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PubMed1979

Maternal-fetal transfer of ascorbic acid in the guinea pig.

Placental transfer of ascorbic acid was studied in the guinea pig using an in situ placental perfusion technique. A total of 14 animals were studied during their last week of gestation. The fetus was shown to have higher plasma total ascorbic acid (TAA) levels than the mother prior to maternal ascorbic acid infusion. However, following maternal venous infusion this normal gradient for TAA (fetal greater than maternal) disappeared and a new gradient was established (maternal greater than fetal). As maternal plasma TAA levels rose, the level of TAA in the placental perfusate steadily increased to a maximal concentration of approximately 0.85 mg/dl. This occurred when maternal plasma TAA levels were above 3.0 mg/dl. These results demonstrate that a saturable or carrier-mediated transport mechanism is involved in the placental transfer of ascorbic acid in this species. The apparent Vmax (the maximal transport rate by the saturable system per gram placenta) and the Kt (or one-half saturation concentration) were estimated to be 8.3 nmoles/minute and 0.12 mM, respectively. Additional results are presented to suggest that dehydroascorbic acid (DHA) may be the predominant form of the vitamin crossing the guinea pig placenta.

Animals↗
PubMed1991

Ascorbic acid accumulation in human skin fibroblasts.

The transport and accumulation of ascorbic acid in normal human skin fibroblasts in culture was investigated by using high-performance liquid chromatographic separation and coulometric electrochemical detection. Results measured as picomole ascorbic acid per microgram cell protein were expressed in molar amounts after determining the volume of skin fibroblasts. Confluent fibroblasts contained undetectable amounts of ascorbic acid. On incubation with micromole per liter amounts of ascorbic acid in the medium, cells showed increasing uptake of ascorbic acid with time, accumulating a 15-fold excess in 3.5 h. Kinetic experiments suggested two transport mechanisms, a high-affinity and a low-affinity transport activity. Both transport activities were temperature sensitive and accumulated ascorbic acid against a concentration gradient.

Ascorbic Acid↗
PubMed1978

Bactericidal action of ascorbic acid on Psuedomonas aeruginosa: alteration of cell surface as a possible mechanism.

Neutralised ascorbic acid is found to exert a strong bactericidal action on Pseudomonas aeruginosa suspended in isotonic phosphate buffer at pH 7.1. Both the bactericidal and bacteriostatic action of ascorbic acid are antagonised by magnesium ions. In the absence of complex formation between magnesium and ascorbic acid it is concluded that ascorbic acid acts by competing with the magnesium binding sites in the cell wall, cell membrane or ribosomes. Using the chequer-board titration method the synergistic action of ascorbic acid and erythromycin is determined; such a potentiation of erythromycin is also adversely affected by magnesium ions. P. aeruginosa cells, washed and suspended in isotonic phosphate buffer containing ascorbic acid, became increasingly susceptible to the action of polymyxin, erythromycin, chloramphenicol, neomycin and tetracycline. It is suggested that ascorbic acid alters the cell surface to render it increasingly permeable to these antibiotics.

Ascorbic Acid↗
PubMed1982

Effects of some xenobiotics on ascorbic acid metabolism in rats.

The administration of xenobiotics, PCB, DDT, or aminopyrine to rats causes a marked increase in urinary excretion of ascorbic acid and in various tissue levels of ascorbic acid. When rats were fed diet containing 200 ppm PCB or 500 ppm DDT (14 days), the incorporations from D-(U-14C) glucose into ascorbic acid in liver were significantly increased. The dietary addition of 200 ppm PCB, 500 ppm DDT, 2,000 ppm pentobarbital or 3,000 ppm chloretone caused a significant increase in the activity of hepatic UDPglucose dehydrogenase, but did not affect the activity of hepatic L-gulonolactone oxidase. Good correlation between the liver level of ascorbic acid and the activity of hepatic UDPglucose dehydrogenase was observed. Subsequently, in rats fed the basal diet (30% casein diet) or the diet containing 200 ppm PCB, the specific activities of ascorbic acid in urine and in various tissues were measured 6 hours, 12 hours and 24 hours after the oral administration of L-(l-14C)ascorbic acid. Dietary PCB accelerated the disappearances of radioactivities in ascorbic acid in urine and various tissues, that is, shortened the half lives of radioactivities in ascorbic acid. It is likely that the administration of xenobiotics, such as PCB or DDT, to rats increases the biosynthesis of ascorbic acid and accelerates concomitantly the turnover of ascorbic acid in body.

Aminopyrine↗
PubMed1975

Changes relevant to catecholamine metabolism in liver and brain of ascorbic acid deficient guinea-pigs.

A chronic deficiency of ascorbic acid was induced in guinea pig. The level of catecholamines, copper and the activities of ceruplasmin, catecholamine oxidase, monoamineoxidase and acetylcholinesterase were checked in brain, liver and serum. Also the levels of ascorbic acid and glutathione were measured in the organs of ascorbic acid-deficient animals. The most important changes due to the ascorbic acid deficiency were observed in the brain were monoamineoxidase, catecholamineoxidase, acetylcholinesterase and the concentration of catecholamines were altered. The statement that brain is the organ most affected by the ascorbic acid deficiency is discussed.

Acetylcholinesterase↗
PubMed2001

Role of ascorbic acid in promoting follicle integrity and survival in intact mouse ovarian follicles in vitro.

Ascorbic acid has three known functions: it is necessary for collagen synthesis, promotes steroidogenesis and acts as an antioxidant. Within the ovary, most studies have concentrated on the role of ascorbic acid in luteal formation and regression and little is known about the function of this vitamin in follicular growth and development. Follicular growth and development were investigated in this study using an individual follicle culture system that allows the growth of follicles from the late preantral stage to Graafian morphology. Follicles were isolated from prepubertal mice and cultured for 6 days. Control media contained serum and human recombinant FSH. Further groups of follicles were cultured in the same media but with the addition of ascorbic acid at concentrations of either 28 or 280 micromol l(-1). Addition of ascorbic acid at the higher concentration significantly increased the percentage of follicles that maintained basement membrane integrity throughout culture (P < 0.001). Ascorbic acid had no effect on the growth of the follicles or on oestradiol production. Metalloproteinase 2 activity tended to increase at the higher concentration of ascorbic acid and there was a significant concomitant increase in the activity of tissue inhibitor of metalloproteinase 1 (P < 0.01). Follicles cultured without the addition of serum but with FSH and selenium in the culture media underwent apoptosis. Addition of ascorbic acid to follicles cultured under serum-free conditions significantly reduced apoptosis (P < 0.05). From these data it is concluded that ascorbic acid is necessary for remodelling the basement membrane during follicular growth and that the ability of follicles to uptake ascorbic acid confers an advantage in terms of granulosa cell survival.

Animals↗
PubMed1989

Ascorbic acid transport and accumulation in human neutrophils.

The transport, accumulation, and distribution of ascorbic acid were investigated in isolated human neutrophils utilizing a new ascorbic acid assay, which combined the techniques of high performance liquid chromatography and coulometric electrochemical detection. Freshly isolated human neutrophils contained 1.0-1.4 mM ascorbic acid, which was localized greater than or equal to 94% to the cytosol, was not protein bound, and was present only as ascorbic acid and not as dehydroascorbic acid. Upon addition of ascorbic acid to the extracellular medium in physiologic amounts, ascorbic acid was accumulated in neutrophils in millimolar concentrations. Accumulation was mediated by a high affinity and a low affinity transporter; both transporters were responsible for maintenance of concentration gradients as large as 50-fold. The high affinity transporter had an apparent Km of 2-5 microns by Lineweaver-Burk and Eadie-Hofstee analyses, and the low affinity transporter had an apparent Km of 6-7 mM by similar analyses. Each transporter was saturable and temperature dependent. In normal human blood the high affinity transporter should be saturated, whereas the low affinity transporter should be in its linear phase of uptake.

Ascorbic Acid↗
PubMedDate not supplied

Ascorbic acid and glycosaminoglycan and lipid metabolism in guinea pigs fed normal and atherogenic diets.

The effect of low and high doses of ascorbic acid on glycosaminoglycan and lipid metabolism was studied in guinea pigs fed both normal and atherogenic diets. The high dose of ascorbic acid (25 mg/100 g body weight/day) decreased the cholesterol level in the liver and aorta but not in the serum in animals fed the normal diet in comparison with those fed the low dose of ascorbic acid (0.1 mg/100 g body weight/day). In animals fed the atherogenic diet, cholesterol decreased in the serum and liver, but not in the aorta. Serum triglycerides were not affected by the dose of ascorbic acid in the group on the normal diet, but in the animals receiving the atherogenic diet, the high dose of ascorbic acid caused serum triglycerides to decrease when compared with the low dose. Hepatic and aortic triglycerides decreased in groups on normal and atherogenic diets receiving the high dose of ascorbic acid. Lipoprotein lipase activity was not affected in the aorta by the dose of ascorbic acid either in the normal or atherogenic diet group. It was increased in the liver and heart in both the groups receiving the low dose of ascorbic acid but decreased in the high dose group. The concentration of all the glycosaminoglycans significantly increased in the aorta of animals on normal diet receiving the high dose of ascorbic acid when compared with the low dose group. In the group on the atherogenic diet, hyaluronic acid was not affected, but all the sulphated glycosaminoglycans increased in the animals receiving the high dose when compared with those receiving the low dose. In the liver all the sulphated glycosaminoglycans increased while hyaluronic acid decreased in both the normal and atherogenic diet groups receiving the high rather than the low dose of ascorbic acid. L-Glutamine:D-fructose-6-phosphate aminotransferase and UDPG dehydrogenase, two key enzymes in the biosynthesis of precursors of glycosaminoglycans, were studied in relation to the dose of ascorbic acid. Hepatic aminotransferase activity was higher both in the normal and atherogenic diet groups when receiving the high rather than the low dose of ascorbic acid. UDPG dehydrogenase was not affected by the dose of ascorbic acid. The activities of the degrading enzymes -- hyaluronidase, beta-glucuronidase, beta-hexosaminidase and aryl sulphatase -- significantly increased both in the normal and atherogenic diet groups when receiving the low rather than the high dose of ascorbic acid. The concentration of PAPS, sulphate activity and sulphotransferase activity were all increased in both the normal and atherogenic diet groups receiving the high dose of ascorbic acid.

Animals↗
PubMed1986

Effects of ascorbic acid in vivo on the fatty acid composition of the tissues of mice treated with Gramoxone.

The effects of the simultaneous administration of ascorbic acid and the LD50 of paraquat (an ingredient of Gramoxone), and of ascorbic acid pretreatment followed by the LD50 of paraquat, were studied on the phospholipid and triglyceride fatty acid levels in homogenates of mouse lung, liver and kidney. Ascorbic acid treatment increases the content of polyunsaturated fatty acids in the lung considerably, i.e. the pulmonary membrane fluidity decreases significantly in response to ascorbic acid. In the liver homogenate, the membrane fluidity is significantly increased by ascorbic acid pretreatment, and significantly decreased by simultaneous ascorbic acid treatment. In the renal tissue, the result of ascorbic acid pretreatment exhibits a similar tendency to that of paraquat treatment, but a more significant one, while the administration of ascorbic acid together with paraquat does not cause a substantial change in the fluidity index compared to the control.

Animals↗
PubMed2000

Human vitamin C (L-ascorbic acid) transporter SVCT1.

In human, vitamin C (l-ascorbic acid) is an essential micronutrient required for an array of biological functions including enzymatic reactions and antioxidation. We describe here the molecular cloning of a novel human cDNA encoding a vitamin C transporter SVCT1. SVCT1 is largely confined to bulk-transporting epithelia (e.g., kidney and small intestine) with a putative alternative-splice product present in thymus. Applying radiotracer and voltage-clamp approaches in cRNA-injected Xenopus oocytes, we found that SVCT1 mediates saturable, concentrative, high-affinity l-ascorbic acid transport (K(0.5) = 50-100 microM) that is electrogenic and can be inhibited by phloretin. SVCT1 displays exquisite substrate selectivity, greatly favoring l-ascorbic acid over its isomers d-isoascorbic acid and dehydroascorbic acid and 2- or 6-substituted analogues, whereas glucose and nucleobases are excluded. We have mapped the SLC23A2 gene (coding for SVCT1) to human chromosome 5 in band 5q31.2-31.3, within a region commonly deleted in malignant myeloid (leukemia) diseases. In addition, we have demonstrated that the human SLC23A1 gene product is a related high-affinity l-ascorbic acid transporter (SVCT2) that is widely distributed in brain, retina, and a host of endocrine and neuroendocrine tissues. The molecular identification of the human l-ascorbic acid transporters now provides the tools with which to investigate their roles in vitamin C metabolism in health and disease.

Amino Acid Sequence↗
PubMedDate not supplied

Anemia associated with changes in iron and iron-59 utilization in copper deficient rats fed high levels of dietary ascorbic acid and iron.

The influence of dietary copper, iron, and ascorbic acid on iron utilization was examined in a 2 x 2 x 2 factorial experiment. Male Sprague-Dawley weanling rats were fed copper-deficient (Cu-, 0.42 microgram Cu/g) or copper-adequate (Cu+, 5.74 micrograms Cu/g) diets that contained one of two levels of iron (38 or 191 micrograms Fe/g) and ascorbic acid (0 or 1% of the diet). These eight diets were fed for 20 d, and rats received an oral dose of 4 microCi iron-59 on d 15. Compared to Cu+ rats, the Cu- rats had 27% lower hemoglobin levels with 45, 59, and 65% lower cytochrome c oxidase (CCO) activities in the liver, heart, and bone marrow, respectively (p less than 0.0001). High dietary iron or ascorbic acid did not alter hemoglobin in Cu+ rats. However, hemoglobin was 23% lower in Cu- rats fed the highest, rather than the lowest levels of iron and ascorbic acid. Liver CCO was decreased (p less than 0.02) in Cu- rats fed high iron. Among Cu- rats, ascorbic acid did not influence CCO but decreased hemoglobin by 17% (p less than 0.001), reduced the percentage of absorbed iron-59 in the erythrocytes by 91% (p less than 0.05) and depressed the percentage apparent absorption of iron (p less than 0.05). These results suggest that the effects of elevated dietary iron and ascorbic acid on iron utilization are influenced by copper status.

Anemia, Hypochromic↗
PubMed1993

Antioxidant and neutrophil-inhibiting properties of new 2-O-methyl-6-(alkylthio)ascorbic acid derivatives.

A series of new 6-(alkylthio)ascorbic acids was synthesized, and their inhibitory effects on lipid peroxidation and the oxidative burst of human neutrophils were tested. Of 12 structurally different lipophilic ascorbic acid derivatives 6-S-n-hexadecyl-2-O-methyl-6-deoxy-6-thio-L-ascorbic acid (7b; B-003) inhibited the Fe2+/ADP-induced lipid peroxidation of rat liver microsomes with an IC50 value of 2 microM. In human neutrophils, 7b most potently inhibited the fMLP-induced oxidative burst in a cell density-dependent manner with an IC50 value of 0.6 microM at 5 x 10(5) cells/mL. Shorter alkyl chain lengths decreased the inhibitory potency for both lipid peroxidation and oxidative burst, but in general no correlation was found between the two parameters. Likewise, 6-S-n-hexadecyl-3-O-methyl-6-thio-L-ascorbic acid (7c; B-015), the regioisomer of 7b, was a potent antioxidant but did not affect the oxidative burst. Since superoxide anions generated by xanthine/xanthine oxidase were not quenched by 7b, it became evident that its target was somewhere between receptor stimulation and NADPH-oxidase activation. By measuring the cellular concentrations of 7b and 7c, an accumulation of the first was found explaining its potency and the dependence on cell density. Expecting a pKa value of 3.3 for 7b and 7.7 for 7c a protonophore action of 7b was likely and could be verified by the drop in intracellular pH (pHi) which did not occur with 7c. Ionophores such as nigericin, CCCP, or propionic acid also lowered the pHi but did not inhibit the oxidative burst, indicating that the pHi drop was not the cause for this inhibition. 7b also strongly inhibited the fMLP-induced secretion of azurophilic (IC50 = 7 microM) and specific (IC50 = 2.5 microM) granules.

Animals↗
PubMed1983

Dietary ascorbic acid and hepatic mixed function oxidase activity in the guinea pig.

Studies were carried out to characterize the response of hepatic mixed function oxidase (MFO) activity to chronic ascorbic acid deficiency and excessive ascorbic acid intake in the guinea pig. When guinea pigs were fed excessive ascorbic acid, there was a small increase in hepatic cytochrome P-450 which was unaccompanied by any alteration in drug-metabolizing enzyme activity. Similarly, induction of MFO activity by phenobarbital was not modified by excessive ascorbic acid administration. Chronic ascorbic acid deficiency resulted in depressed metabolism of aniline, aminopyrine, ethoxycoumarin and benzphetamine, but not of ethylmorphine, in comparison with animals fed diets containing control and/or excessive amounts of ascorbic acid. In contrast to the metabolism of all drugs studied, the 7 alpha-hydroxylation of cholesterol was depressed by both inadequate and excessive vitamin C intake, demonstrating the unique sensitivity of cholesterol 7 alpha-hydroxylase to dietary ascorbate.

Animals↗
PubMed1995

Anodic voltammetric study of ascorbic Acid at platinum and gold rotating disc electrodes.

Anodic Voltammetry of ascorbic acid at platinum and gold rotating disc electrodes has been examined in acidic and alkaline media. Ascorbic acid is oxidised by a single two electron wave at platinum and one electron two step at gold electrode. The best medium for electroanalysis is 0.1 mol 1(-1) sulphuric acid in which it shows obedience to the Levich relationship at both electrodes. The limiting current is linearly proportional to ascorbic acid concentration with Zero intercept and shows excellent rapid voltammetric determination. Electrode Kinetic parameters for mass and charge transfer have been determined. Voltammetric method has been used to determine the number of electrons involved in the reaction and the reaction mechanism has been elucidated.

Acids↗
PubMed1983

Ascorbic acid inhibition of Campylobacter jejuni growth.

The inhibitory effect of ascorbic acid on Campylobacter jejuni is described. In vitro growth of clinical strains, as measured spectrophotometrically, was inhibited by 0.5 mg of freshly prepared L-ascorbic acid per ml. Alkaline-treated or aged L-ascorbic acid increased inhibition, as did copper; however, L-cysteine, L-cystine, and glutathione prevented inhibition. Biochemical analysis of the medium and cultures indicated that one or more of the oxidation products of L-ascorbic acid, e.g., L-dehydroascorbic acid or L-diketogulonic acid, were more effective inhibitors than was reduced L-ascorbic acid.

Ascorbic Acid↗
PubMed1991

Decreased resistance to antibiotics and plasmid loss in plasmid-carrying strains of Staphylococcus aureus treated with ascorbic acid.

The effect of ascorbic acid on plasmid-coded antibiotic resistance in Staphylococcus aureus was investigated. Several strains of S. aureus were cultured in the presence of 1 mM ascorbate for 6 h. This treatment induced an increased loss of resistance markers in 4 of 6 strains tested, and agarose gel electrophoresis showed this disappearance of plasmid DNA in ascorbate-induced susceptible colonies. The presence of ascorbate induced a 50-75% decrease in minimal inhibitory concentrations of different antibiotics for resistant strains. When ascorbate is added, formerly subinhibitory concentrations of penicillin or tetracycline have an increased inhibitory effect on resistant strains and even induced the death of 25-93% of the initial population. These results suggest that ascorbate can induce the loss of several plasmids of S. aureus, and that the levels of antibiotic resistance are also affected by the presence of this compound.

Ascorbic Acid↗
PubMed1972

Platelet ascorbic acid levels in normal subjects and in disease.

The platelet ascorbic acid concentration was measured in 26 normal subjects and found to be 20 times as high as in plasma. This is in agreement with previous reports in the literature. The platelets of patients with uraemia, leukaemia, and megaloblastic anaemia had a lower than normal platelet ascorbic acid content. In uraemia and megaloblastic anaemia the plasma ascorbic acid concentration was normal suggesting that a platelet defect may be responsible for the low platelet ascorbic acid content. In leukaemia the low platelet ascorbic acid content is probably secondary to a low plasma level.

Acute Disease↗