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PubMed2000

Dietary taurine alters ascorbic acid metabolism in rats fed diets containing polychlorinated biphenyls.

The effect of dietary taurine on ascorbic acid metabolism and hepatic drug-metabolizing enzymes was investigated in rats fed diets containing polychlorinated biphenyls (PCB) to determine whether taurine has an adaptive and protective function in xenobiotic-treated animals. Young male Wistar rats (60 g) were fed diets containing 0 or 0.2 g/kg diet PCB with or without 30 g/kg diet of taurine for 14 d. The rats fed the PCB-containing diets had greater liver weight, higher ascorbic acid concentrations in the liver and spleen and greater hepatic cytochrome P-450 contents than control rats that were not treated with PCB (P < 0.01). In PCB-fed rats, urinary ascorbic acid excretion was enhanced, and serum cholesterol concentration (especially HDL-cholesterol) was significantly elevated compared with those in control rats. Dietary taurine significantly potentiated the increases in the urinary excretion of ascorbic acid and the rise in the levels of cytochrome P-450 which were caused by PCB treatment. On the other hand, the supplementation of taurine to control diet did not alter these variables. Taurine may enhance the hepatic drug-metabolizing systems, leading to the stimulation of the ascorbic acid metabolism in rats fed diets containing PCB.

Animals↗
PubMed1989

Effects of ascorbic acid in alkaptonuria: alterations in benzoquinone acetic acid and an ontogenic effect in infancy.

The effects of ascorbic acid on the excretion of homogentisic acid and its derivative benzoquinone acetic acid were studied in two adults and three infants. The administration of relatively large amounts of ascorbic acid to the adults was followed by a disappearance of benzoquinone acetic acid from the urine, whereas the level of excretion of homogentisic acid did not change. This could have relevance to the pathogenesis of ochronotic arthritis. In the 4-mo-old infant and the 5-mo-old infant ascorbic acid in the urine may have doubled the amount of homogentisic acid, presumably through an effect on the immature p-hydroxyphenylpyruvic acid oxidase. Dietary reduction of the intake of tyrosine and phenylalanine substantially reduced the excretion of homogentisic acid.

Aged↗
PubMed1987

Ascorbic acid, HDL, and total plasma cholesterol in the elderly.

The relationships between ascorbic acid (plasma and dietary) and plasma HDL cholesterol (HDL-C), total plasma cholesterol (T-C) and T-C:HDL-C ratio were examined in a population of 235 males and 445 females, age 60-98 years. Many known or suspected determinants of HDL-C and T-C, including age, sex, triceps skinfold thickness, fasting blood glucose, alcohol intake, and others, were considered as covariates due to their potential confounding or modifying effects on the relationships under study. The results show that plasma ascorbic acid is significantly (p less than 0.05) correlated with HDL-C (r = 0.09), T-C:HDL-C (r = 0.10), but not with T-C (r = 0.03). There is a strong age interaction with the largest effect of ascorbic acid in the youngest age group studied (60-69 years). The effects of dietary ascorbic acid are similar but slightly reduced in magnitude.

Aged↗
PubMed1984

Is leucocyte ascorbic acid an unreliable estimate of vitamin C deficiency?

Leucocyte ascorbic acid levels failed to identify six of seven elderly patients shown to be deficient on an oral vitamin C saturation test. Compared to those with a normal saturation test, patients judged deficient had lower levels for triceps skinfold thickness, mean arm muscle circumference and Quetelet's index; there was a significant association with the habit of eating alone, and with a dietary intake of less than 30 mg of ascorbic acid daily (the recommended daily allowance in the U.K.). No significant difference was found in the values for haemoglobin, serum albumin or potassium concentrations between the two groups, and no association shown between a deficient saturation test and smoking, season, sublingual varicosities or an abnormal bleeding time.

Aged↗
PubMed1976

Influence of ascorbic acid on selenium nutrition in the chick.

Experiments were conducted to determine the nature of the effect of dietary ascorbic acid on selenium nutrition in the chick. Results showed that ascorbic acid resulted in increased activities of the selenium-containing enzyme glutathione peroxidase in plasma, accompanied by an apparent reduction in the dietary selenium requirement of the vitamin E-deficient chick. The ascorbic acid contents of plasma, liver, kidney and adrenals were not affected by selenium or vitamin E deficiencies, indicating that selenium-vitamin E deficient chicks are not rendered scrobutic. Absorption experiments using ligated duodenal loops or oral doses indicated that dietary ascorbic acid promoted the enteric absorption of selenium but did not affect the absorption of vitamin E. These results support the hypothesis previously reported that factors which inhibit the oxidation of dietary selenium promote its absorption and, perhaps, its post-absorptive utilization in metabolically active components of the cell.

Animals↗
PubMed2000

Chemical characteristics of dehydro-L-ascorbic acid.

Dehydro-L-ascorbic acid (DAA) exists mainly in its C2 hydrated bicyclic form (5) in an aqueous solution, and monocyclic DAA (3), which is the expected reaction product immediately after the oxidation of AA, has not been observed by NMR spectroscopy. The formation mechanism for 5 from 3 and the stability of 5 were examined by the semi-empirical molecular orbital method (MOPAC). It was indicated that the protonation reaction was the key step in the formation of 5, therefore, the formation of 5 is thought to be more difficult under physiological conditions which mostly involve in the neutral or slightly alkaline state. However, by NMR, it was confirmed that, even in a neutral or slightly alkaline state very close to physiological conditions, the predominant form of DAA existing in an aqueous solution immediately after the enzymatic oxidation of AA was confirmed to be 5, although the possible existence of other forms of DAA at very low concentrations could not be completely excluded.

Dehydroascorbic Acid↗
PubMedDate not supplied

Induction of cell death by ascorbic acid derivatives in human renal carcinoma and glioblastoma cell lines.

Sodium-L-ascorbate, L-ascorbic acid, D-isoascorbic acid, sodium 5,6-benzylidene-L-ascorbate and sodium-6-beta-O-galactosyl-L-ascorbate, which produce ascorbyl radicals during the oxidative degradation, also induced cytotoxicity against cultured human renal carcinoma (TC-1) and glioblastoma multiform tumor (T98G) cell lines. On the other hand, L-ascorbic acid 2-phosphate magnesium and L-ascorbic acid 2-sulfate dipotassium salt, which do not produce the ascorbyl radical, were inactive. This suggests the possible role of the ascorbyl radical for cell death induction. T98G cells were more resistant to ascorbate analogs than TC-1 and HL-60 cells, possibly due to higher intracellular glutathione concentrations. Ascorbate treatment induced rapid elevation of both intracellular concentration of cAMP and Ca2+ in HL-60 cells, but not in TC-1 and T98G cells. However, the elevation of cAMP by theophyline and N,2-dibutyryl adenosine 3,5 cyclic monophosphate (dibutyryl cAMP) resulted in a decrease in the viable cell number. This suggests the possible role of cAMP for ascorbate-induced cell death.

Apoptosis↗
PubMed1984

Ascorbic acid changes in brain.

The level of ascorbic acid in the brain of growing rats was not influenced by efforts to accelerate neural activity. Treatments used to depress neural activity included thyroidectomy which produced a 13%-20% loss of ascorbic acid in cortical and cerebellar tissue and diazepam which produced a significant rise in the cerebellum. Ethanol and barbital were without effect.

Animals↗
PubMed2006

Results of a prospective randomised multicentre controlled trial comparing a new 2-L ascorbic acid plus polyethylene glycol and electrolyte solution vs. sodium phosphate solution in patients undergoing elective colonoscopy.

BACKGROUND: Elective colonoscopy is used increasingly to screen at risk patients for colonic malignancy. Bowel preparation quality is a critical factor for successful screening. Preparations used include high doses of potent laxatives, e.g. sodium phosphate solution or high volume polyethylene glycol. Because of constraints and limited patient acceptability, there remains a need for a more acceptable bowel preparation with at least equivalent cleansing to existing preparations. AIM: To determine if a 2-L polyethylene glycol solution with electrolytes and ascorbic acid (polyethylene glycol + ascorbic acid) produces equivalent bowel cleansing to sodium phosphate solution, and is acceptable to patients and well tolerated. METHODS: This was a single blind, parallel group, equivalence study comparing polyethylene glycol + ascorbic acid with sodium phosphate solution in 352 patients undergoing elective colonoscopy. A blinded, independent expert scored a video recording of each colonoscopy. Patients completed a questionnaire reporting acceptability of the bowel preparation process. RESULTS: Clinically successful bowel preparation was reported in 72.5% of cases prepared using polyethylene glycol + ascorbic acid and in 63.9% of cases prepared using sodium phosphate solution (treatment difference +8.6%, 95% confidence interval -2.3%, +19.4%). The new solution was well accepted and better tolerated than sodium phosphate solution. CONCLUSIONS: The new 2-L solution of polyethylene glycol + ascorbic acid was at least as efficacious as sodium phosphate solution with comparable efficacy and a better tolerability profile.

Ascorbic Acid↗
PubMed1990

Inhibition of beta-glucuronidase in human urine by ascorbic acid.

The effects of oral supplementation of ascorbic acid (1500 mg d-1) on urinary beta-glucuronidase (beta-G) activity was assessed in a double-blind crossover study design over a 3-week period. The subjects on ascorbic acid treatment displayed a statistically significant (P less than 0.05) decrease in beta-G with an approximate decrease of 25%.

Adult↗
PubMed2003

Relation of serum ascorbic acid to Helicobacter pylori serology in US adults: the Third National Health and Nutrition Examination Survey.

PURPOSE: To examine the relation between serum ascorbic acid and Helicobacter pylori serology from a probability sample of US adults. SUBJECTS AND METHODS: Data from 6,746 adults (ages 20 to 90 years) enrolled in the Third National Health and Nutrition Examination Survey (NHANES III), 1988-1994 were analyzed. Multiple logistic regression models were examined taking into account sample weights and the complex survey design of NHANES III, and controlling for the effects of potential confounders. Because race appeared to modify the association between serum ascorbic acid and seropositivity to H. pylori, we conducted the analyses stratified by race. RESULTS: A total of 2,189 adults (32%) had a positive serology for H. pylori, and, of these, 1,175 (54%) were positive for the CagA antigen. Among whites, a 0.50 mg/dL increase in serum ascorbic acid level was associated with decreased seroprevalence of H. pylori (Odds Ratio (OR) = 0.89, 95% confidence interval (CI) CI 0.82-0.96, p < 0.01). In analyses that controlled for seroprevalence of H. pylori, a 0.50 mg/dL increase in serum ascorbic acid level among whites was independently associated with a decreased seroprevalence of the pathogenic cagA-positive strain of H. pylori (OR = 0.31, 95% CI 0.12-0.79, p < 0.05). Serum ascorbic acid levels were not significantly associated with H. pylori serology among non-whites (all p > 0.05). CONCLUSIONS: Higher serum levels of ascorbic acid were associated with a decreased seroprevalence of H. pylori and of the pathogenic cagA-positive strain of H. pylori among whites. If these associations are related causally and are not the result of residual confounding by factors such as socioeconomic status, ascorbic acid may affect the risk of H. pylori infection and in turn, the risk for peptic ulcer disease and gastric cancer among white Americans.

Adult↗
PubMed2004

[Comparison of intravenous ascorbic acid versus intravenous iron for functional iron deficiency in hemodialysis patients].

The effect of intravenous ascorbic acid was compared with that of intravenous iron in the treatment of functional iron deficiency, as defined as serum ferritin levels over 300 ng/ml and serum iron levels below 50 microg/dl, in patients on chronic hemodialysis. Thirteen patients on chronic hemodialysis with functional iron deficiency received intravenous injections of ascorbic acid, 100 mg, three times a week, after hemodialysis. The therapy was continued until serum ferritin decreased to below 300 ng/ml (3 months at the maximum). The iron and control group were composed of patients who had serum iron levels below 50 microg/dl within 3 months after serum ferritin rose to over 300 ng/ml. Seven patients with the iron group received more than a total of 10 intravenous injections of saccharated ferric oxide (40 mg/dose) after hemodialysis, and seven patients with the control group received no iron preparation during the 3 months. In the ascorbic acid group, while hemoglobin did not change from 10.9 +/- 0.5 g/dl (mean +/- SE) during the three-month period, serum iron increased significantly from 37 +/- 4 microg/dl to 49 +/- 4 microg/dl after one month (p<0.01), and remained elevated until the end of the three-month period. Serum ferritin decreased significantly from 607 +/- 118 ng/ml to 354 +/- 30 ng/ml after 3 months (p<0.01). In the iron group, hemoglobin and serum iron increased significantly from the respective pre-treatment levels during the 2-month period, and serum ferritin rose significantly after 3 months. In the control group, hemoglobin, serum iron and ferritin levels decreased significantly from the respective pre-treatment levels during the 3 months. The recombinant erythropoietin dose remained stable for three months in the ascorbic acid, iron, and control groups, respectively. These results suggest that in hemodialysis patients with a functional iron deficiency, treatment with intravenous ascorbic acid can prevent iron overload due to treatment with intravenous iron, and provide a useful adjuvant means of maintaining hemoglobin and serum iron levels.

Aged↗
PubMed2000

Differential effects of acute administration of haloperidol and clozapine on ethanol-induced ascorbic acid release in rat striatum.

Antipsychotic drugs were initially considered to act predominantly through their antagonism at dopamine D(2)-like receptors. However, reports have demonstrated that the typical neuroleptic drug haloperidol and the atypical neuroleptic drug clozapine showed differential actions in clinical, behavioral and biochemical studies. Since ascorbic acid has a potential usefulness in psychological therapeutics, the present study investigates the actions of these two drugs on ethanol-induced ascorbic acid release in the striatum in order to help explain the different mechanisms of these drugs. The results showed that clozapine, at the doses of 15 and 30 mg/kg, i.p., had no effect on basal ascorbic acid release. However, a synergistic tendency at a dose of 15 mg/kg and a significant synergism at a dose of 30 mg/kg were observed on ascorbic acid release when clozapine was used with ethanol. In contrast, haloperidol, at the doses of 0.5, 1.0 and 2.0 mg/kg, i.p., administered alone did not affect the basal release of striatal ascorbic acid, and when used together with ethanol had neither a potentiating nor an antagonizing effect on ethanol-induced ascorbic acid release. Chlorpromazine, a nonselective dopamine receptor antagonist, at the dose of 5 mg/kg, i.p., affected neither the basal nor the ethanol-induced ascorbic acid release. Ritanserin, a 5-HT(2) receptor antagonist, at the dose of 1 mg/kg, s.c., significantly antagonized ethanol-induced ascorbic acid release. These results demonstrate that clozapine dose-dependently potentiates the stimulatory effect of ethanol on striatal ascorbic acid release and this effect of clozapine may not be related to its dopamine D(2) receptor antagonism.

Animals↗
PubMed1975

Stimulation of ion transport by ascorbic acid through inhibition of 3':5'-cyclic-AMP phosphodiesterase in the corneal epithelium and other tissues.

Ascorbic acid stimulates active transport of Cl-minus by the isolated intact cornea. The effect is not present in corneas previously stimulated by the theophylline, an inhibitor of 3':5"-cyclic-AMP phosphodiesterase (EC 3.1.4.17), and vice versa, theophylline has no action after stimulation with ascorbic acid. This indicated inhibition of 3':5'-cyclic-AMP phosphodiesterase by ascorbic acid. Assay of phosphodiesterase using 3-H-labeled cyclid AMP of frog and rabbit corneal epithelial homogenates showed an inhibitory effect of ascorbic acid. Concentration of 5 mM produced 16% inhibition with 20 mM producing 46%. This compares with 58% inhibition by theophylline at 5 mM. Phosphodiesterase activity is mostly soluble in frog corneal epithelium but in rabbit 45% is particulate. Soluble and particulate fractions are inhibited by ascorbate, but in rabbits greater inhibition (50%) was observed in the particulate fraction than in the soluble fraction. Other tissues showed inhibition also: frog retina 12%, rat brain (caudate nucleus) 48%, rabbit brain 14%, rabbit liver 16%. It is concluded that ascorbate produces an increase in cyclic AMP content of corneal epithelium and other tissues by inhibition of 3':5'-cyclic-AMP phosphodiesterase. This action may be one of the main functions of the high ascorbic acid content of ocular tissues and explain some of the effects of high dosis of ascorbate in other systems.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1978

[Biochemical changes in guinea pigs after the application of high doses of ascorbic acid].

The effect of high doses of ascorbic acid (AA) (200 mg/kg body weight, s. c.) on the values of some biochemical parameters has been studied in guinea pigs (glucose, lactic acid, SH substances and GSH in blood, proteins and urea, and the LDH, MDH, ASAT, ALAT, and gamma-GT activities in the serum, the acid phosphatase activity in the liver, the gamma-GT activities in the liver and the kidney, and on the levels of SH substances and GSH in various organs). Ascorbic acid was administered to the animals in a single dose or in dialy doses for different periods (4 days, 2 weeks, and 7 weeks). The majority of the studied parameters showed a transient increase or decrease of the values which, however, after long term AA administration mostly returned to normal values. After 7 weeks, the level of urea in the serum remained increased (by approximately 30%) contrary to the decreased level of lactic acid, the gamma-GT activity in the serum, and the GSH level in some organs. In the experimental series carried out in the different seasons of the year, the results differed in some cases especially after short term AA administration. However, in a few cases, even the values obtained from the control animals tended to differ. If similar changes are to be expected in man after AA administration, then on the basis of our results it can be assumed that in the indicated cases the therapeutic long-term application of large AA doses does not present any hazard to the patient.

Animals↗
PubMed1996

Ascorbic acid and atherosclerotic cardiovascular disease.

In this chapter, we have briefly reviewed the current scientific knowledge of the role of vitamin C in the prevention of atherosclerosis and its associated clinical manifestations. There is good evidence from animal studies that vitamin C can slow the progression of experimental atherosclerosis. Most of these studies, however, were done either in guinea pigs, using ascorbic acid depletion, or in cholesterol-fed rabbits, using ascorbic acid supplementation. Both animal models have limitations, as guinea pigs are not a well-established (nor well-studied) model of atherosclerosis, and rabbits develop atherosclerosis at high serum beta-VLDL cholesterol levels, and in addition can synthesize ascorbic acid. In contrast, humans develop atherosclerosis spontaneously and readily at moderately elevated serum LDL cholesterol levels and have lost the ability to synthesize ascorbic acid. Thus, the animal studies discussed, although quite promising and suggestive of an anti-atherogenic effect of ascorbic acid, need to be expanded to primates before more definitive conclusions can be drawn. Similar to the animal data, the current evidence from epidemiological studies on the role of vitamin C in the prevention of CVD is inconclusive, with some studies showing a very strong correlation between increased vitamin C intake and incidence of CVD events and other studies showing no correlation at all. Studies on CVD risk factors indicate that vitamin C may moderately decrease total serum cholesterol levels, increase HDL levels, and exert a hypotensive effect. These findings are particularly intriguing and should be pursued vigorously in basic research studies to elucidate biological mechanisms. In addition, it appears that large placebo-controlled, double-blind, randomized trials of vitamin C supplementation (without simultaneous supplementation with vitamin E) in populations with a wide range of vitamin C body levels are needed in order to confirm or refute a role for vitamin C in the prevention of CVD. Unfortunately, no such trials are currently being conducted. The possible mechanisms by which ascorbic acid may affect the development of atherosclerosis and the onset of acute coronary events include effects on arterial wall integrity related to biosynthesis of collagen and GAGs, altered cholesterol metabolism mediated by vitamin C-dependent conversion of cholesterol to bile acids, and effects on triglyceride levels via modulation of lipoprotein lipase activity. A particularly intriguing possible mechanism for the anti-atherogenic effect of vitamin C is prevention of atherogenic, oxidative modification of LDL. Numerous in vitro studies have demonstrated that ascorbic acid strongly inhibits LDL oxidation by a variety of mechanisms. The potential effects of ascorbic acid on platelet function and EDRF metabolism are particularly intriguing, as they might have widespread consequences for the prevention of atherosclerotic lesion development as well as acute clinical events. Thus, both metabolic and antioxidant functions may contribute to the possible reduction of CVD risk by vitamin C.

Animals↗
PubMed2000

Inhibition of formation of oxidative volatile components in fermented cucumbers by ascorbic acid and turmeric.

Two naturally occurring antioxidants, ascorbic acid and turmeric, were effective in inhibiting formation of hexanal, (E)-2-penenal, (E)-2-hexenal, (E)-2-heptenal, and (E)-2-octenal when slurries of fermented cucumber tissue were exposed to oxygen. Added ascorbic acid prevented formation of most of these oxidative aldehydes at 175 ppm or greater. Turmeric, which is used commercially as a yellow coloring in cucumber pickle products, was found to almost completely prevent aldehyde formation at 40 ppm.

Ascorbic Acid↗
PubMed1975

Quantification of plasma cholesterol and triglyceride levels in hypercholesterolemic subjects receiving ascorbic acid supplements.

In order to assess the possible effects of ascorbic acid on plasma cholesterol and triglyceride levels and plasma lipoprotein composition, nine hypercholesterolemic subjects were treated with oral ascorbic acid (4 g/day) for 2 months. The data demonstrate: 1) no significant change in plasma cholesterol or triglyceride levels; 2) no significant change in the cholesterol or triglyceride concentrations of the major lipoprotein classes; and 3) the unexpected appearance of extra pre-beta bands on lipoprotein electrophoresis by the end of the ascorbic acid treatment period.

Adult↗