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PubMed2000

The effects of ascorbic acid on dopamine-induced death of PC12 cells are dependent on exposure kinetics.

The role of ascorbic acid on dopamine (DA) oxidation-mediated cytotoxicity was studied using the PC12 cell line. DA cytotoxicity was slightly attenuated by ascorbic acid, whereas the cytotoxicity of 6-hydroxydopamine (6-OHDA), a DA oxidation product, was markedly potentiated. To elucidate the relationship between the ascorbic acid effect and the degree of DA oxidation, ascorbic acid was added in a time-dependent fashion after DA treatment. We found greater cell death the later ascorbic acid was applied. Treatment of cells with glutathione alleviated DA- and 6-OHDA-induced cell death, while L-buthionine sulfoximine potentiated DA and 6-OHDA cytotoxicity. Ascorbic acid combined with glutathione eliminated the toxicity of DA and 6-OHDA. These results suggest that the interaction between DA and ascorbic acid is dependent upon the degree of DA oxidation and glutathione availability.

Animals↗
PubMed1999

Ascorbic acid metabolism in rats and guinea pigs after the administration of ethanol.

Ascorbic acid metabolism was studied in guinea pigs and rats after the administration of ethanol and a high dose of ascorbic acid (AA). Male guinea pigs were maintained for 30 days as follows: (1) controls (1 mg AA/100 g body wt.); (2) ethanol (1 mg AA/100 g body wt. + 900 mg ethanol/100 g body wt); (3) ascorbic acid (25 mg AA/100 g body wt.); (4) ascorbic acid + ethanol (25 mg AA/100 g body wt. + 900 mg ethanol/100 g body wt.). Rats were also grouped into four groups as in the case of guinea pigs, but the dose of AA was 200 mg/100 g body weight. Rats adjusted to ethanol intoxication by enhancing the biosynthesis of ascorbate as evidenced by elevated activity of L-gulono lactone oxidase (GLO). Hence ascorbate levels were not lowered in rats after administration of alcohol. However, alcohol administration lowered tissue levels of ascorbate in guinea pigs. But the supplementation of ascorbate along with alcohol raised the tissue level of this vitamin. Guinea pigs responded to the ascorbate deficiency during alcohol administration by lowering the degradation of ascorbate, as seen by the lower activity of the degrading enzyme gulono lactone hydrolase. It is concluded that on the administration of alcohol, guinea pigs are dependent upon additional exogenous supplies of ascorbic acid, whereas rats are not.

Animals↗
PubMed1983

Ascorbate radical and ascorbic acid level in human serum and age.

Free radical in human serum was observed by an electron spin resonance (ESR) technique and was assigned to ascorbate radical. Quantitative estimation revealed that the ESR intensity could be used as an expedient mean. The ESR intensity of ascorbate radical, the concentrations of total ascorbic acid and oxidized form of ascorbic acid were determined on sera of 200 healthy individuals whose ages ranged from 12 to 96 years. The ESR intensity as well as the concentrations of total and oxidized form of ascorbic acid declined with age. There were significant correlations between the ESR intensity and the concentrations of total and oxidized form of ascorbic acid. From these results, the clinical significance of the concentrations of total ascorbic acid, ascorbate radical and the oxidized form was discussed in relation to age.

Adolescent↗
PubMed1989

Ascorbic acid analysis using high-performance liquid chromatography with coulometric electrochemical detection.

A method for the detection of ascorbic acid using high-performance liquid chromatography with coulometric electrochemical detection and a technique for stabilization of the vitamin are described. Since less than 1 pmol of ascorbic acid can be detected, this assay provides significantly greater sensitivity than nearly all of the currently available procedures. Stabilization of 10 pmol or less of ascorbic acid at room temperature for up to 4 h and for several weeks at -70 degrees C facilitates storage of a large number of samples and measurement of ascorbic acid using an automated sampling device. This method was used to quantitate the amounts of ascorbic acid in human polymorphonuclear leukocytes and bovine adrenomedullary chromaffin granules. The calculated concentrations found for human neutrophils (1.35 mM) and bovine chromaffin granules (10.0 mM) are in agreement with previously published data. The assay is suitable for the determination of ascorbic acid in biological samples where only a small amount of tissue is available or very low amounts of ascorbic acid are found. This method is the first application of coulometric electrochemical detection to ascorbic acid HPLC analysis.

Animals↗
PubMed1981

Differential inhibitory effects of ascorbic acid on the binding of dopamine agonists and antagonists to neostriatal membrane preparations: correlations with behavioral effects.

Ascorbic acid was a potent inhibitor of the binding of both dopamine agonists (3H-dopamine and 3H-ADTN) and also of dopamine antagonists (3H-spiroperidol and 3H-domperidone) to neostriatal membrane preparations. Against dopamine agonists, ascorbic acid caused a dose-dependent inhibition of binding with about 90% effect at 6 mM ascorbic acid. Against dopamine antagonists there was U-shaped dose response curve for ascorbic acid. That is, 6 mM ascorbic acid caused no significant inhibition, while 0.006 mM caused a slight inhibition, and intermediate concentrations caused extensive inhibition. Almost identical inhibitory effects were obtained with sodium ascorbate. In other experiments, 500 mg/kg of ascorbic acid given to mice 1 hour prior to the dopamine releasing agent d-amphetamine, was able to greatly attenuate the increase in locomotor activity usually seen after amphetamine. These latter data may have important implications for a possible role for ascorbic acid in dopaminergic neurotransmission.

Animals↗
PubMed1985

Effect of L-ascorbic acid supplementation on the toxicity of pirimiphos-methyl to albino rats.

The effect of L-ascorbic acid supplementation on Pirimiphos-methyl induced toxicity was studied in albino rats. Biochemical estimations were made in rats administered orally the insecticide at 100 and 200 mg/kg body weight with or without oral supplementation of L-ascorbic acid at 200 mg/kg b.w. The biochemical assessments included estimations of brain and plasma cholinesterases, levels of ascorbic acid in liver, kidney and adrenals, urinary levels of ascorbic acid and glucuronic acid. A lower degree of inhibition of the cholinesterases were evident in ascorbic acid supplemented rats. Marked elevation in urinary levels of ascorbic acid and glucuronic acid was observed in the insecticide treated rats. Results of this study suggests that L-ascorbic acid supplementation partially offsets Pirimiphos-methyl induced toxicity.

Acetylcholinesterase↗
PubMed1989

Ascorbic acid facilitates chicken myoblast fusion in vitro.

Addition of low concentrations of ascorbic acid (5 micrograms/ml to 10 micrograms/ml) to myogenic chick embryo cultures resulted in an early fusion. At 30 h cultures receiving small amounts of ascorbic acid presented fusion rates 3 times that of the control. However, control rates of fusion were not different from those of experimentals at 50 h. No such effect was seen with ascorbic acid added at 24 h of culture, or with ascorbic acid addition to a calcium-deprived system. These findings demonstrate that the calcium binding properties of ascorbic acid can induce precocious myogenic fusion.

Animals↗
PubMed2003

[Methemoglobinemia due to prilocaine after plexus anesthesia. Reduction by prophylactic administration of ascorbic acid?].

OBJECTIVE: This study investigated in vivo and in vitro kinetics of o-toluidine-induced methemoglobinemia and the influence of ascorbic acid on resulting methemoglobin concentrations. o-Toluidine is a metabolite of prilocaline and ascorbic acid is recommended for treatment of methemoglobinemia as an alternative to methylene blue. METHODS: We measured the formation of methemoglobin in vitro in a whole blood culture system of 8 healthy individuals 30, 60, and 360 min after the addition of different concentrations of o-toluidine (0.5, 5, 50 micrograms/ml) with and without addition of ascorbic acid (0.5 and 5 mg/ml). In a prospective randomized clinical study, a total of 72 patients of ASA risk I-III were investigated. The 3 groups of 24 patients received either an axillary, an infraclavicular vertical brachial plexus, or a combined femoral and ischiadic blockade. In each plexus anesthesia group, 12 patients were given 2,000 mg ascorbic acid intravenously before applying the local anesthetics. For surgery of the upper limb the patients received 40 ml 1% prilocaine and 10 ml 0.5% bupivacaine, for surgery of the lower limb they received 60 ml 1% prilocaine and 0.25 mg adrenaline. Blood samples for measurement of methemoglobin concentrations were taken before and 30, 60, 120, 180 and 360 min after the injection of the regional anesthetic. A p < 0.05 was considered to be significant. RESULTS: There was a dose-dependent increase of methemoglobin due to addition of o-toluidine after 360 min in vitro. The application of 0.5 mg/ml ascorbic acid to the whole blood samples with 0.5 and 5 micrograms/ml o-toluidine resulted in a further increase of methemoglobin formation whereas there was no difference in the samples with 50 micrograms/ml. The higher concentration of 5 mg/ml ascorbic acid attenuated the methemoglobin formation only with 50 micrograms/ml o-toluidine. No effect was observed with lower concentrations of o-toluidine. In the in vivo study plexus anesthesia with prilocaine resulted in an increase of the methemoglobin concentration with a maximum after 120-180 min. The highest measured methemoglobin concentration found was 11.3%. The methemoglobin concentration already showed a decrease 360 min after the application of the regional anesthetic 2,000 mg ascorbic acid given intravenously before plexus anesthesia was not able to influence the resulting methemoglobin concentrations. CONCLUSIONS: In vitro high concentrations of ascorbic acid are able to reduce the resulting methemoglobin concentration 360 min after addition of 50 micrograms/ml o-toluidine. The application of 2,000 mg ascorbic acid i.v. before plexus anesthesia with prilocaine does not reduce the concentration of methemoglobin.

Adult↗
PubMed1975

Further comments on the ascorbic acid requirement.

Recommended Daily Allowances (US RDA) of the Food and Drug Administration for ascorbic acid are higher than Recommended Dietary Allowances (set by the Food and Nutrition Board) for adults. There is a 6-fold margin between the requirement to prevent scurvy and the US RDA. The high requirement reported for the rhesus monkey may be needed to compensate for oxidative catabolism of ascorbic acid in this species. The rate of production of ascorbic acid, in mammals that synthesize it has been listed as 3-19 g/70 kg per day. If this high rate of synthesis represents the requirement of such animals, mutations that caused a loss of ascorbic-acid-synthesizing ability would be eliminated by natural selection on diets that failed to supply these large quantities. The loss of ascorbic-acid-synthesizing ability by human beings could indicate a low requirement, which has enabled our species to spread to regions of the earth where dietary sources of ascorbic acid are poor.

Animals↗
PubMedDate not supplied

Investigation of atmospheric oxidation of propyl gallate in an anionic surfactant system in the absence and presence of ascorbic acid.

The antioxidant efficiency of two hydrophilic species, ascorbic acid (AA) and propyl gallate (PG), in an anionic surfactant system are studied. Ascorbic acid and propyl gallate are dissolved/solubilized in a microemulsion formed by water, pentanol, and sodium dodecyl sulfate. The determination of propyl gallate decomposition/oxidation kinetics shows enhanced oxidation of PG with increasing pentanol concentration in the system. When ascorbic acid and propyl gallate are both present in water, in surfactant aqueous solution, and in the studied microemulsion systems, the molecular complex AAPG is formed. After some time the complex decomposes.

Anions↗
PubMedDate not supplied

The effects of L-ascorbic acid and prostaglandins on isolated tracheal smooth muscle.

On the isolated tracheal smooth muscle, L-ascorbic acid alone induced a dose-related relaxation. When L-ascorbic acid was added in a standard concentration of 10(-5) g/ml to increasing concentrations of PGE2, an increase of relaxation was evident. The opposite effect was observed when PGF2 alpha was added in presence of L-ascorbic acid: a depression of tracheal smooth muscle contraction occurred. L-ascorbic acid increased the relaxing effect of isoprenaline on the tracheal smooth muscle. The relaxation effect of L-ascorbic acid was abolished by propranolol. These data support the hypothesis, that the effect of L-ascorbic acid may be related to stimulation of beta adrenergic receptors.

Animals↗
PubMedDate not supplied

[Correlation of the nitrate and ascorbic acid content in vegetables and fruits].

Comparison of the evidence on the content of nitrates and ascorbic acid in vegetables and fruits shows that the content of ascorbic acid in fruits exceeds that of nitrates whereas in a number of vegetables the nitrate content is greater than that of ascorbic acid. With increase in the amount of nitrogen fertilizers introduced, the content of nitrates in vegetables grows more intensively as compared to ascorbic acid. The range of these variations is relative to the type and grade of vegetables. During the storage of beet and cabbage the decreased content of ascorbic acid correlated well with the amount of nitrogen-containing mineral fertilizers introduced. It is recommended that fruits and berries be used first of all as a source of ascorbic acid, while rhubarb, fall radish and salad be restricted in the diet.

Ascorbic Acid↗
PubMed1975

Cerebral monoamine metabolism in guinea-pigs with ascorbic acid deficiency.

Guinea-pigs kept on a diet deficient in vitamin C showed, after 3 weeks, a marked decrease of ascorbic acid in brain and blood leucocytes as well as of the activity of alkaline phosphatase in blood plasma. Pair-fed animals did not exhibit these changes. The alpha-methyl-p-tyrosine (alpha MpT)-induced diminution of noradrenaline in the hypothalamus and the rest of the brain was attenuated in pair-fed animals, but restored in guinea-pigs deficient in ascorbic acid. The cerebral noradrenaline content (without administration of alpha MpT) showed a decrease in both pair-fed and ascorbic acid deficient animals. The noradrenaline of the heart exhibited a similar tendency. The alpha MpT-induced dopamine decrease in the striatum of ascorbic acid deficient animals was attenuated and the dopamine content (without alpha MpT administration) decreased. Pair-fed animals showed a similar tendency. The striatal concentration of homovanillic acid (HVA) was diminished in both pair-fed and ascorbic acid deficient guinea-pigs. The cerebral content of 5-hydroxyindoleacetic acid showed a decrease in pair-fed as well as in ascorbic acid deficient animals. It is concluded that ascorbic acid deficiency enhances the turnover of brain noradrenaline, whereas under-nutrition without ascorbic acid deficiency (pair-feeding) diminishes the turnover of cerebral noradrenaline, 5-hydroxytryptamine and striatal dopamine.

Alkaline Phosphatase↗
PubMed1983

Interactions of ascorbic acid supplementation and bleomycin instillation on murine lung connective tissue metabolism.

The effects of ascorbic acid supplementation on the pulmonary toxicity induced by bleomycin were examined. Swiss-Webster mice were fed an ascorbate-free diet supplemented with ascorbic acid at 0%, 0.2%, or 1.0% of the diet for 2 weeks. Bleomycin (0.15 units) was instilled intratracheally and the mice were killed 1 week later. Bleomycin caused pulmonary inflammation and edema as noted by the increases in lung wet weight and lung wet-weight-to-dry-weight ratios. The activity of prolyl hydroxylase was increased 1.4-fold to 1.6-fold in response to bleomycin, but only minor increases were observed in the collagen and elastin content of the lung. Prior dietary ascorbic acid supplementation did not reverse the effects induced by bleomycin. Interestingly, each dietary level of supplemental ascorbic acid resulted in a slight increase in the elastin and collagen content of the lung in comparison with lungs from mice consuming no ascorbic acid in their diet. The data suggest that high levels of ascorbic acid supplementation may aggravate the response to bleomycin.

Animals↗
PubMed1998

The salubrious effects of ascorbic acid on cyclophosphamide instigated lipid abnormalities in fibrosarcoma bearing rats.

The combined effect of cyclophosphamide and ascorbic acid on plasma lipids and lipoprotein profiles are important since, ascorbic acid encumbered the lipid abnormalities initiated by cyclophosphamide during cancer chemotherapy. Hence, the study was launched to appraise the salutary role of ascorbic acid in cyclophosphamide administered fibrosarcoma bearing rats. Fibrosarcoma cell line induced rats were treated with cyclophosphamide (10 mg/kg body weight) and ascorbic acid (200 mg/kg body weight) individually and in combination for 28 days. The concentration of plasma lipids and lipoprotein profiles were determined in control and experimental animals. The untreated, as well as cyclophosphamide administered fibrosarcoma bearing rats, divulged significantly increased levels of plasma total cholesterol, triglycerides, phospholipids, VLDL- and LDL-cholesterol, as compared with their respective control animals. In contrast, ester and HDL-cholesterol levels exhibited a marked decrease in these animals. Similar observations were also noticed in liver lipid values, as well. However, these lipid abnormalities were corrected by the co-administration of ascorbic acid. These results suggested, that some clinical entanglement of cyclophosphamide was refrained by co-administration of ascorbic acid in tumor stress condition.

Animals↗