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PubMed2005

Improvement of sympathetic response to exercise by oral administration of ascorbic acid in patients after myocardial infarction.

BACKGROUND: Recent studies indicated that excessive oxidative stress in an animal heart failure model injures both the sympathetic nerve endings and receptors, resulting in disturbance of norepinephrine release and sensitivity to norepinephrine. However, it has not been clarified whether this phenomenon is expressed clinically in patients with heart disease. Therefore, we examined the efficacy of ascorbic acid administration as an antioxidant vitamin in relation to the heart rate and norepinephrine response to exercise in patients after myocardial infarction. METHODS: In this randomized crossover trial, 21 male patients who had had myocardial infarction underwent symptom-limited ergometer cardiopulmonary exercise testing twice, that is, without and with ascorbic acid (2 g) administration. Plasma norepinephrine concentrations were assessed at rest and at peak exercise, and heart rate responsiveness to the norepinephrine increment from rest to peak exercise (DeltaHR/logDeltaNE) was calculated. RESULTS: In the exercise test after ascorbic acid administration, peak oxygen consumption (VO(2)) improved over baseline. Ascorbic acid administration significantly increased the change in heart rate and norepinephrine from rest to peak exercise and DeltaHR/logDeltaNE. The increment in heart rate was significantly correlated with peak VO(2) in each test. CONCLUSION: Ascorbic acid intake before exercise improved exercise capacity through enhancement of the heart rate and norepinephrine response to exercise in patients after myocardial infarction. These findings suggest that ascorbic acid intake improves sympathetic dysfunction resulting from injury by excessive oxidative stress after myocardial infarction.

Aged↗
PubMed2005

Electrochemical behavior of a covalently modified glassy carbon electrode with aspartic acid and its use for voltammetric differentiation of dopamine and ascorbic acid.

Aspartic acid was covalently grafted on to a glassy carbon electrode (GCE) by amine cation radical formation in the electrooxidation of the amino-containing compound. X-ray photoelectron spectroscopic (XPS) measurement and cyclic voltammetric experiments proved the aspartic acid was immobilized as a monolayer on the GCE. Electron transfer to Fe(CN)6(4-) in solution of different pH was studied by cyclic voltammetry. Changes in solution pH resulted in the variation of the charge state of the terminal group; surface pK(a) values were estimated on the basis of these results. Because of electrostatic interactions between the negatively charged groups on the electrode surface and dopamine (DA) and ascorbic acid (AA), the modified electrode was used for electrochemical differentiation between DA and AA. The peak current for DA at the modified electrode was greatly enhanced and that for AA was significantly reduced, which enabled determination of DA in the presence of AA. The differential pulse voltammetric (DPV) peak current was linearly dependent on DA concentration over the range 1.8 x 10(-6)-4.6 x 10(-4) mol L(-1) with slope (nA micromol(-1) L) and intercept (nA) of 47.6 and 49.2, respectively. The detection limit (3delta) was 1.2 x 10(-6) mol L(-1). The high selectivity and sensitivity for dopamine was attributed to charge discrimination and analyte accumulation. The modified electrode has been used for determination of DA in samples, in the presence of AA, with satisfactory results.

Ascorbic Acid↗
PubMed1997

Influence of maternal nicotine exposure on neonatal rat lung structure: protective effect of ascorbic acid.

The aims of this study were (1) to determine and quantify the adverse effects of maternal nicotine exposure during pregnancy and lactation on neonatal rat lung development, and (2) to establish whether ascorbic acid will protect the neonatal rat lung against the adverse effects of maternal nicotine exposure. Pregnant rats received nicotine (1 mg/kg body mass/day) subcutaneously during gestation and lactation. A second group received nicotine and ascorbic acid (1 mg/kg body mass/day). The control animals received saline subcutaneously. The results illustrate that maternal nicotine exposure results in (a) a decreased (P < 0.001) radial alveolar count (RAC), (b) an increase (P < 0.001) in destructive index (DI), (c) an increased (P < 0.001) linear intercept (Lm), (d) an increased (P < 0.001) abnormal alveolar attachment index (AAA) (e) and an increase in septal cellularity. Ascorbic acid does not protect fetal lung development against the adverse effects of maternal nicotine exposure. However, after birth ascorbic acid prevents further deterioration of the DI, AAA and Lm, whereas the RAC and thus the number of alveoli was even higher than in control neonatal rat lung. No further increase in cellularity occurred. The reason for this response to ascorbic acid supplementation is under investigation.

Abnormalities, Drug-Induced↗
PubMed1993

Ascorbic acid and cholesterol gallstones.

Decreased activity of cholesterol 7 alpha-hydroxylase, the rate-limiting enzyme in the catabolism of cholesterol to bile acids, is known to result in increased biliary cholesterol concentration and supersaturation of bile. Supersaturation of bile by cholesterol is a necessary condition for cholesterol gallstone formation. In guinea pigs, the hepatic concentration of ascorbic acid affects the catabolism of cholesterol: hypovitaminosis C reduces cholesterol 7 alpha-hydroxylase activity. Cholesterol gallstones are frequently found in ascorbic acid-deficient guinea pigs. Risk factors for cholesterol gallstones in humans include obesity, aging, estrogen treatment, pregnancy and diabetes. Plasma ascorbic acid levels are reduced in these groups. Vegetarian diets, which typically have high ascorbic acid contents, protect against gallstones. Since ascorbic acid effects the rate-limiting step in the catabolism of cholesterol in the guinea pig and many human risk groups for cholesterol gallstones are associated with reduced ascorbic acid levels, ascorbic acid may play a contributory role in human gallbladder disease.

Animals↗
PubMed1994

Ascorbic-acid-mediated iron release from cellular ferritin and its relation to the formation of DNA strand breaks in neuroblastoma cells.

Ascorbic acid at pharmacologically attainable concentrations effectively inhibited the growth of the catecholamine-positive neuroblastoma cell line SK-N-SH; it inhibited LS cells to a smaller extent and catecholamine-negative SK-N-LO cell growth least effectively. In all three cell lines high concentrations of H2O2 were found. Since ascorbic acid was shown to release iron from ferritin in vitro and to keep it in the reduced state, we suggested that it acted as a pro-oxidant in ferritin-rich neuroblastoma cells in the presence of H2O2 and Fe2+ (Fenton reaction), implying iron release from cellular ferritin. We show here that iron could be mobilized from cellular ferritin by 1 mM ascorbic acid in iron-59-preloaded SK-N-SH and LS cells, but not in SK-N-LO cells. In agreement with these results, DNA strand break formation by ascorbate was only observed in SK-N-SH and LS cells. In SK-N-LO cells, DNA strand breaks could be induced by a combination of 1 mM ascorbic acid and 100 microM H2O2. Since cell-damaging effects caused by chemotherapy further facilitate iron release from ferritin, we conclude that ascorbate could be a powerful enhancer of some cytostatic drugs in neuroblastoma therapy.

Ascorbic Acid↗
PubMed1993

Ascorbic acid is an abettor in calcium urolithiasis: an experimental study.

Two sets of animal experiments using guinea pigs were planned to evaluate the effect of ascorbic acid supplementation on the lithogenic process. In the first set of experiments, 10, 40, and 60 mg doses of ascorbic acid/100g body weight/day were given for 105 days. Neither of the ascorbic acid doses given induced crystalluria, calcification or stone formation, thereby confirming our previous findings that ascorbic acid in the doses used by clinicians does not cause urolith formation. In the second set of experiments, ascorbic acid was supplemented in hypercalciuric (induced by calcium carbonate feeding) and hyperoxaluric (induced by sodium oxalate feeding) animals for 45 days. The results indicated that it exacerbated the calcification process in renal and bladder tissue.

Animals↗
PubMed1983

Intestinal absorption of oxalate in scorbutic and ascorbic acid supplemented guinea pigs.

Radiolabelled U-14C oxalic acid uptake was measured in the intestine of scorbutic and ascorbic acid (AA) supplemented guinea pigs. The feeding of vitamin C deficient diet to the animals for 26 days resulted in a significant fall in the ascorbic acid levels in the various tissues studied. Supplementation of vitamin C (10, 25 or 50 mg per 200 g body weight) increased ascorbic acid levels of spleen, adrenals, liver and leucocytes. The intestinal uptake of oxalate follows a passive diffusion mechanism in normally fed guinea pigs. The oxalate uptake rate was significantly increased (p less than 0.001) in the vitamin C administered group. Vitamin C depletion significantly decreased the oxalate uptake rate as compared to control animals. The changes observed in the uptake rate appear to be related with the chemical aberrations produced in the brush border membranes.

Animals↗
PubMed1981

The effect of ascorbic acid on the amine-nitrite and nitrosamine mutagenicity in bacteria injected into mice.

Ascorbic acid was tested for its ability to increase or decrease the induction of bacterial mutations by dimethylnitrosamine (DMN) or aminopyrine plus nitrite within intact mice. No evidence was found of the mutagenicity of ascorbic acid itself when tested alone or in the presence of copper ions. Similarly, no increase or decrease in the DMN-induced mutation frequency was observed. However, ascorbic acid was found to decrease the aminopyrine/nitrite-induced mutation frequency to an extent which was dependent on the experimental conditions used.

Amines↗
PubMed1979

Natural hypocholesterolemic agent: pectin plus ascorbic acid.

An addition of 5% citrus pectin and 0.5% ascorbic acid to high-fat diet of guinea pigs prevented total cholesterol accumulation in blood serum and the liver. Two groups of persons were given a preparation containing a daily dose of 15 g pectin and 450 mg ascorbic acid for 6 weeks. In 21 healthy persons with mild hypercholesterolemia total serum cholesterol dropped significantly by 24 mg/100 ml (8.6%), while the concentration of high density lipoprotein cholesterol remained unchanged. In 11 hyperlipemic outpatients (type IIa, IIb and IV) total serum cholesterol dropped by 68 mg/100 ml (18.7%). The changes in triglyceridemia proved inconsistent.

Animals↗
PubMed2004

Ascorbic acid prevents contrast-mediated nephropathy in patients with renal dysfunction undergoing coronary angiography or intervention.

BACKGROUND: Contrast agents can cause a reduction in renal function that may be due to the generation of reactive oxygen species. Conflicting evidence suggests that administration of the antioxidant acetylcysteine prevents this renal impairment. The action of other antioxidant agents has not been investigated. METHODS AND RESULTS: We conducted a randomized, double-blind, placebo-controlled trial of ascorbic acid in 231 patients with a serum creatinine concentration > or =1.2 mg/dL who underwent coronary angiography and/or intervention. Ascorbic acid, 3 g at least 2 hours before the procedure and 2 g in the night and the morning after the procedure, or placebo was administered orally. Contrast-mediated nephropathy was defined by an absolute increase of serum creatinine > or =0.5 mg/dL or a relative increase of > or =25% measured 2 to 5 days after the procedure. Contrast-mediated nephropathy occurred in 11 of the 118 patients (9%) in the ascorbic acid group and in 23 of the 113 patients (20%) in the placebo group (odds ratio [OR], 0.38; 95% confidence interval [CI], 0.17 to 0.85; P=0.02). The mean serum creatinine concentration increased significantly in the placebo group (from 1.36+/-0.50 to 1.50+/-0.54 mg/dL, P<0.001) and nonsignificantly in the ascorbic acid group (from 1.46+/-0.52 to 1.52+/-0.64 mg/dL, P=0.07). The mean increase in serum creatinine concentration was greater in the placebo group than in the ascorbic acid group (difference of 0.09 mg/dL; 95% CI, 0.00 to 0.17; P=0.049). CONCLUSIONS: Prophylactic oral administration of ascorbic acid may protect against contrast-mediated nephropathy in high-risk patients undergoing a coronary procedure.

Acute Kidney Injury↗
PubMed1982

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

The rate of free radical formation in aqueous solutions of ascorbic acid in the presence of chelating agents was measured by the ESR-stopped-flow method. Addition of ethylenediamine tetraacetate and trimetaphosphoric acid to the ascorbic acid-oxygen system results in only a minimal change in the rate of ascorbate free radical formation compared to that in absence of inhibitors. Evidence suggests that radical formation arises via secondary reactions involving products.

Ascorbic Acid↗
PubMed1984

Effect of ascorbic acid on ulceration in alkali-burned corneas.

Alkali-burned corneas were treated with 2% ascorbic acid. Topical applications and subconjunctival injections were given for 32 days. Treatment with ascorbic acid significantly decreases the incidence of corneal ulcerations and perforations compared to the control group that received the vehicle. These results confirm previous studies and strongly suggest that ascorbic acid presents a potential for use in the alkali-burned human eye.

Animals↗
PubMed1979

Steady-state turnover and body pool of ascorbic acid in man.

The time course of radioactivity in plasma and urine after oral administration of a single dose of (1-14C)ascorbic acid has been followed in healthy nonsmoking male volunteers. The investigation was carried out under steady state conditions with regard to ascorbic acid intake (30 to 180 mg/day). Using pharmacokinetic principles, turnover, pool size, and rates of metabolism and excretion could be calculated. It was found that the half-life of ascorbic acid was inversely related to the dosage and that the pool could be increased to about 20 mg/kg bodyweight by increasing the dosage. It was concluded that on a daily intake of about 100 mg ascorbic acid this pool size would be reached in 95% of the population.

Adult↗
PubMed2003

8-Isoprostaglandin F2a and ascorbic acid concentration in the aqueous humour of patients with exfoliation syndrome.

BACKGROUND/AIMS: The authors investigated the concentrations of 8-isoprostaglandin F(2a), a marker of oxidative stress in vivo, and ascorbic acid, a protectant against oxidative damage, in the aqueous humour of patients with exfoliation syndrome (XFS) and cataract and compared the results with those in age matched patients with cataract, but without XFS, to determine whether XFS is associated with increased oxidative stress. METHODS: Aqueous humour was aspirated at the beginning of phacoemulsification cataract surgery from 27 eyes of 27 cataract patients with XFS and 27 eyes of 27 age matched cataract patients without XFS. 8-Isoprostaglandin F(2a)concentration in the aqueous was determined with a commercial immunoassay; ascorbic acid concentration was measured with a microplate assay method. RESULTS: The mean concentration of 8-isoprostaglandin F(2a)in the aqueous from patients with XFS (2429 (SD 2940) pg/ml; range 400-10500 pg/ml) was significantly higher than that measured in the aqueous of age matched control patients (529.1 (226.8) pg/ml; range 325-1000 pg/ml); (p = 0.0028). Furthermore, mean ascorbic acid concentration in XFS patients (0.75 (0.39) mM; range 0.28-1.70 mM) was significantly lower than that found in control patients (1.19 (0.47) mM; range 0.53-2.4 mM); (p = 0.0005). There was a reverse correlation between 8-isoprostaglandin F(2a)and ascorbic acid concentration. CONCLUSION: 8-Isoprostaglandin F(2a)was significantly increased in the aqueous of patients with XFS, and ascorbic acid was decreased, providing evidence of a role for free radical induced oxidative damage in the pathobiology of XFS.

Antioxidants↗
PubMed1984

Effect of age and sex on the ascorbic acid content of kidney, skeletal muscle and pancreas of common Indian toad, Bufo melanostictus.

Ascorbic acid decreases from age-group I to II in Kidney, skeletal muscle, and increases in the Pancreas of female. There is no significant change in the Pancreas of male toad. There is an increase in the ascorbic acid content from age group II to III except in the Pancreas of females, where there is a decline of the content. Ascorbic acid remains constant in age-group IV except in the kidney of female, skeletal muscle of both sexes showing an increase and decrease of the value respectively. Sex difference shows a higher content in kidney of group IV, in skeletal muscle of group II and III and in pancreas of group II and is less in kidney of age-group II of females over their male counterparts.

Age Factors↗
PubMed2000

[In vitro activity of ascorbic acid].

The aim of this study was to determine the in vitro activity of ascorbic acid (vitamin C) against 43 Helicobacter pylori clinical isolates obtained from gastric biopsy taken by endoscopy. The MIC was determined by an agar dilution method. The ascorbic acid was included as two-fold dilutions in the agar to obtain a final concentration from 4000 mg/l to 62 mg/l. Brain-heart infusion agar supplemented with yeast extract and 10% fetal calf serum, 10(6) CFU/spot inoculum and microaerobic incubation for 2 to 5 days were used. MIC(50) 500 mg/l, MIC(90) 1000 mg/l and the range from 62 to 2000 mg/l. No differences in susceptible or resistant isolates were observed. Ascorbic acid showed good in vitro activity against the H. pylori clinical isolates tested in this study, which could explain some of the beneficial properties of vitamin C.

Ascorbic Acid↗