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PubMed1991

Ascorbic acid enhances the effects of 6-hydroxydopamine and H2O2 on iron-dependent DNA strand breaks and related processes in the neuroblastoma cell line SK-N-SH.

Neuroblastoma cells accumulate ascorbic acid and iron. It was hypothesized that these features could be exploited for sensitizing neuroblastoma cells for therapy in combination with reactive oxygen intermediates. In the present study the effects of 6-hydroxydopamine (6-OHDA) and H2O2 on metabolic parameters critical for cell survival were investigated in cells with low and high ferritin content in the presence and absence of ascorbate. Human neuroblastoma SK-N-SH cells were pretreated with 100 microM FeSO4 and 10 microM desferrioxamine, respectively, for 24 h yielding cells with different ferritin contents. The effects of 6-OHDA and H2O2 (25 microM-250 microM) in the absence and presence of 1 mM ascorbic acid on DNA strand break formation, activation of poly(ADP-ribose) polymerase, and finally decrease in NAD+ and ATP concentration were investigated. All these parameters were influenced by 6-OHDA and H2O2 in a concentration-dependent manner in a similar way. The effects were most pronounced in ferritin-rich cells and in the presence of ascorbic acid. Using isolated CCC PM2 DNA, 6-OHDA and ascorbic acid caused strand breaks that were prevented in the presence of mannitol or desferrithiocine. H2O2-mediated strand breaks were observed only in the presence of ascorbic acid. Based on these data and data published by others a model explaining the deleterious effects of ascorbic acid on neuroblastoma cells is presented. It is suggested that continuous application of a high dosage of ascorbic acid might be a useful approach in neuroblastoma therapy.

Adenosine Triphosphate↗
PubMed1981

Anorectic drugs and vitamin C: role in appetite and brain ascorbic acid in guineapigs.

The role of daily administration of anorectic drugs (fenfluramine, mazindol and diethylpropion) with or without Vitamin C supplement, in the appetite and brain ascorbic acid, had been investigated in guineapigs receiving a daily Vitamin C-deficient diet for 24 days. Food intake was reduced by diethylpropion in the scorbutic male and female guineapigs but to a smaller extent by fenfluramine or mazindol. Supplementary Vitamin C daily significantly inhibited the anorectic actions of these drugs. In relation to the brain ascorbic acid level in the scorbutic gunieapigs, the initial stable level of brain ascorbic acid was significantly reduced by fenfluramine in both sexes by day 24, (P less than 0.05). Both mazindol and diethylpropion did not cause such reductions in the initial brain ascorbic acid. The three anorectic drugs prevented the rise in brain ascorbic acid normally associated with supplementary Vitamin C. It appears that brain ascorbic acid level can make metabolic readjustment during anorexia caused by diethylpropion and mazindol but not that caused by fenfluramine in guineapigs.

Animals↗
PubMed1987

Induced synthesis of metallothionein by ascorbic acid in mouse liver.

The concentration of metallothionein in mouse tissues after administration of ascorbic acid was determined by the Cd-hem method. The concentration of metallothionein in the liver was increased significantly after an intraperitoneal injection of L-ascorbic acid at the dose of 1000 mg/kg. A simultaneous injection of cycloheximide inhibited the increase of the metallothionein concentration. Mortality of mice injected with a lethal dose of cadmium was decreased significantly by the pre-injection of L-ascorbic acid. All of these results indicate that metallothionein is induced in the liver after the administration of ascorbic acid.

Animals↗
PubMed1996

[Effect of heparin and ascorbic acid on growth behavior of cultivated corneal epithelial cells of the rabbit].

Although ascorbic acid and heparin are used for local therapy of corneal wounds that heal poorly (e.g., after chemical burns), little has been known up to now about the mechanisms underlying their effectiveness at the cellular level. The aim of the present study was therefore to evaluate the effect of heparin and ascorbic acid on the growth behaviour of corneal cells in vitro. For this purpose cell cultures from a corneal epithelial cell line were used. Stimulation of the cells with heparin at concentrations ranging from 10 to 200 micrograms/ml for 6 days led to a dose-dependent rise in growth rate (population doublings per day) of 0.48 +/- 0.50 to 2.19 +/- 1.65 (mean value +/- standard deviation, n = 10) with an EC50 of 132 micrograms/ml. In contrast, the addition of ascorbic acid at concentrations ranging from 0.5 to 3.0 mM led on average to a 40% dose-dependent inhibition of cell proliferation after 6 days, with an IC50 of 0.7 mM as-corbic acid. On the basis of these results, the use of heparin at concentrations of 180-200 micrograms/ml appears advantageous. In contrast, the local application of ascorbic acid for chemical burns with no stromal involvement should be subjected to a critical reassessment.

Animals↗
PubMed1992

Ascorbic acid status in uremics.

Plasma levels of ascorbic acid (AA) and dehydroascorbic acid (DHA) were estimated in 27 patients of end stage renal failure (ESRF) on standard conservative therapy (group A) and 9 patients of ESRF on maintenance haemodialysis (MHD; group B). Fourteen healthy subjects matched for age and sex served as control (group C). The dietary intake of vitamin C was significantly decreased in group A than in group B compared to control. Similarly, plasma AA was significantly lowered to 0.801 +/- 0.283 mg per cent in group A compared to 1.421 +/- 0.47 mg per cent in control. While it was just lowered to 1.058 +/- 0.272 mg per cent in group B. Although plasma level of DHA was raised to 0.243 +/- 0.486 mg per cent and 0.166 +/- 0.54 mg per cent in groups A and B respectively, the increase was not statistically significant. In our present study, the DHA/AA ratio was found to be inversely proportional to the plasma AA. Further, this ratio has been claimed to be a better indicator of overall reducing atmosphere (i.e., profile of vitamin C) of the body.

Ascorbic Acid↗
PubMedDate not supplied

Stimulatory effects of ascorbic acid on hyaluronic acid synthesis of in vitro cultured normal and glaucomatous trabecular meshwork cells of the human eye.

The outflow of aqueous humor of the primate eye occurs across the filter system of the trabecular meshwork (TM) into Schlemm's canal. Cells of TM derived from a normal (TM-N-cells) and a glaucomatous human eye (TM-G-cells) were established in monolayer culture. The present comparative experiments were performed with cells kept in a defined serum-free medium (the aqueous humor is nearly protein-free!). Under these conditions the cells stay alive for several months in a non-proliferating state. TM-G-cells exhibited a lower synthesis rate of glycosaminoglycans-especially of hyaluronic acid (HA)--than TM-N-cells. Addition of 50-200 micrograms/ml ascorbic acid (the aqueous humor is characterized by a high ascorbic acid concentration of about 150 micrograms/ml) to the culture medium resulted in a significant dose-dependent stimulation of HA-synthesis and secretion, which was relatively stronger in case of TM-G-cells than with TM-N-cells. Thus, the results suggest a role of ascorbic acid in the probably membrane-localized HA-synthesis. Functions of ascorbic acid and HA for the morphological and functional integrity of the TM-cells in vitro and the outflow apparatus in vivo were discussed.

Adult↗
PubMed1975

Failure of ascorbic acid to inhibit FANFT-induced bladder cancer.

L-ascorbic acid has been shown to reduce the elevated level of urinary chemiluminescence found in patients with bladder cancer. Thus, it has been suggested that vitamin C might be efficacious in bladder tumor prophylaxis. However, there is no clinical evidence to support this thesis. We evaluated whether L-ascorbic acid given concomitantly with the urinary carcinogen FANFT was capable of reducing the incidence of subsequent bladder tumors. No inhibitory effect was observed. Unless evidence is obtained demonstrating bladder tumor prevention by L-ascorbic acid its routine administration to patients with bladder cancer is not indicated.

Animals↗
PubMed1985

Ascorbic acid therapy in a thermal burn model of corneal ulceration in rabbits.

We studied the effect of topical and systemic ascorbic acid on a rabbit model of corneal ulceration produced by thermal burn. Central stromal ulceration occurred in 77% to 100% of eyes in all treatment groups. The rate of ulceration was accelerated in animals treated with systemic ascorbic acid. Ulceration began after 5.80 +/- 2.14 days in control eyes and 2.75 +/- 1.26 days in the eyes of rabbits treated with both topical and systemic ascorbic acid (P less than .02). Subconjunctival ascorbic acid alone did not affect the rate of ulceration (average onset, 6 +/- 1 days). Once ulceration occurred in animals treated with both topical and systemic ascorbic acid, the incidence of perforation and descemetocele formation was increased and that of healing was decreased. The time required for healing was not significantly altered by treatment (9.50 +/- 2.28 days for control eyes vs 5.75 +/- 2.78 days for treated eyes) (P greater than .05).

Animals↗
PubMed1981

Effect of ascorbic acid on copper and cholesterol in adult cynomolgus monkeys fed a diet marginal in copper.

The effects of prolonged consumption of high levels of dietary ascorbic acid on copper metabolism and cholesterol in adult monkeys fed a diet low or marginal in copper were investigated. Small reductions in serum copper and in serum ceruloplasmin levels were observed when high levels of ascorbic acid were fed. During the period of copper depletion there was a gradual but significant (p less than 0.001) increase in serum cholesterol. The level of ascorbic acid supplementation had no effect during this phase. When copper was added back to the diet, serum cholesterol levels leveled off or declined in the monkeys receiving the low (1 mg/day/kg body weight) dose of ascorbic acid. Cholesterol levels continued to increase in the group receiving the higher ascorbic acid supplement (25 mg/day/kg body weight). These data suggest that high levels of ascorbic acid supplementation may make dietary copper relatively unavailable for regulating cholesterol metabolism.

Animals↗
PubMed1996

Ascorbic acid reverses endothelial vasomotor dysfunction in patients with coronary artery disease.

BACKGROUND: In the setting of atherosclerosis, endothelial vasomotor function is abnormal. Increased oxidative stress has been implicated as one potential mechanism for this observation. We therefore hypothesized that an antioxidant, ascorbic acid, would improve endothelium-dependent arterial dilation in patients with coronary artery disease. METHODS AND RESULTS: Brachial artery endothelium-dependent dilation in response to hyperemia was assessed by high-resolution vascular ultrasound before and 2 hours after oral administration of either 2 g ascorbic acid or placebo in a total of 46 patients with documented coronary artery disease. Plasma ascorbic acid concentration increased 2.5-fold 2 hours after treatment (46+/-8 to 114+/-11 micromol/L, P=.001). In the prospectively defined group of patients with an abnormal baseline response (<5% dilation), ascorbic acid produced marked improvement in dilation (2.0+/-0.6% to 9.7+/-2.0%), whereas placebo had no effect (1.1+/-1.5% to 1.7+/-1.5%, P=.003 for ascorbic acid versus placebo). Ascorbic acid had no effect on hyperemic flow or arterial dilation to sublingual nitroglycerin. CONCLUSIONS: Ascorbic acid reverses endothelial vasomotor dysfunction in the brachial circulation of patients with coronary artery disease. These findings suggest that increased oxidative stress contributes to endothelial dysfunction in patients with atherosclerosis and that endothelial dysfunction may respond to antioxidant therapy.

Adult↗
PubMed1980

The effect of ascorbic acid on the interaction of adrenaline and neostigmine on neuromuscular transmission.

Ascorbic acid is used in the laboratory as a stabilizing agent to delay the oxidation of adrenaline solutions. The rat isolated phrenic nerve-diaphragm preparation was used to study the interaction of ascorbic acid, adrenaline and neostigmine on neuromuscular transmission. While ascorbic acid itself did not affect the response of the preparation to phrenic nerve stimulation, it significantly reduced the response of the preparation to neostigmine and the augmentation of this response by adrenaline. The results emphasize the need to consider the consequences of including preservatives or stabilizing agents in drug solutions when quantitative comparisons are made.

Animals↗
PubMedDate not supplied

Sialoresponsin and an antiviral action of ascorbic acid.

Several pathogens, both viral and bacterial, employ the enzyme neuraminidase (N-acetylneuraminate glycohydrolase, EC 3.2.1.1.8). The neuraminidase renders ineffective the hemagglutinin inhibitory mucins that confine the pathogens in a coating of host mucins. Sialoresponsin is a receptor "decoy" that inhibits neuraminidase. Several known antiviral agents, including ascorbic acid, inhibit neuraminidase. It is proposed that ascorbic acid may mediate an antiviral effect through the incorporation of ascorbic acid or some derivative of ascorbic acid as a part of the sialoresponsin molecule. Whether ascorbic acid works alone as a pharmacological inhibitor, or is incorporated in sialoresponsin as a physiological inhibitor; it may be useful against pathogens that employ neuraminidase.

Ascorbic Acid↗
PubMed1985

Inhibition of ascorbic acid uptake by endotoxin: evidence of mediation by serum factor(s).

The effect of bacterial endotoxin on the ascorbic acid uptake by 3T6 fibroblasts was studied. Endotoxin inhibited ascorbic acid uptake by fibroblasts in a dose dependent manner. The inhibition by endotoxin takes place only in the presence of unheated serum; decomplementing serum by heat inactivation at 56 degrees C for 30 minutes eliminates endotoxin's inhibitory effect on ascorbic acid uptake. The effect of endotoxin appears to be instantaneous since the inhibition seen in the cells without any preexposure was similar to the cells preexposed to endotoxin for up to 6 hours. Polymyxin B sulfate which is known to bind the lipid A portion of endotoxin did not reverse the inhibition of ascorbic acid uptake caused by endotoxin.

Animals↗
PubMed1998

Histochemical observation and cellular distribution of ascorbic acid in persimmon leaves.

This study was carried out to resolve the discrepancy of data for the proportion of ascorbic acid and dehydroascorbic acid in persimmon leaves at the final stage of the season and to clarify their cellular distributions using histochemical and biochemical techniques. Fresh persimmon leaves were collected and used on July 31, September 5 and October 7, 1996. Ascorbic acid and dehydroascorbic acid in subcellular fractions were determined by the HPLC method that was found to be the most reliable for separation. The percent of dehydroascorbic acid in the total leaves was found to be almost constant (between 32 and 37%) in all preparations tested. In all preparations, more than 90% of the ascorbic acid and dehydroascorbic acid was found in the soluble fraction. The histochemical detection of ascorbic acid and an electron micrograph of persimmon leaf cells showed that the reactive color, after the reduction of silver nitrate under acidic conditions, in the leaves of all three preparations was mainly found on the face side of columned-type palisade parenchyma cells where chloroplasts were not rich and large vacuoles were seen. On the inner side of the palisade parenchyma cells where chloroplasts were the richest, only weak color development was observed. This study demonstrates that the percent of dehydroascorbic acid in persimmon leaves did not exceed 40% at least until October 7. It also shows that in persimmon leaf cells, ascorbic acid is mainly localized in the cytosol of palisade parenchyma tissue cells where large vacuoles are seen.

Ascorbic Acid↗
PubMedDate not supplied

Modifications induced by ascorbic acid on alkaline phosphatase fluorescence.

Ascorbic acid, isoascorbic acid and dehydroascorbic acid quench the tryptophyl fluorescence of alkaline phosphatase. The quenching is protein aspecific, although its extent reflects the different inhibitory efficiency of the compounds. The kinetic inactivation and emission deactivation of alkaline phosphatase isoenzymes present also striking similarities. The fluorescence modifications, moreover, show a particular pattern, indicative of a transition phenomenon. The quenching effects displayed by the ascorbic system on alkaline phosphatase can then supply an interesting insight into other aspects of the inhibitor-enzyme interaction.

Alkaline Phosphatase↗
PubMed1990

[Studies on sensor for L-ascorbic acid using biotissue slice].

Bioselective membrane electrode for L-ascorbic acid has been made with tissue slices. It is made from porcine liver tissue slice covering an oxygen electrode. The influence of buffer mediator, pH, temperature, antiseptics, slice thickness, etc. on the response characteristics of the electrode was examined. In the presence of copper ions, a linear relationship between dynamic response of the electrode and the logarithm of concentration of L-ascorbic acid was observed for the range of 21.14 micrograms/ml to 352.3 micrograms/ml, with a correlation coefficient of 0.9996 and the Michaelis constant of 0.8 mmol/L. The electrode has been used to determine L-ascorbic acid in drugs, the analytical results were satisfactory.

Animals↗
PubMed1979

Inhibition by ascorbic acid (vitamin C) of chemical detection of blood in urine.

Review of results of 9,620 consecutive urinalyses revealed 892 urines that contained microscopic evidence of erythrocytes and 98 for which there were discrepancies between microscopic evidence of hematuria (greater than 20 erythrocytes/high-power field) and chemical detection of blood (0 or "1+" when results should be "3+"). Eleven specimens (from ten patients) showed negative results of chemical tests for blood and greater than 40 erythrocytes/high-power field (HPF). Nine of these patients were receiving ascorbic acid supplementation. In a random sample of 20 patients with greater than 40 erythrocytes/HPF and strongly positive tests for blood, none was receiving ascorbic acid, a significant difference by chi-square analysis. In a prospective study, low levels of ascorbic acid inhibited chemical detection of blood. At 25 mg/dl ascorbic acid, 10--20 erythrocytes/HPF could not be detected; at 35 mg/dl ascorbic acid, greater than 20 erythrocytes/HPF were undetectable. For quantitation of the low level at which ascorbic acid inhibits chemical detection of blood, fresh urine specimens should be analyzed. Ascorbic acid is oxidated in vitro to products that partially inhibit detection of blood yet do not assay as ascorbic acid.

Ascorbic Acid↗
PubMed1978

Protective role of ascorbic acid in fishes exposed to organochlorine pollution.

Protective role of ascorbic acid on the toxic effect of aldrin pollution in an air-breathing fish Channa punctatus Bloch is reported. Fishes fed with aldrin mixed diet at 0.25% showed 25% mortality in 30 days. Mortality is preceded by certain changes in peripheral blood such as polycythemia and leucocytosis with increased thrombocyte but decreased neutrophil population. However, a massive dose of ascorbic acid (500 mg/100 g diet) was found to considerably neutralize the toxic effect as evidenced by 10-fold decrease in mortality and significantly lowered haematological response. The significance of these studies in the light of physiological role of ascorbic acid as a micronutrient for protection against pollution stress is discussed.

Aldrin↗