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PubMed1995

Intracameral ascorbic acid, glutathione and protein levels in albino and pigmented rabbits.

We performed a comparative investigation into differences between albino and pigmented rabbits in respect of intracameral concentrations of ascorbic acid, glutathione and total protein with high-performance liquid chromatography. The intracameral concentrations of reduced ascorbic acid, total ascorbic acid, reduced glutathione, total glutathione and protein in albino rabbits were similar (p > 0.05) to those in pigmented rabbits.

Animals↗
PubMed2002

Up-regulation and polarized expression of the sodium-ascorbic acid transporter SVCT1 in post-confluent differentiated CaCo-2 cells.

Human cells acquire vitamin C using two different transporter systems, the sodium-ascorbic acid co-transporters with specificity for ascorbic acid, and the facilitative glucose transporters with specificity for dehydroascorbic acid. There is no information on the mechanism of vitamin C transport across the intestinal barrier, a step that determines the bioavailability of vitamin C in humans. We used the colon carcinoma cell line CaCo-2 as an in vitro model for vitamin C transport in enterocyte-like cells. The results of transport kinetics, sodium dependence, inhibition studies, and reverse transcriptase-PCR analysis indicated that CaCo-2 cells express the sodium-ascorbate co-transporters SVCT1 and SVCT2, the dehydroascorbic acid transporters GLUT1 and GLUT3, and a third dehydroascorbic acid transporter with properties expected for GLUT2. Analysis by real time quantitative PCR revealed that the post-confluent differentiation of CaCo-2 cells was accompanied by a marked increase (4-fold) in the steady-state level of SVCT1 mRNA, without changes in SVCT2 mRNA levels. Functional studies revealed that the differentiated cells expressed only one functional ascorbic acid transporter having properties expected for SVCT1, and transported ascorbic acid with a V(max) that was increased at least 2-fold compared with pre-confluent cells. Moreover, post-confluent Caco-2 cells growing as monolayers in permeable filter inserts showed selective sorting of SVCT1 to the apical membrane compartment, without functional evidence for the expression of SVCT2. The identification of SVCT1 as the transporter that allows vectorial uptake of ascorbic acid in differentiated CaCo-2 cells has a direct impact on our understanding of the mechanism for vitamin C transport across the intestinal barrier.

Ascorbic Acid↗
PubMed2005

A spectroscopic study on applicability of spectral analysis for simultaneous quantification of l-dopa, benserazide and ascorbic acid in batch and flow systems.

The usefulness of derivative spectrophotometry for simultaneous assay of l-dopa, benserazide and ascorbic acid in pharmaceuticals was studied. The parameters of derivatisation depends on composition of solution in which particular compound was determined. For quantification of l-dopa in mixtures with benserazide or ascorbic acid the first derivative was used. Its determination in ternary mixture (l-dopa+benserazide+ascorbic acid) is possible by third derivative spectra. Benserazide was assayed in presence of l-dopa using first derivative while in ternary mixture by third derivative. Direct determination of ascorbic acid is possible applying first derivative only in presence of l-dopa. The elaborated derivative spectrophotometric methods were used for assaying of l-dopa and benserazide in their commercial form "Madopar". The proposed spectrophotometric derivative method of simultaneous determination of l-dopa and benserazide was combined with FIA technique.

Ascorbic Acid↗
PubMed2001

Fluorimetric determination of total ascorbic acid by a stopped-flow mixing technique.

A simple, rapid and automatic fluorimetric method for the determination of total ascorbic acid is described. The method makes use of the stopped-flow mixing technique in order to achieve the rapid oxidation of ascorbic acid by dissolved oxygen to dehydroascorbic acid, which then reacts with o-phenylenediamine to form a fluorescent quinoxaline. The initial rate and fluorescence signal of this system are directly proportional to the ascorbic acid concentration. The calibration graph was linear over the range 0.1-30 microg ml(-1) (kinetic method) and 0.25-34 microg ml(-1) (equilibrium method). The precision (% RSD) was close to 0.5%. The method has been used for the determination of ascorbic acid in pharmaceutical formulations, fruit juices, soft drinks and blood serum.

Ascorbic Acid↗
PubMed1977

The effect of additives on the free radical formation in aqueous solutions of ascorbic acid.

The relative rate constants for the decay of ascorbate free radical in aqueous solutions in the presence of heavy metal ions, hydrogen peroxide and sulphite were measured the ESR-spectroscopy. The oxidation of ascorbic acid showed a strong pH dependence, reaching a maximum rate at pH 9.6. It was shown that the ascorbic acid radical decay generally follows overall second order kinetics, being however first order in the presence of hydrogen peroxide. The protective effect of sulphur dioxide is proposed to have nutritional implications.

Ascorbic Acid↗
PubMed1985

Ascorbic acid enhances the formation of prostaglandin E1 in washed human platelets and prostacyclin in rat aortic rings.

Effects of ascorbic acid at physiologically achieved concentrations were examined on the metabolism of exogenous dihomo-gamma -linolenic acid and arachidonic acid (AA) in washed human platelets, and of AA in rat aortic rings. In the presence of ascorbic acid an increased formation of PGF1 alpha, PGE1 and PGE2 was observed in platelets. Also this vitamin induced an increased production of prostacyclin (measured as its stable metabolite 6-keto-PGF1 alpha) from exogenously provided substrate in aortic rings. In addition, from endogenous stores of AA in aortic rings ascorbic acid induced an increased generation of prostacyclin as revealed by inhibition of ADP-induced platelet aggregation.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

The influence of ascorbic acid on lipid peroxidation in guinea pigs intoxicated with cadmium.

Cadmium (as CdCl2) administered at a dose of 1 mg Cd/animal/day in drinking water to guinea pigs with a low intake of ascorbic acid (2 mg/animal/day) increased lipid peroxidation (LPO) in the kidney, liver and serum after 5 wk of treatment. A high intake of ascorbic acid (100 mg/animal/day) decreased LPO (determined from malondialdehyde levels) in the kidney, liver and serum of Cd-treated guinea pigs. Administration of Cd to guinea pigs with a low intake of ascorbic acid significantly increased LPO in the kidney at 5 wk, in comparison with controls given low levels of ascorbic acid but no Cd. However, at 12 wk, LPO in the kidney of Cd-treated guinea pigs was significantly lower than in the controls. These results indicate that the level of lipid peroxides in the kidney of guinea pigs with a low intake of ascorbic acid depends on the amount of accumulated cadmium.

Administration, Oral↗
PubMed1979

[Erythrocyte protective synergism of ascorbic acid and alpha-mercaptopropionylglycine].

The antitoxic action of 1-ascorbic acid and alpha-mercaptopropionyl glycine was examined via the formation of Ehrlich-Heinz bodies in human venous red cells following in vitro intoxication with 100 mg/ml acetylphenylhydrazine. Marked synergism was noted, especially when small amounts of glucose were added. Both substances displayed a marked affinity for red cells and penetrated them on contact without an incubation period. Optimum amounts for maximum synergy were alpha-mercaptopropionyl glycine 0.01-0.02, 1-ascorbic acid 0.01-0.02 ml and glucose 40 mg per ml of blood. At this dose, appearance of Ehrlich bodies was appreciably retarded. In addition, changes in the size and quality of such bodies pointed to enhanced cell resistance to the poison used.

Amino Acids, Sulfur↗
PubMed1998

Effect of ascorbic acid on infarct size in experimental focal cerebral ischaemia and reperfusion in a primate model.

Temporary occlusion of major cerebral blood vessels occasionally becomes necessary during surgical procedures. Ascorbic acid (Vitamin C) is an important non-enzymatic scavenger of free radicals and its protective effect on the brain in permanent focal cerebral ischaemia has been proven in a primate model of focal cerebral ischaemia [16]. Additional damage caused by reperfusion of the infarcted area has been shown in the rat model [22]. This study was undertaken to study the efficacy of ascorbic acid in decreasing infarct size in ischaemic reperfused brain. Maccaca radiata monkeys in the treated group were given two grams of ascorbic acid, parentally immediately before clipping the middle cerebral artery and the control group was given placebo. Reperfusion was done after four hours. Mean infarct size in all the three brain slices in the ascorbic acid pretreated group was 7.3% +/- 2.7 and in the placebo group 22.1 +/- 6.7 under similar conditions. The mean infarct size in the ascorbic acid pretreated group of monkeys was significantly lower when compared with the placebo group (p = 0.0003).

Animals↗
PubMedDate not supplied

[Effect of a malic acid load on the blood and urine content in animals of the products of a malate dehydrogenase reaction and the correlation of reduced and oxidized forms of ascorbic acid].

Addition of 150 mg of malic acid per a day to food of rabbits caused an increase in content of reduced ascorbic acid and pyruvic acid in blood; at the same time the content of oxydized forms of ascorbic acid was decreased. Similar alterations were observed in urine of guinea-pigs, which received 100 mg of malic acid per a day. The data obtained suggest that under these conditions the increased reduction, of ascorbic acid was due to increased formation of NADP with H2 in the course of reaction, catalyzed by malate dehydrogenase.

Administration, Oral↗
PubMed1993

The influence of ascorbic acid on selected parameters of cell immunity in guinea pigs exposed to cadmium.

The study investigated the possibility of influencing immunotoxic effects of Cd through ascorbic acid. Guinea pigs with high and low intake of ascorbic acid were perorally exposed to cadmium chloride (1 mg Cd/animal/day). The daily vitamin C intake was 2 and 100 mg per animal, respectively. Phagocytic activity of polymorphonuclear leucocytes and monocytes as well as the percentage of active and total T lymphocytes in peripheral blood of animals were evaluated. Five- and 12-week experiments showed a mutual potentiation of negative effects of Cd on the immune system by suboptimal intake of ascorbic acid. Toxic effects of Cd on the immune system can be reduced by a sufficient intake of vitamin C.

Animals↗
PubMed2001

Relation of serum ascorbic acid to mortality among US adults.

PURPOSE: To examine the relation between serum ascorbic acid (SAA), a marker of dietary intake (including supplements), and cause-specific mortality. SUBJECTS AND METHODS: We analyzed data from a probability sample of 8,453 Americans age > or = 30 years at baseline enrolled in the Second National Health and Nutrition Examination Survey (NHANES II), who were followed for mortality endpoints. We calculated relative hazard ratios as measures of disease association comparing the mortality rates in three biologically relevant SAA categories. RESULTS: Participants with normal to high SAA levels had a marginally significant 21% to 25% decreased risk of fatal cardiovascular disease (CVD) (p for trend = 0.09) and a 25% to 29% decreased risk of all-cause mortality (p for trend <0.001) compared to participants with low levels. Because we determined that gender modified the association between SAA levels and cancer death, we analyzed these associations stratified by gender. Among men, normal to high SAA levels were associated with an approximately 30% decreased risk of cancer deaths, whereas such SAA levels were associated with an approximately two-fold increased risk of cancer deaths among women. This association among women persisted even after adjustment for baseline prevalent cancer and exclusion for early cancer death or exclusion for prevalent cancer. CONCLUSIONS: Low SAA levels were marginally associated with an increased risk of fatal CVD and significantly associated with an increased risk for all-cause mortality. Low SAA levels were also a risk factor for cancer death in men, but unexpectedly were associated with a decreased risk of cancer death in women. If the association between low SAA levels and all-cause mortality is causal, increasing the consumption of ascorbic acid, and thereby SAA levels, could decrease the risk of death among Americans with low ascorbic acid intakes.

Adult↗
PubMed2001

Ascorbic acid protects against peroxidative modification of low-density lipoprotein, maintaining its recognition by LDL receptors.

Peroxidatively modified low-density lipoprotein (LDL) may contribute to atherosclerotic processes; therefore, protecting LDL against peroxidation may thus reduce or retard the progression of atherosclerosis. We have evaluated the protective effects of ascorbic acid on copper-catalyzed LDL peroxidative modification. The protective effects of ascorbic acid on copper-catalyzed LDL peroxidative modification were examined by measurement of concentration of lipid hydroperoxides in LDL and by the provision of LDL cholesterol to lymphocytes via LDL receptor-mediated pathway. The measurement of concentration of lipid hydroperoxides in LDL showed that ascorbic acid inhibited peroxidative modification of LDL. Also, ascorbic acid preserved the ability of LDL to be recognized by LDL receptors in peripheral blood lymphocytes to the same extent as native LDL. These findings indicate that ascorbic acid may protect LDL against peroxidative modification, maintaining its ability to act as a ligand for LDL receptors in vivo.

Adult↗
PubMed1982

Ascorbic acid and iron levels in plasma and liver of vitamin C deficient guinea pigs after iron overload and desferrioxamine administration.

The effect of desferrioxamine on the reduction of tissue iron and the corresponding level of tissue ascorbic acid have been investigated in female guinea pigs on Vitamin C deficient diet. Plasma and liver AA concentrations were measured after stopping treatment (day 0) and on the following 24 days. Vitamin C intake with the diet enhances rapid absorption of iron into the tissue with corresponding increased catabolism of tissue ascorbic acid. Desferrioxamine reduced tissue iron concentrations without causing pronounced loss of liver ascorbic acid. It is concluded that alterations in tissue ascorbic acid are caused by iron overload in guinea pigs without the pronounced involvement of desferrioxamine.

Animals↗
PubMed1998

Ascorbic acid inhibits the increase in low-density lipoprotein (LDL) susceptibility to oxidation and the proportion of electronegative LDL induced by intense aerobic exercise.

BACKGROUND: We have previously reported the finding of an acute increment in the susceptibility of low-density lipoprotein (LDL) to oxidation and in the proportion of electronegative LDL [LDL(-)] after intense exercise. We have now studied the effect of oral supplementation with 1 g ascorbic acid, immediately before a 4-h athletic race, on the susceptibility of LDL to oxidation, the proportion of LDL(-), and the alpha-tocopherol and lipid peroxides content in LDL, in order to inhibit such deleterious changes, and to confirm the oxidative nature of modifications of LDL induced by exercise. METHODS: We studied seven highly trained runners who received a supplement of 1 g ascorbic acid and a control group of seven who did not receive the supplement. The susceptibility of LDL to oxidation was assessed by measurement of conjugated dienes after CuSO4-induced oxidation, the proportion of LDL(-) was determined by anion exchange chromatography, alpha-tocopherol was quantified by reverse-phase high performance liquid chromatography, and lipid peroxides were measured by the thiobarbituric acid-reactive substances (TBARS) method. RESULTS: After exercise, in the control group there was an increase in both the susceptibility of LDL to oxidation (change in lag phase from 51.4 +/- 4.7 min to 47.0 +/- 4.6 min, P < 0.05) and the proportion of LDL(-) (from 11.1 +/- 1.4% to 13.0 +/- 2.2%, P < 0.05), but these did not occur in the ascorbic acid group (change in lag phase from 49.7 +/- 2.3 min to 50.4 +/- 4.2 min, and in LDL(-) from 9.7 +/- 1.7% to 10.1 +/- 1.7%). No significant changes in the absolute amount of LDL alpha-tocopherol were observed after exercise (ascorbic acid group: 6.65 +/- 0.94 mol/mol apoB before the race, 7.13 +/- 0.88 mol/mol apoB after the race; control group: 7.34 +/-0.69 mol/mol apoB before the race, 7.06 +/- 0.69 mol/mol apoB after the race), but significant differences were found when increments or decrements of alpha-tocopherol were tested (alpha-tocopherol increased 9.9 +/- 11.5% in the ascorbic acid group, and decreased 0.6 +/- 7.3% in the control group; P < 0.018). TBARS did not change after exercise. CONCLUSIONS: We conclude that 1 g ascorbic acid inhibits the increase in LDL susceptibility to oxidation after exercise, preventing this acute pro-atherogenic effect. In addition, the observation that LDL(-) enhancement is prevented by ascorbic acid supports the hypothesis that at least some of the circulating LDL(-) originates from oxidative processes.

Adult↗
PubMed2003

Alteration in the glutathione, glutathione peroxidase, superoxide dismutase and lipid peroxidation by ascorbic acid in the skin of mice exposed to fractionated gamma radiation.

BACKGROUND: In spite of the immense therapeutic gains produced by the fractionated irradiation (IR) regimen, radiation burden on the skin increases significantly. Protection of skin might enable use of higher radiation doses for better therapeutic gains. Ascorbic acid (AA), an essential ingredient of the human diet, is known to be a free radical scavenger and radioprotective agent. This study was undertaken to evaluate the effect of ascorbic acid on the radiation-induced changes in the status of glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and lipid peroxidation (LPx) in the skin of mice exposed to 10, 16 and 20 Gy of fractionated gamma radiation. METHODS: One group of the animals was administered daily with double distilled water (DDW), while the other group received 250 mg/kg b. wt. of ascorbic acid once daily, consecutively for 5, 8 or 10 days, before hemibody (below rib cage) exposure to 2 Gy/day of gamma-rays. Skin biopsies from both the groups were collected for the biochemical estimations. RESULTS: The irradiation of animals resulted in a dose-dependent decline in the activities of superoxide dismutase, glutathione peroxidase and glutathione contents. Ascorbic acid pretreatment resulted in a significant increase in the activities of both the enzymes and glutathione in the irradiated mouse skin. Normal concentrations of glutathione could not be restored even by day 6 post-irradiation. Conversely, lipid peroxidation increased in a dose-dependent manner in both the groups reaching a peak concentration by 3 h post-irradiation, while the ascorbic acid pretreatment inhibited the radiation-induced increase in lipid peroxidation. CONCLUSIONS: The ascorbic acid treatment arrested the decline in the activities of superoxide dismutase and glutathione peroxidase, glutathione contents and inhibited the radiation-induced lipid peroxidation in the skin of mice exposed to different doses of fractionated gamma radiation.

Animals↗
PubMedDate not supplied

[Content of different forms of ascorbic acid in the tissues of rabbits with experimental myocardial infarct].

It was established that experimental myocardial infarction leads to a decrease in the ascorbic acid content in the left heart ventricle in the ischemic are and to a negligible rise in the dehydroascorbic acid concentration within the first hours after artery ligation followed by its lowering at the 24th hour. Meanwhile 24 hours after the operation the right heart ventricle manifests a 22% increase in the ascorbic acid content along with the rise of the deketogulonic acid level, whereas the content of dehydroascorbic acid does not appreciably change. The concentration of ascorbic acid in the liver of animals with experimental myocardial infarction drops by 27% as compared with intact animals. The data obtained attest to upset ascorbic acid metabolism in the acute stage of experimental myocardial infarction thus suggesting that it is desirable to apply vitamin C to the treatment of patients with myocardial infarction.

Animals↗
PubMed2003

[The effect of topical ascorbic acid application on the healing of rat tympanic membrane perforations].

OBJECTIVES: We investigated the effect of topical administration of ascorbic acid on the healing process of tympanic membrane perforations in rats. DESIGN AND METHODS: Thermal myringotomy was induced in both ears of 22 albino rats. The right and left ears were assigned to topical applications of ascorbic acid and saline solution, respectively. The same procedure was performed after 48 hours. Perforations were examined daily by otomicroscopy and healing periods were determined. For histopathologic examination, a single rat in which closure of the tympanic membranes was not completed was sacrificed on days 5, 7, 10, and 12. Data were analyzed with the use of the Student's t-test. RESULTS: The mean durations of healing in the right and left ears were 7.6 and 8.3 days, respectively. No significant differences were found between the applications of ascorbic acid and saline solution with regard to the duration of closure and histopathologic healing criteria. CONCLUSION: Our data suggest that topical application of ascorbic acid have no beneficial effect on the healing of rat tympanic membrane perforations.

Administration, Cutaneous↗