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PubMed1982

The effect of ascorbic acid on a proliferating cell system.

Ascorbic acid, alone and in combination with copper sulphate, was injected into the sub-blastodermal space in the early chick embryo at 17 hours of incubation. There was a marked stunting of the embryonal axis. The absence of interphase cells indicate that ascorbic acid is lethal to the resting cell and results in a reversal of differentiation. Copper counteracts the effect of ascorbic acid and protects the blastoderm when given before ascorbic acid. A parallel action in neoplasia is of importance in the therapeutic use of this vitamin.

Animals↗

PubMed1978

Some studies on ascorbic acid metabolism in hydrazine-treated rats.

The metabolism of ascorbic acid was studied in hydrazine-treated rats. Hydrazine was administered i.p. at a dose of 1.28 mg/day (20% LD50) for each 100 g body weight for 7 days. Hydrazine administration at the present dose did not appear to have an effect on the total ascorbic acid level of liver, kidney, spleen and testis. The adrenal and plasma total ascorbic acid levels were, however, elevated. The activity of liver D-glucuronoreductase and that of liver and kidney dehydroascorbatases were diminished after hydrazine administration. The changes in the activities of liver enzymes were accompanied by a fall in the reduced ascorbic acid level and an elevation in the dehydroascorbic acid level. The uronolactonase activity of liver, on the other hand, remained independent of hydrazine treatment. It has been suggested that hydrazine treatment at the present dose reduced the biosynthesis of L-ascorbic acid from D-glucuronolactone as substrate. In spite of diminished synthesis, the normal level of total ascorbic acid in the liver of hydrazine-treated rats was maintained by reducing the degradation of L-ascorbic acid. The rise in the plasma total ascorbic acid level after hydrazine treatment was ascribed to reduced catabolism and urinary excretion of ascorbic acid, while the elevation in adrenal total ascorbic acid level might result from increased uptake of ascorbic acid by the gland from blood or from nonfunctional accumulation.

Alcohol Oxidoreductases↗

PubMed1991

Ascorbic acid in Drosophila and changes during aging.

The ascorbic acid content of Drosophila melanogaster was found to be high in the absence of a dietary source. The amount of ascorbic acid per fly declined with aging in both the Oregon R and Swedish C strains. The median life span at 25 degrees C was 45 days for Swedish C and 59 days for Oregon R. The amount of ascorbic acid in Swedish C flies (0.078 micrograms/fly) was higher than that for Oregon R (0.058 micrograms/fly) for newly emerged flies but the rate of decline with aging was greater for Swedish C than Oregon R. The decline in ascorbic acid content with aging was 70.4% for Swedish C versus 19.9% for Oregon R. A brief cold shock was found to significantly increase the amount of ascorbic acid in Oregon R flies. Feeding the precursor of ascorbic acid synthesis, L-gulonolactone, did not improve the life span. Life-time feeding of ascorbic acid did not improve the life span of either Swedish C or Oregon R flies.

Aging↗

PubMed1999

A family of mammalian Na+-dependent L-ascorbic acid transporters.

Vitamin C (L-ascorbic acid) is essential for many enzymatic reactions, in which it serves to maintain prosthetic metal ions in their reduced forms (for example, Fe2+, Cu+), and for scavenging free radicals in order to protect tissues from oxidative damage. The facilitative sugar transporters of the GLUT type can transport the oxidized form of the vitamin, dehydroascorbic acid, but these transporters are unlikely to allow significant physiological amounts of vitamin C to be taken up in the presence of normal glucose concentrations, because the vitamin is present in plasma essentially only in its reduced form. Here we describe the isolation of two L-ascorbic acid transporters, SVCT1 and SVCT2, from rat complementary DNA libraries, as the first step in investigating the importance of L-ascorbic acid transport in regulating the supply and metabolism of vitamin C. We find that SVCT1 and SVCT2 each mediate concentrative, high-affinity L-ascorbic acid transport that is stereospecific and is driven by the Na+ electrochemical gradient. Despite their close sequence homology and similar functions, the two isoforms of the transporter are discretely distributed: SVCT1 is mainly confined to epithelial systems (intestine, kidney, liver), whereas SVCT2 serves a host of metabolically active cells and specialized tissues in the brain, eye and other organs.

Amino Acid Sequence↗

PubMed1989

High-affinity sodium-dependent uptake of ascorbic acid by rat osteoblasts.

Ascorbic acid is essential for the formation of bone by osteoblasts, but the mechanism by which osteoblasts transport ascorbate has not been investigated previously. We examined the uptake of L-[14C]ascorbate by a rat osteoblast-like cell line (ROS 17/2.8) and by primary cultures of rat calvaria cells. In both systems, cells accumulated L-[14C]ascorbate during incubations of 1-30 min at 37 degrees C. Unlike propionic acid, which diffuses across membranes in protonated form, ascorbic acid did not markedly alter cytosolic pH. Initial ascorbate uptake rate saturated with increasing substrate concentration, reflecting a high-affinity interaction that could be described by Michaelis-Menten kinetics (apparent Km = 30 +/- 2 microM and Vmax = 1460 +/- 140 nmol ascorbate/g protein/min in ROS 17/2.8 cells incubated with 138 mM extracellular Na+). Consistent with a stereoselective carrier-mediated mechanism, unlabeled L-ascorbate was a more potent inhibitor (IC50 = 30 +/- 5 microM) of L-[14C]ascorbate transport than was D-isoascorbate (IC50 = 380 +/- 55 microM). Uptake was dependent on both temperature and Na+, since it was inhibited by cooling to 4 degrees C and by substitution of K+, Li+ or N-methyl-D-glucamine for extracellular Na+. Decreasing the external Na+ concentration lowered both the affinity of the transporter for ascorbate and the apparent maximum velocity of transport. We conclude that osteoblasts possess a stereoselective, high-affinity, Na+-dependent transport system for ascorbate. This system may play a role in the regulation of bone formation.

Animals↗

PubMed1985

Studies on the antimutagenic activity of ascorbic acid in vitro and in vivo.

The possibility that ascorbic acid, as a nucleophile, may inhibit mutagenicity induced by electrophilic metabolites of N-nitroso compounds was examined. In vitro data are presented to show that ascorbic acid does not decrease the mutagenicity of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in a modified Ames bacterial mutagenicity system if deionized water is used to prepare the incubation medium. However, ascorbic acid prevents the mutagenicity of MNNG in vitro if added to bacteria in a medium prepared with either sterile tap water or deionized water and Cu2+ ions and that this antimutagenic response is blocked by EDTA. Additional in vitro experiments suggest that when ascorbic acid and Cu2+ ions are mixed in aqueous solution, H2O2 and free radicals derived from H2O2 are formed and these compounds may deactivate N-nitroso compounds. In vivo data are presented to show that ascorbic acid supplementation to guinea pigs (2000 mg/kg body weight/day) has no effect on the mutagenicity of N-nitrosodimethylamine, MNNG, N-methylnitrosourea and streptozotocin using the intrahepatic host-mediated bacterial mutagenicity assay. Additional in vivo studies demonstrate that simultaneous oral administration of ascorbic acid prevents the mutagenicity that follows the intragastric nitrosation of aminopyrine by nitrite while dietary pre-treatment with ascorbic acid does not. These findings suggest that ascorbic acid can block the intragastric formation of mutagenic N-nitroso compounds but that ascorbic acid has no effect on mutagenicity of N-nitroso compounds once they are formed.

Animals↗

PubMed2006

An immunohistological study of anhydrous topical ascorbic acid compositions on ex vivo human skin.

BACKGROUND: Ascorbic acid has numerous essential and beneficial functions in normal and photoaged skin. Ionisation of ascorbic acid in aqueous topical formulations leads to oxidative degradation. Ascorbic acid in an anhydrous vehicle would inherently have greater stability. OBJECTIVE: The objective of this study was to observe the effects of two anhydrous formulations containing microfine particles of ascorbic acid on neocollagenesis and cytokeratin production in ex vivo human skin. METHODS: Vitamin C preparations were applied topically onto the surface of freshly excised human abdominal skin. Following an exposure time of 48 h with appropriate controls, skin discs were cut into sections, placed on slides and assessed using immunohistochemical (antibodies: collagen type I, III, cytokeratin) staining. Analysis was performed using microscopy and descriptive rating. RESULTS: Both formulations resulted in increased production of collagen types I and III and cytokeratin. CONCLUSION: The application of anhydrous formulations containing microfine particles of ascorbic acid to ex vivo human skin in this study resulted in neocollagenesis and increased production of cytokeratin. This approach appears to enable biological effects of ascorbic acid in the skin using a vehicle which would provide it greater stability than an aqueous vehicle.

Abdomen↗

PubMed2000

A simple and rapid method for the routine assay of total ascorbic acid in serum and plasma using ascorbate oxidase and o-phenylenediamine.

A simple and rapid analysis of total ascorbic acid (AsA) in serum and plasma and its automated analysis are described. AsA is oxidized by ascorbate oxidase (AsA oxidase) to dehydroascorbic acid that then reacts with o-phenylenediamine (OPDA) to form a quinoxaline derivative that absorbs at 340 nm. The change in absorbance is directly proportional to the total AsA concentration. The assay was validated with a linear concentration range of 0.8-80 mg/L, and the within-day and between-day assays precision did not exceed 8.6% and 12.5%, respectively. On 47 sera, the manual enzymatic procedure gave 0.2 mg/L on average lower values than those of an automated enzymatic procedure with a correlation coefficient of 0.847. On another 66 sera, results by automated enzymatic method correlated well with the HPLC method and the regression equation is Y (enzymatic, automated)=0.97 X (HPLC)+0.1, r=0.980, Sy.x=0.6 mg/L. An experienced analyst can perform about 24 manual assays per hour whereas the automated procedure gave a rate of 100 assays per hour.

Ascorbate Oxidase↗

PubMed1982

Effect of dietary level of sulfur-containing amino acids on liver drug-metabolizing enzymes, serum cholesterol and urinary ascorbic acid in rats fed PCB.

Effects of dietary level of sulfur-containing amino acids (S-AA) on liver drug-metabolizing enzymes, serum cholesterol and ascorbic acid metabolism in growing rats fed diets containing 300 ppm of polychlorinated biphenyls (PCB) were investigated. Maximum gain in body weight was observed with 0.5% S-AA diets with or without PCB addition. Metabolic parameters increased by PCB were liver weight, activities of hepatic aminopyrine N-demethylase and aniline hydroxylase, serum total cholesterol, serum high density lipoprotein cholesterol, serum corticosterone and urinary metabolites of the glucuronic acid pathway including ascorbic acid, glucuronic acid and glucaric acid. In the PCB-treated animals, maximum values of liver weight, aminopyrine demethylase activity, serum cholesterol, serum corticosterone, urinary ascorbic acid and glucaric acid were obtained with about 0.8% S-AA. For the maximum induction of these metabolic responses, 0.5% S-AA was not enough. Urinary glucuronic acid and the ratio of lower density lipoprotein cholesterol versus high density lipoprotein cholesterol were decreased with a supplement of S-AA to PCB-containing diets.

Amino Acids, Sulfur↗

PubMed1993

Kinetic properties of light-dependent ascorbic acid oxidation by melanin.

The kinetic properties of ascorbic acid oxidation by light-activated melanin granules demonstrate the presence of a specific reactive site on the melanin granule saturable by ascorbic acid. Increased light intensity increased the Vmax and reduced the Km of this reaction, indicating increased affinity of the active site for ascorbic acid. The kinetics of this reaction are not markedly changed in a reduced-oxygen environment. Ascorbic acid oxidation is competitively inhibited by isoascorbic acid, an epimer of ascorbic acid, while other tested reducing agents are inactive. The Ki for isoascorbic acid is 1 mM, about the same as the Km of ascorbic acid.

Animals↗

PubMed2003

Quercetin-dependent reduction of salivary nitrite to nitric oxide under acidic conditions and interaction between quercetin and ascorbic acid during the reduction.

A salivary component, nitrate, is reduced to nitrite in the oral cavity. Polyphenols in foods are mixed with nitrite in the saliva to be swallowed into the stomach. An objective of the present study is to elucidate reactions between a polyphenol quercetin and a nitrite under acidic conditions. Nitric oxide, which is formed by the reactions between nitrous acid and quercetin or ascorbic acid (AA), can be measured using an oxygen electrode in the saliva as well as a buffer solution. The initial oxidation of quercetin was inhibited by AA, and quercetin enhanced the oxidation of AA, suggesting AA-dependent reduction of quercetin radicals, which might be formed during the oxidation of quercetin by nitrous acid. On the basis of the above results, the usefulness of an oxygen electrode for the measurement of nitrite-dependent nitric oxide formation under acidic conditions is proposed and the possible mechanism of reduction of nitrous acid by quercetin and the interaction between quercetin and AA, which is a normal component in the gastric juice, for the reduction of nitrous acid is discussed.

Ascorbic Acid↗

PubMed2005

Experimental spinal cord injury induced an increase of extracellular ascorbic acid concentration in anesthetized rats: a microdialysis study.

Ascorbic acid plays important roles in mammalian central nervous system. We employed an on-line analytical system to monitor the extracellular ascorbic acid concentrations in anesthetized rat spinal cord before and after the experimental injury. A microdialysis probe (216 microm od, 200 microm id, 3 mm in length) was implanted into an anesthetized rat spinal cord (Thoratic-12). Microdialysis perfusate (2 microl/min) was collected in the sample loop (20 microl) of an on-line injector for direct injection onto a High Performance Liquid Chromatography (HPLC) system equipped with an electrochemical detector. Normal ascorbic acid concentrations in the spinal cord extracellular fluids ranged from 1.8 microM to 10.8 microM (mean +/- S.D. 5.6 +/- 2.4 microM, n = 8). The experimental spinal cord injury, induced by a lesion at T-10, gradually yet significantly increased the extracellular ascorbic acid levels. The effect of exogenous glutamate perfusion (0.2 mM, 2 mM, and 20 mM) through the microdialysis probe also increased the extracellular ascorbic acid concentrations in a dose dependent manner. These results suggested that the injury-induced ascorbic acid accumulation may result from elevated extracellular glutamate levels that are commonly observed in spinal cord injury. This on-line, continuous and automatic monitoring system can be applied to future investigations on the roles of ascorbic acid in spinal cord injuries.

Anesthesia↗

PubMed1984

A study of blood ascorbic acid in leprosy.

The basal level of blood ascorbic acid was studied in 70 cases of polar leprosy. The level was found to be significantly reduced in both polar types, more so in tuberculoid. In untreated cases of these two polar forms, the differences were highly significant. No significant differences were found between untreated and treated cases of either form of leprosy, indicating that dapsone (DDS) has no effect on the ascorbic acid level. In lepromatous leprosy, the level was not affected by erythema nodosum leprosum (ENL). The deficiency of ascorbic acid in leprosy might be due to the disease per se and/or associated with nutritional factors. In trophic ulcers after supplement therapy for 60 days, the low level of ascorbic acid became close to the control group with marked improvement in the healing of the ulcers clinically. In addition, lactic and pyruvic acids were also measured and found to be significantly raised. After ascorbic acid supplement, the levels fell to near the control values, indicating that ascorbic acid played a role in controlling the infection as well as possible thiamine deficiency and also checked the disturbance caused by DDS on lactate and pyruvate metabolism. The present study suggested that supplementing DDS therapy with ascorbic acid might provide a beneficial effect on the general condition of the leprosy patients and the early healing of trophic ulcers.

Ascorbic Acid↗

PubMed1995

Ascorbic acid during cerebral ischemia in newborn piglets.

We measured ascorbic acid (reduced and oxidized) in brain, CSF and blood, before, during and after cerebral ischemia in newborn piglets. Bilateral carotid ligation induced a 54% decrease in cerebral blood flow (p < 0.01) and a 43% decrease in the cerebral metabolic rate of oxygen (p < 0.01). After ischemia and reperfusion, we obtained a 60% decrease (p < 0.01) in total brain ascorbic acid content. CSF ascorbic acid increased during reperfusion: +60% at 30 min (p < 0.001) and +160% at 120 min (p < 0.05). Blood ascorbic acid content did not change. These changes and the absence of massive oxidation of ascorbic acid in brain tissue suggest release of ascorbic acid by the brain during ischemia.

Animals↗

PubMed1982

Ascorbic acid uptake in guinea pig intestinal mucosa.

Cellular accumulation of ascorbic acid was investigated in vitro in distal intestinal mucosa of guinea pig. With 14C-ascorbic acid present at 8 microM/L in the bathing media, tissue/media (T/M) concentration ratios of at least 5 were routinely achieved. Recently absorbed ascorbic acid appeared to be free in solution in the cellular fluid in that it diffused from tissue exposed to poisons with a disappearance half-time of approximately 10 minutes. Ascorbic acid uptake was highly dependent on the presence of sodium in the bathing media; total Tris substitution resulted in a 97% decrease in uptake. Also, metabolically depleted tissue did not accumulate ascorbic acid against a concentration gradient. Uptake of 14C-ascorbic acid from a bathing solution concentration of 8 microM/L was reduced 67% in the presence of 0.8 mM/L nonlabeled ascorbic acid. Recently absorbed 14C-ascorbic acid moved more rapidly back into the lumen when the luminal solution contained nonlabeled ascorbic acid (5 mM) than when it contained mannitol (5 mM). This demonstration of counter transport substantiates a carrier mechanism in the brush border.

Animals↗

PubMed1993

Ascorbic acid recycling in human neutrophils.

Ascorbic acid (vitamin C) accumulation in activated human neutrophils is increased as much as 10-fold above the mM concentrations present in normal neutrophils. Internal concentrations as high as 14 mM are achieved when external vitamin is at physiologic concentration. The mechanism is by oxidation of external vitamin to dehydroascorbic acid, preferential transmembrane translocation of dehydroascorbic acid, and intracellular reduction to ascorbic acid within minutes. These data indicate that vitamin C accumulation is enhanced in activated human neutrophils and that human neutrophils utilize and recycle oxidized external vitamin C under physiologic conditions.

Adult↗

PubMed1976

Bioavailability of ascorbic acid in orange juice.

Several orange juice preparations were analyzed for biologically active and inactive ascorbic acid derivatives --L-ascorbic acid , dehydro-L-ascorbic acid, and inactive 2,3-diketo-L-gulonic acid. Fresh orange juice contained from 4 to 7 mg/100 ml of inactive ascorbic acid. In contrast, pasteurized orange juice contained from 15 to 30 mg/100 ml of inactive ascorbic acid (up to 400% more than fresh orange juice). Samples of fresh orange juice contained as much as 100% more active ascorbic acid than samples of pasteurized orange juice. There is great variability in prepared orange juice derivatives with a substantial decrease in bioavailability of active ascorbic acid.

Ascorbic Acid↗

PubMed2002

Development of an integrated capillary electrophoresis/sensor for L-ascorbic acid detection.

A CE/biosensor for measuring ascorbic acid was developed by coupling a polyaniline optical sensor and capillary electrophoresis (CE). The capillary column was partially modified with a thin film of polyaniline redox sensitive material. Ascorbic acid was detected by monitoring the changes in optical absorbance occurring to the polyaniline film upon the reduction reaction. The sensor response (change in optical absorbance at 650 nm) is proportional to the concentration of ascorbic acid over a range of 2.5-250 mg/L and the response range has shown a clear dependence on the characteristics of the polymerized film. High specificity and sensitivity of the present method, low sample consumption, short times of response (ca. 2 min) and the reproducibility of the results demonstrate that the CE/polyaniline-sensor could be further employed in the study of the relation between the content of L-ascorbic acid in body fluids and clinical parameters, e.g., cell ageing.

Ascorbic Acid↗