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PubMed1994

Protection by ascorbic acid against oxidative injury of isolated hepatocytes.

1. The ability of ascorbic acid to protect from prooxidant-induced toxic injury was investigated in isolated, intact rat hepatocytes, whose ascorbic acid content had been restored by means of exogenous supplementation. 2. Ascorbate-supplemented and ascorbate-non-supplemented cells in suspension were treated with a series of different prooxidants (allyl alcohol, diethyl maleate, carbon tetrachloride, menadione), and the development of lipid peroxidation and cell injury was evaluated. 3. With allyl alcohol and diethyl maleate, ascorbic acid was able to protect cells from both lipid peroxidation and cell injury. The same protection was offered by ascorbate also in hepatocytes obtained from vitamin E-deficient animals. 4. With carbon tetrachloride, ascorbate supplementation did not affect the initial steps of lipid peroxidation, but nevertheless provided a marked protection against lipid peroxidation and cell injury at later times of incubation. The protection was unaffected by the vitamin E content of cells. 5. With menadione, a toxin which does not induce lipid peroxidation, ascorbic acid did not protect cells against injury. 6. It is concluded that ascorbic acid can act as an efficient antioxidant in isolated rat liver cells, with protection against cell injury. The antioxidant effect appears primarily to involve membrane lipids, and can be independent from the cellular content of vitamin E, thus suggesting that ascorbic acid can play a direct and independent role in the intact cell, in addition to its synergistic interaction with vitamin E described in other models.

1-Propanol↗
PubMed1995

Intracellular ascorbic acid inhibits the Na(+)-Ca2+ exchanger in cultured rat astrocytes.

The effect of ascorbic acid on Ca2+ uptake in cultured rat astrocytes was examined in the presence of ouabain and monensin, which are considered to drive the Na(+)-Ca2+ exchanger in the reverse mode. Ascorbic acid at 0.1-1 mM inhibited Na(+)-dependent Ca2+ uptake significantly but not Na(+)-dependent glutamate uptake in the cells, although the inhibition required pretreatment for more than 30 min. The effect of ascorbic acid on the Ca2+ uptake was blocked by simultaneous addition of ascorbate oxidase (10 U/ml). Na(+)-dependent Ca2+ uptake was also inhibited by isoascorbate at 1 mM but not by ascorbate 2-sulfate, dehydroascorbate, and sulfhydryl-reducing reagents such as glutathione and 2-mercaptoethanol. The inhibitory effect of ascorbic acid was observed even in the presence of an inhibitor of lipid peroxidation, o-phenanthroline, or a radical scavenger, mannitol, and the degrading enzymes such as catalase and superoxide dismutase. On the other hand, the inhibitory effect was not observed under the Na(+)-free conditions that inhibited the uptake of ascorbic acid in astrocytes. When astrocytes were cultured for 2 weeks in a medium containing ascorbic acid, the content of ascorbic acid in the cells was increased and conversely Na(+)-dependent Ca2+ uptake was decreased. These results suggest that an increase in intracellular ascorbic acid results in a decrease of Na(+)-Ca2+ exchange activity in cultured astrocytes and the mechanism is not related to lipid peroxidation.

Animals↗
PubMed1994

Expression of a rabbit renal ascorbic acid transporter in Xenopus laevis oocytes.

We examined the expression of renal ascorbic acid transporter(s) in Xenopus laevis oocytes after microinjection of cells with poly(A)+ RNA extracted from rabbit kidney cortex. Concomitant expression of the Na+-glucose cotransporter served as a control in these studies. Injection of poly(A)+ RNA into oocytes produced over a fivefold increase in the uptake of [14C]ascorbic acid (570 microM) compared with water-injected cells. Size fractionation of the kidney cortex mRNA by sucrose gradient revealed that the mRNA species that induced ascorbic acid transporter expression in oocytes was present in a fraction centered around 2.0 kilobases (kb) and had a size range of 1.8-3.1 kb. Injection of the active fraction into oocytes produced a > 40-fold increase in ascorbic acid uptake compared with water-injected controls. Expression of ascorbic acid transporter(s) was noticeable as early as 2 days after injection and was maximal after 7 days; it was also dependent on the amount of mRNA injected into oocytes. The induced uptake of [14C]ascorbic acid after injection of mRNA into oocytes was 1) Na+ dependent, as indicated by the almost complete lack of transport on removal of Na+ from the incubation medium; 2) significantly inhibited by unlabeled ascorbic acid and its structural analogue isoascorbic acid but not by D-glucose; and 3) saturable as a function of increasing the substrate concentration in the incubation medium (100-1,000 microM), with an apparent Km of 258 +/- 72.5 microM and a maximum velocity of 29.6 +/- 2.8 pmol.oocyte-1.2 h-1. These data demonstrate that X. laevis oocytes are a suitable system to functionally express the mammalian renal ascorbic acid transporter.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

Effect of ascorbic acid on serum lipid levels and depot cholesterol of the baboon (Papio ursinus).

Twelve young male baboons were kept on a diet low in ascorbic acid for 3 months before the experiment. Six animals then received intravenous injections of ascorbic acid 60 mg/kg body mass every third day, while an isotonic saline solution was administered to 6 control animals. The serum ascorbic acid concentration of the animals treated with ascorbic acid levelled off after 9 days, at about 1,1 mg/100 ml. Ascorbic acid treatment resulted in a significant increase (P smaller than 0,005) in serum cholesterol values during the initial stages of treatment, but these returned to normal when the body pool was replenished with ascorbic acid. Ascorbic acid also brought about a significant lowering in serum triglyceride values (P smaller than 0.05). In an acute experiment ascorbic acid caused a 12,7% increase in serum cholesterol level 2 hours after the intravenous injection of ascorbic acid 60 mg/kg body mass. The blood glucose value and serum triglyceride concentration were not affected. The results prove that ascorbic acid treatment causes mobilisation of cholesterol from body depots into the bloodstream.

Animals↗
PubMedDate not supplied

Ascorbic acid in the brain.

Ascorbic acid is highly concentrated in the central nervous system. Measurement of the extracellular concentration of ascorbate in animals, mainly by the technique of voltammetry in vivo, has demonstrated fluctuation in release from neuropil, both spontaneously and in response to physical stimulation of the animal and to certain drugs. Although in the adrenal medulla ascorbate is co-released with catecholamines, release of ascorbate from brain cells is associated principally with the activity of glutamatergic neurones, mainly by glutamate-ascorbate heteroexchange across cell membranes of neurones or glia. This phenomenon is discussed in relation to a possible role of ascorbate as a neuromodulator or neuroprotective agent in the brain.

Animals↗
PubMed2004

A study on degradation kinetics of ascorbic acid in amla (Phyllanthus emblica L.) during cooking.

The kinetics of ascorbic acid degradation in amla (Phyllanthus emblica L.) as well as in pure ascorbic acid solutions at initial concentrations present in amla over a temperature range of 50-120 degrees C (steady-state temperature) has been studied. The ascorbic acid degradation followed first-order reaction kinetics where the rate constant increased with an increase in temperature. The temperature dependence of degradation was adequately modeled by the Arrhenius equation. The activation energies were found to be 4.09 kcal/mole for amla and 4.49 kcal/mole for pure vitamin solution. The degradation kinetics of ascorbic acid was also evaluated in normal open pan cooking, pressure-cooking and a newly developed and patented fuel-efficient EcoCooker (unsteady state heating process). A mathematical model was developed using the steady-state kinetic parameters obtained to predict the losses of ascorbic acid from the time-temperature data of the unsteady state heating processing method. The results obtained indicate the ascorbic acid degradation is of a similar order of magnitude in all the methods of cooking.

Ascorbic Acid↗
PubMed1987

Re-evaluation of ascorbic acid deficiency in hemodialysed patients.

In 92 uremic patients under chronic hemodialysis without ascorbic acid supplementation, serum ascorbic acid was measured before hemodialysis and between two sessions. The results indicated a more serious ascorbic acid deficiency of patients than in previous studies. This difference might be explained by the highly specific enzymatic method applied in the present study, excluding any potential interference of various serum reducing substances.

Adult↗
PubMed1992

Influence of ascorbic acid supplementation on copper metabolism in rats.

An attempt was made to unravel further the mechanism by which high dietary concentrations of ascorbic acid influence copper metabolism. The addition of ascorbic acid to the diet of rats caused about a twofold increase in plasma ascorbate concentrations and reduced group mean plasma and tissue concentrations of Cu. The effect of 10 g ascorbic acid/kg diet was greater than that of 1 g/kg. Ascorbic acid feeding reduced blood haemoglobin concentrations and packed cell volume values. Dietary ascorbic acid caused a significant decrease in apparent Cu absorption from the intestine. Ascorbate, intravenously administered together with 64Cu, caused an increase in 64Cu in the liver. Ascorbate, at concentrations occurring in plasma after ascorbic acid feeding, promoted the uptake of 64Cu by isolated hepatocytes. Thus, ascorbate stimulated the efficiency of hepatic uptake of Cu. Ascorbate, intravenously administered together with 64Cu, stimulated accumulation of 64Cu in bile of rats with a bile duct cannula. In rats fed on ascorbic acid, intravenously administered 64Cu was recovered in bile at increased rates. Dietary ascorbic acid enhanced the recovery of intraperitoneally administered 64Cu in faeces. The ascorbate-induced stimulation of biliary 64Cu excretion may reflect an increased hepatic uptake of 64Cu and be caused by an increased specific activity of Cu in liver pools. It is suggested that dietary ascorbic acid reduces tissue Cu concentrations primarily by interfering with intestinal Cu absorption. Ascorbate increases the efficiency of hepatic uptake of Cu, but this effect may not be causatively related with the reduced tissue Cu concentrations after ascorbic acid feeding.

Animals↗
PubMed2002

Enhancement of glutathione cardioprotection by ascorbic acid in myocardial reperfusion injury.

The present experiment determined the effects of glutathione and ascorbic acid, the two most important hydrophilic antioxidants, on myocardial ischemia-reperfusion injury and evaluated their relative therapeutic values. Isolated rat hearts were subjected to ischemia (30 min) and reperfusion (120 min) and treated with ascorbic acid, glutathione monoethyl ester (GSHme), or their combination at the onset of reperfusion. Administration of 1 mM GSHme alone, but not 1 mM ascorbic acid alone, significantly attenuated postischemic injury (P < 0.05 versus vehicle). Most interestingly, coadministration of ascorbic acid with GSHme markedly enhanced the protective effects of GSHme (P < 0.01 versus vehicle). The protection exerted by the combination of GSHme and ascorbic acid at 1 mM each was significantly greater than that observed with 1 mM GSHme alone (P < 0.05). Moreover, treatment with GSHme alone or GSHme plus ascorbic acid markedly reduced myocardial nitrotyrosine levels, suggesting that these treatments attenuated myocardial peroxynitrite formation. These results demonstrated that 1) GSHme, but not ascorbic acid, exerted protective effects against ischemia-reperfusion injury; and 2) the protective effects of GSHme were further enhanced by coadministration with ascorbic acid, suggesting a synergistic effect between GSHme and ascorbic acid.

Animals↗
PubMed1994

Long term administration of testosterone on ascorbic acid metabolism in castrated rats.

Orchidectomy caused a significant decrease in the concentration of ascorbic acid and ascorbic acid-2-sulphate in tissues while administration of testosterone to these animals reverses this effect. Concentration of ascorbic acid in liver in experimental groups correlates with the activity of L-qualano-lactone oxidase and dehydroascorbatase in this tissue.

Animals↗
PubMed1986

Studies on ascorbic acid and cholesterol levels in Nigerian nomadic groups.

Studies on plasma and leukocyte ascorbic acid and cholesterol concentrations in 102 nomads from rural communities in Oyo State of Nigeria, as well as in 88 controls, showed no significant differences between study group and controls with respect to leukocyte ascorbic acid values; no correlation was found between ascorbic acid and cholesterol levels; no cases of clinical scurvy were observed. These findings are compared with similar results from Kenya and elsewhere. The findings suggest low but acceptable levels of plasma ascorbic acid in nomadic groups; there was no correlation between ascorbic acid and cholesterol concentrations in cases where plasma vitamin C deficiency was mild or moderate with close to normal levels of leukocyte ascorbic acid; prolonged low levels of plasma ascorbic acid may exist without overt clinical manifestations of scurvy.

Adult↗
PubMed1969

New method for the estimation of platelet ascorbic acid.

Present techniques for the estimation of platelet ascorbic acid allow interference by other substances in the sample. A new and more specific method of analysis is presented. The proposed method owes its increased specificity to resolution of the extract by thin-layer chromatography. By this means ascorbic acid is separated from other reducing substances present. The separated ascorbic acid is eluted from the thin layer and estimated by a new and very sensitive procedure: ascorbic acid is made to react with ferric chloride and the ferrous ions so formed are estimated spectrophotometrically by the coloured derivative which they form with tripyridyl-Striazine. Results obtained with normal blood platelets were consistently lower than simultaneous determinations by the dinitrophenylhydrazine (DNPH) method.

Ascorbic Acid↗
PubMed1981

The role of superoxide and hydroxyl radicals in the degradation of hyaluronic acid induced by metal ions and by ascorbic acid.

Purified commercial hyaluronic acid contains significant amounts of iron. Addition of Fe2+ to solutions of it causes depolymerization, which is inhibited by catalase and scavengers of the hydroxyl radical (. OH) but not by superoxide dismutase. Fe3+ is ineffective. Ascorbic acid also depolymerizes hyaluronic acid, apparently because it can reduce Fe3+ in the reaction mixtures to Fe2+. Ascorbate-induced depolymerization is inhibited by the specific iron chelator desferrioxamine, by catalase, and by scavengers of the hydroxyl radical. The relevance of these observations to rheumatoid arthritis and inflammatory joint diseases is discussed.

Arthritis, Rheumatoid↗
PubMed2000

Possible role of ascorbic acid in the oxidative damage induced by inhaled crystalline silica particles.

The selective interaction of ascorbic acid with crystalline silica (quartz) has been studied by measuring the ascorbic acid consumption (by means of UV/vis and IR spectroscopy) and the release of silicon when quartz particles or amorphous silica (Aerosil 50) is incubated in ascorbic acid solution. At a physiological ascorbic acid concentration, quartz, and not amorphous silica, reacts, suggesting the formation of a 1:1 silicon-ascorbate complex, while at higher concentrations, the reacting amount of ascorbic acid exceeds the amount of silicon that is released. Silicon tetrahedra bearing free silanols at the quartz surface are selectively attached by ascorbic acid. The particle-derived hydroxyl radical yield in the presence of hydrogen peroxide is increased on ascorbic acid-treated quartz in comparison with the original sample. The results presented herein are relevant because the depletion of ascorbic acid from the lung lining layer and the increased potential in particle-derived free radical generation may both contribute to the oxidative damage following inhalation of crystalline silica.

Ascorbic Acid↗
PubMed1997

Ascorbic acid enhances hydroxyl radical formation in iron-fortified infant cereals and infant formulas.

UNLABELLED: Infant cereals and formulas are usually fortified with iron to prevent iron deficiency. To enhance iron bioavailability, supplemental ascorbic acid is recommended. Ascorbic acid is considered to be an antioxidant in vivo, but has pro-oxidant effects when exposed to non-protein-bound iron. We measured formation of free radicals in cereals and infant formulas after addition of ascorbic acid. The production of hydroxyl radicals was assessed by hydroxylation of salicylic acid to 2.5-dihydroxybenzoic acid (2,5-DHBA). Production of 2.5-DHBA increased with increasing ascorbic acid doses added. Addition of 0.8 mM ascorbic acid to breast milk produced less radicals (0.03 +/- 0.05 microM) than addition of ascorbic acid to low-iron formula (0.13 +/- 0.08 microM. P = 0.019), medium-iron formula (0.34 +/- 0.12 microM, P < 0.0001) or high-iron formula (0.44 +/- 0.08 microM. P < 0.0001). Even when iron content in breast milk was adjusted to a level comparable with that of formulas, production of 2,5-DHBA was lower. Breast milk seems to contain substances that reduce hydroxyl radical formation. CONCLUSION: Supplemental ascorbic acid causes hydroxyl radical formation in iron-fortified infant nutrients in vitro.

Ascorbic Acid↗
PubMed1991

Expression of Ascorbic Acid Oxidase in Zucchini Squash (Cucurbita pepo L.).

The expression of ascorbic acid oxidase was studied in zucchini squash (Cucurbita pepo L.), one of the most abundant natural sources of the enzyme. In the developing fruit, specific activity of ascorbic acid oxidase was highest between 4 and 6 days after anthesis. Protein and mRNA levels followed the same trend as enzyme activity. Highest growth rate of the fruit occurred before 6 days after anthesis. Within a given fruit, ascorbic acid oxidase activity and mRNA level were highest in the epidermis, and lowest in the central placental region. In leaf tissue, ascorbic acid oxidase activity was higher in young leaves, and very low in old leaves. Within a given leaf, enzyme activity was highest in the fast-growing region (approximately the lower third of the blade), and lowest in the slow-growing region (near leaf apex). High expression of ascorbic acid oxidase at a stage when rapid growth is occurring (in both fruits and leaves), and localization of the enzyme in the fruit epidermis, where cells are under greatest tension during rapid growth in girth, suggest that ascorbic acid oxidase might be involved in reorganization of the cell wall to allow for expansion. Based on the known chemistry of dehydroascorbic acid, the end product of the ascorbic acid oxidase-catalyzed reaction, we have proposed several hypotheses to explain how dehydroascorbic acid might cause cell wall "loosening."

Journal Article↗
PubMed2001

Effect of Ascorbic Acid and Its Hydrophobic Derivative Palmitoyl Ascorbate on the Redox State of Primary Human Fibroblasts.

Ascorbic acid (AA) and its derivatives participate in vitro in oxidative-reductive reactions both as antioxidants and as prooxidants. The physiological relevance of these prooxidant effects of AA and its derivatives remains unclear. There is little evidence that AA can initiate formation of reactive oxygen species (ROS) or lipid peroxidation in cells or tissue. In order to examine the effect of AA and its derivative palmitoyl ascorbate on in situ intracellular ROS production and lipid peroxidation, 2('),7(')-dichlorofluorescin diacetate (DCFH-DA) and cis-parinaric acid were used as fluorescent probes in cultural neonatal foreskin fibroblasts. The results demonstrated that the effect of AA depended on the in vitro growth conditions. AA induced augmentation of the intracellular ROS concentration in newly plated (24 hours) cells. However, in cells cultured for 72 hours, AA had a different effect: it moderately reduced intracellular ROS concentration but stimulated lipid peroxidation in the cytoplasmic membrane. Palmitoyl ascorbate demonstrated significant inhibition of intracellular DCFH-DA oxidation presumably caused by inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase.

Journal Article↗
PubMedDate not supplied

Uptake and release of ascorbic acid by rat Leydig cells in vitro.

The mechanism by which ascorbic acid is transported into rat Leydig cells in vitro was investigated. Transport of [14C]ascorbic acid was temperature-dependent and inhibited in the absence of sodium in the incubation medium. The uptake of [14C]ascorbic acid was saturable (apparent Km approximately equal to 33 microM, Vmax approximately equal to 20 pmol/10(6) cells/min) and stereospecific. Uptake was not affected by removing glucose from the incubation medium, indicating that no significant uptake was occurring via the glucose transport system. Transport of [14C]ascorbic acid into Leydig cells was not affected by testosterone concentrations up to 7 microM or by LH at a concentration that causes maximum androgen secretion. Leydig cells preloaded with [14C]ascorbic acid rapidly released radioactivity into the incubation medium, a process that was unaffected by the presence of LH. The results suggest that ascorbic acid uptake by Leydig cells is by an electroneutral, sodium-dependent co-transport mechanism as in some, but not all, other types of cells.

Animals↗