the normal increase seen in creatine kinase activity during muscle differentiation was not altered by the addition of ascorbic acid. We conclude that the action of ascorbic acid on AChR number cannot be explained by changes in cell growth, survival, differentiation, or protein synthesis. Therefore, in addition to a minor stimulation of AChR clustering, ascorbic acid specifically affects some aspect of the AChR biosynthetic pathway.

Animals↗