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At least 775 records · Page 43Linked to original sources
PubMed1991

Inhibiting effect of ascorbic acid on the growth of human mammary tumor xenografts.

The effect of ascorbic acid on the growth of a human mammary tumor in mice has been investigated using the 6-d subrenal capsule assay method. The results indicated that ascorbic acid administered in the drinking water significantly inhibited the growth of the tumor fragments implanted beneath the renal capsule of mice. Administration of a mixture of ascorbic acid and cupric sulfate orally or intraperitoneally significantly inhibited tumor growth in these mice, whereas neither alone was effective. These results support the hypothesis that certain oxidation or degradation products of ascorbic acid were active antineoplastic agents for the human mammary tumor studied. The activity of D-isoascorbic acid, an isomer of ascorbic acid, was similar to that of ascorbic acid. This suggests that the antitumor activity of ascorbic acid was not due to the metabolism of ascorbic acid as a vitamin, but due to its chemical properties.

Animals↗
PubMedDate not supplied

[Effect of massive doses of ascorbic acid on oxidative and glycolytic processes in the tissues].

Ascorbic acid in a dose of 500 mg/kg was given perorally to guinea pigs once in 24 hours. Investigations were carried out on animals receiving ascorbic acid in single doses and also with its administration of 7, 14, 21, 60 and 90 days. Subject to studies were tissue respiration and glycolysis of the skin, liver and kidneys as well as oxidative phosphorylation in hepatic homogenates. With introduction of large doses of ascorbic acid the tissue respiration of the kidneys and the effectiveness of oxidative phosphorylation in the liver were found to be on the increase. Both effects depended on the time during which massive doses of ascorbic acid were administered. The liver and kidney glycolysis did not show any changes with any duration of the ascorbic acid loading. The skin glycolysis intensity gained somewhat in strength with ascorbic acid administration for 21 days.

Animals↗
PubMed1982

Nicotine and ascorbic acid effects on cold-restraint ulcers in rats.

Rats were orally administered 1-ascorbic acid, nicotine 1-ascorbic acid and nicotine, or distilled water for 10 days. Following this treatment they were fasted for 24 h and then restrained in a cold environment for 2 h. Nicotine alone produced significantly more gastric ulcers than any other treatment. 1-Ascorbic acid increased ulceration relative to controls. The combined effects of 1-ascorbic acid and nicotine resulted in reduced ulcer incidence and severity. It appears that l-ascorbic acid and nicotine do not act synergistically to augment stress-induced gastric ulcer.

Animals↗
PubMedDate not supplied

Mercury excretion and intravenous ascorbic acid.

We tested the hypothesis that intravenous ascorbic acid increases urinary excretion of mercury in subjects with low mercury levels from dental amalgam, food, and other sources. From 89 adult volunteers we selected 28 subjects with the highest mercury excretions (2 to 14 micrograms/24 h). We administered intravenous infusions of 500 ml lactated Ringer's solution with and without addition of 750 mg of ascorbic acid/kg body weight, up to 60 g ascorbic acid. Average mercury excretion during the 24 h after infusion of ascorbic acid was 4.0 +/- 0.5 micrograms (mean +/- SEM), which was not significantly more than after infusion of Ringer's solution alone (3.7 +/- 0.5 micrograms). Lead excretion was similarly unaffected. If ascorbic acid administered intravenously benefits some persons with suspected adverse reactions to mercury, the benefit in subjects similar to ours appears unrelated to short-term enhanced excretion of mercury or lead.

Adolescent↗
PubMed1998

The role of ascorbic acid in oral cancer and carcinogenesis.

L-ascorbic acid is an essential dietary vitamin in humans, primates and certain mammals and is endogenously synthesised in some species. Epidemiological and ecological studies have shown that L-ascorbic acid has a protective effect against cancer, in particular non-hormone-dependent malignancies, such as oropharyngeal neoplasms. Experimental in vivo and in vitro studies, however, have yielded more controversial results, suggesting that the effects of L-ascorbic acid are dose- and perhaps, time-dependent with different effects depending on the species or organ studied. An update of the epidemiological and experimental evidence linking L-ascorbic acid to oral cancer and carcinogenesis is discussed together with a brief review of the possible mechanisms of action of L-ascorbic acid.

Animals↗
PubMedDate not supplied

In vivo antineoplastic activity of ascorbic acid for human mammary tumor.

The effect of ascorbic acid on the growth of human mammary tumor xenografts was investigated using the 6-day subrenal capsule assay method. The results showed that ascorbic acid (1 or 5 g/liter) administered in the drinking water significantly inhibited the growth of tumor fragments implanted beneath the renal capsule of immunocompetent mice. The results agree with other work carried out in animal experiments with animal tumors. Administration of ascorbic acid in the mouse diet did not affect the growth of the human mammary tumor fragments within the 6-day experimental period. Tumor growth was inhibited when mice were fed a diet containing ascorbic acid (50g/kg diet) together with cupric sulfate (18 or 90 mg/liter) in the drinking water. The results support the hypothesis that certain oxidation and degradation products of ascorbic acid are active antineoplastic agents for the human mammary carcinoma studied.

Animals↗
PubMed1979

Influence of dietary ascorbic acid on plasma lipid levels in the rainbow trout.

Rainbow trout maintained on ascorbic acid deficient and three grades of ascorbic acid supplemented diets (160--1280 mg ascorbic acid pr kg feed) for a period of 53 weeks, were studied for effects on plasma lipid levels. Fish fed the diet with no ascorbic acid manifested lethargy, lordosis, scoliosis, internal hemorrhages and low body weight. With regard to blood properties, ascorbic acid deficient fish had low hematocrit and high plasma levels of triglycerides and cholesterol but low level of free fatty acids. Plasma level of free fatty acids was low also in fish fed the diet containing the highest amount of ascorbic acid.

Administration, Oral↗
PubMed1992

Inhibition of ascorbic acid transport in human neutrophils by glucose.

Because of the structural similarity between glucose and ascorbic acid, we investigated the effect of glucose on uptake and accumulation of ascorbic acid in isolated normal human neutrophils. Ascorbic acid accumulation was determined using high-performance liquid chromatography with coulometric electrochemical detection, in conjunction with liquid scintillation spectrometry. Ascorbic acid accumulation in neutrophils is mediated by a high and a low affinity transport activity. In neutrophils from different volunteers, glucose inhibited uptake and accumulation of ascorbic acid by both transport activities 3-9-fold. The mechanism of inhibition was different for each transport activity: inhibition of the high affinity transport activity was noncompetitive, while inhibition of the low affinity activity was competitive. Glucose-induced inhibition of both ascorbic acid transport activities occurred in neutrophils of all donors tested and was fully reversible. Although the mechanism of ascorbic acid accumulation appeared to be different than that for glucose transport, other monosaccharides and glucose transport inhibitors also inhibited ascorbic acid accumulation. These are the first data to suggest that ascorbic acid accumulation in neutrophils can be regulated by compounds of similar structure.

Adult↗
PubMed1986

Effects of estrogen and progestogen on the ascorbic acid status of female guinea pigs.

Female, adult guinea pigs were fed a low ascorbic acid diet ad libitum. Oral administrations of either estinyl (5 micrograms) or progestogen (250 micrograms) in combination with 5 mg of ascorbic acid (minimum requirement) daily for 21 d, resulted in significantly lower (P less than 0.05) concentrations of ascorbic acid in plasma, liver, adrenals and urine than in animals receiving only 5 mg of the vitamin. None of these animals showed any clinical signs of ascorbic acid deficiency. Clinical manifestations of scurvy were exhibited, however, when animals receiving no ascorbic acid supplement were treated with the steroid hormones for 7 d. All of these animals died by d 10. On the other hand, the animals receiving neither ascorbic acid nor the steroids remained free from any signs of scurvy, except one (out of six), which died by d 12. In vitro studies revealed a markedly higher rate of oxidation of ascorbic acid in the presence of either estinyl or progestogen than in untreated controls. These results were further supported by a higher level of plasma ceruloplasmin in animals receiving a combination of estrogen and progestogen than in animals receiving no hormones. An in vivo dose-related effect of ascorbic acid indicated that the steroid-mediated lowering effect of the vitamin status could be counteracted by increasing the dose of ascorbic acid from 5 to 10 mg/d for 2 wk. These results suggest that the interactions between oral contraceptive hormones and ascorbic acid may be of clinical importance only in the case of borderline intake of the vitamin.

Adrenal Glands↗
PubMed1984

A direct correlation between the levels of ascorbic acid and H2O2 in aqueous humor.

There is evidence that H2O2 present in aqueous humor arises from ascorbic acid which is also present in this fluid, but the extent to which peroxide is derived from ascorbic acid is not known. We have measured the concentrations of H2O2 and ascorbic acid normally present in the aqueous humor of various species and also under conditions in which the level of ascorbic acid in the fluid was experimentally altered. In aqueous humor of rabbit and guinea pig the concentration of ascorbic acid was 10 times higher than that present in aqueous of rat and frog. Similarly, the concentration of H2O2 was four to 10 times higher in rabbit and guinea pig aqueous compared to that in rat and frog. Consistent with the higher concentration of ascorbic acid in posterior compared to anterior aqueous humor in the rabbit, the concentration of H2O2 was also significantly higher in the posterior aqueous. When ascorbic acid in rabbit aqueous humor was elevated by intraperitoneal administration of the compound, there was a significant increase in the level of H2O2 in both anterior and posterior aqueous humor. Moreover, when the level of ascorbic acid was lowered experimentally by placing guinea pigs on an ascorbic acid deficient diet, a 10-fold decrease in the level of both ascorbic acid and H2O2 was observed in the aqueous humor. Upon returning the animals to a normal diet, the concentrations of both compounds returned to control values. The direct correlation between the concentrations of ascorbic acid and H2O2 in aqueous humor suggests that ascorbic acid is the primary source of H2O2 in this fluid.

Animals↗
PubMedDate not supplied

[Effect of ascorbic acid on uric acid formation in men and animals].

The effect of the level of ascorbic acid on the formation of uric acid in the animals and human organisms has been learned. Activation of the hydroxylation of adenyl purins and uric acid by ascorbic acid has been found. A hypothesis was made about the activation of formation of glucocorticoids by ascorbic acid. Glucocorticoids, perhaps, lower the level of uric acid. Hypothesis was confirmed by experiments.

Adenine↗
PubMed1982

The attenuation of exercise-induced bronchospasm by ascorbic acid.

In order to study the potential benefit of ascorbic acid in asthma we investigated its role in exercise-induced bronchospasm (EIB). Twelve asthmatic subjects were recruited on the basis of findings compatible with EIB. On two subsequent days the subjects ingested 500 mg. of ascorbic acid or a placebo. The study was performed in a double-blind randomized fashion. Partial and maximal expiratory flow volume (PEFV and MEFV) curves were used to determine pulmonary function changes. Pretreatment with ascorbic acid led to a significant attenuation of the bronchospasm seen five minutes after exercise compared to placebo, as measured by FVC (0.23 +/- 0.08 L decrease after ascorbic acid, 0.48 +/- 0.14 L decrease after placebo) and by FEV1 (0.24 +/- 0.06 decrease after ascorbic acid, 0.44 +/- 0.14 decrease after placebo) Mean +/- SE). These results suggest a mild antibronchospastic action of ascorbic acid in subjects with EIB.

Adult↗
PubMed1996

Inhibitory action of palytoxin on ascorbic acid transport into cultured bovine adrenal chromaffin cells.

The effect of palytoxin on the transport of ascorbic acid into cultured bovine adrenal chromaffin cells was examined by measuring the accumulation of radiolabeled ascorbic acid within cells. Ascorbic acid transport into these cells was inhibited by palytoxin in a concentration-dependent manner, and this inhibitory action of palytoxin was shown to be noncompetitive and irreversible. Neither the Na+/K+-pump activity in the intact cells nor the Na+,K+-adenosine 5'-triphosphatase activity in the plasma membranes was significantly influenced by this toxin at concentrations inhibiting ascorbic acid transport. In contrast to the effect of palytoxin on ascorbic acid transport, glucose transport into these cells was not significantly affected by this toxin. These findings indicate that palytoxin can inhibit ascorbic acid transport into adrenal chromaffin cells without affecting Na+,K+-adenosine 5'-triphosphatase activity in the plasma membranes. Furthermore, because palytoxin discriminated between ascorbic acid transport and glucose transport, the data provide new evidence that the transport of ascorbic acid and that of glucose may be mediated by different mechanisms in the adrenal medullary cell.

Acrylamides↗
PubMed1992

Effect of ascorbic acid on neutrophil functions and hypoxanthine/xanthine oxidase-generated, oxygen-derived radicals.

The chemiluminescence of isolated neutrophils, stimulated with N-formyl-L-methionyl-L-leucyl-L-phenylalanine, latex, lipopolysaccharide from Escherichia coli, zymosan A, or 4 beta-phorbol 12 beta-myristate 13 alpha-acetate was inhibited up to 99% by the dose-dependent oxygen radical scavenging activity of 6 mmol/l ascorbic acid. The chemiluminescence of neutrophils in blood, stimulated with 4 beta-phorbol 12 beta-myristate 13 alpha-acetate, or with zymosan A was inhibited 35% or 48%, respectively, by 6 mmol/l ascorbic acid. Ascorbic acid, up to 6 mmol/l, did not inhibit the release of beta-N-acetylglucosaminidase and elastase from isolated neutrophils activated by the above stimulatory agents. During neutrophil/nylon fibre interaction ascorbic acid reduced the oxygen radical production dose-dependently (77% inhibition of the chemiluminescence response at 6 mmol/l ascorbic acid), whereas the adherence was unaffected. Hypoxanthine/xanthine oxidase-generated oxygen radicals were scavenged by ascorbic acid in a dose-dependent manner (99% inhibition of the chemiluminescence response at 100 mumol/l ascorbic acid). From these results, ascorbic acid can highly be recommended for animal experiments and clinical studies in patients with trauma, shock and sepsis and for studies to prevent or reduce reperfusion injuries.

Antioxidants↗
PubMed1990

[Some recent discoveries of metabolism and function of ascorbic acid].

Some newer knowledge concerning the metabolism of the ascorbic acid as well as its importance for the pituitary gland, the adrenal glands, the immune system and the bone formation are described. A large enrichment of the ascorbic acid is present in the pituitary gland and in the adrenal glands. In the pituitary gland the compound is constituent of the Cu-containing peptidyl-glycine-alpha-amidizating-monooxygenase which among others is necessary for the formation of alpha-MSH a lack of ascorbic acid diminishes the formation of alpha-MSH at stress the increased binding of ACTH to the cells of the middle and inner layer of the adrenal cortex leads to the fact that about 40 to 60% of the quantity of ascorbic acid are delivered. This evokes an increase of the activity of the adenylate cyclase as well as of the C21-hydroxylase: The synthesis and secretion of glucocorticosteroids increases. When there is a deficiency of ascorbic acid the content of cortisol in the plasma increases. The ascorbic acid is a constituent of the dopamine-beta-hydroxylase.

Adrenal Glands↗
PubMedDate not supplied

Simultaneous determination of ascorbic acid and acetylsalicylic acid in pharmaceutical formulations.

A direct, simple, and practical first-derivative spectrophotometric method is described for simultaneous determination of ascorbic acid and acetylsalicylic acid. The effects of the solvent, excipients, and spectral variables on the analytical signal were investigated. The drugs were determined simultaneously with a 0.01 M methanolic hydrochloric acid solution as the solvent, and the signals were evaluated directly by using the zero-crossing method at 245.0 and 256.0 nm for acetylsalicylic acid and ascorbic acid, respectively. The method allows the simultaneous determinations of acetylsalicylic acid and ascorbic acid in the ranges of 6.6 x 10(-6) to 1.5 x 10(-4)M and 3.4 x 10(-6) to 2.0 x 10(-4)M, respectively, with standard deviation of <2.0%. The proposed method was applied to determinations of these drugs in tablets.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

Prooxidant action of two antioxidants: ascorbic acid and gallic acid.

The addition of two antioxidants, ascorbic acid or gallic acid to distilled water resulted in the rapid increase in the reduction potential, which a few seconds later was replaced with much higher oxidation potential. The addition of these compounds to culture medium dose-dependently increased the oxidation potential only. Ascorbic acid analogs, which had apoptosis-inducing activity, showed similar oxidation potential, whereas inactive analogs did not. The combination of ascorbate and hydrogen peroxide additively enhanced both the oxidation potential and cytotoxic activity. These data demonstrate that both ascorbic acid and gallic acid act as prooxidants for the induction of apoptotic cell death.

Antioxidants↗