Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ASCORBIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,153 records · Page 64Linked to original sources
PubMed1986

Effects of dietary methionine, cystine and potassium sulfate on serum cholesterol and urinary ascorbic acid in rats fed PCB.

Liver weight, liver and urinary ascorbic acid levels and serum cholesterol concentration were higher in rats fed polychlorinated biphenyls (PCB) than in controls. The influences of methionine, cystine and potassium sulfate on these metabolic responses were studied. Methionine or equivalent moles of cystine or potassium sulfate were added to a basal diet containing 10% soy protein isolate. The basal diet contained 0.3% of total sulfur-containing amino acids (S-AAs). When methionine was added to the basal diet, maximum gain in body weight was obtained with 0.5% of dietary S-AAs, while the highest values in serum cholesterol and urinary ascorbic acid were obtained with 0.8% of dietary S-AAs in rats fed PCB. Dietary addition of cystine had little effect on body weight gain. Nevertheless, in rat fed PCB, urinary ascorbic acid and serum cholesterol were significantly higher in rats fed the cystine-supplemented diet than in those fed the unsupplemented diet. Addition of potassium sulfate had no effect on body weight gain, urinary ascorbic acid or serum cholesterol. These results suggest that more S-AAs are required for the highest metabolic response to PCB than for maximum growth, and the higher requirement for S-AAs cannot be replaced by inorganic sulfate.

Animals↗
PubMed1982

Impairment of absorption of ascorbic acid following ingestion of aspirin in guinea pigs.

A study was undertaken to investigate the interactions between aspirin and ascorbic acid in guinea pigs. Animals received by gastric intubation either a single dose of radiolabelled ascorbic acid alone or ascorbic acid with aspirin and the exhalation of CO2 was monitored for 400 min following administration. Animals receiving the vitamin only reached plasma peak levels within 90 min following administration while coadministration of the vitamin with aspirin, not only resulted in lower plasma peak levels, but also delayed their attainment until after 160 min. The bioavailability of ascorbic acid during the first 400 min was reduced by half following simultaneous administration of aspirin. The initial rate of exhalation of CO2 was decreased by 70% following coadministration of aspirin. These observations indicate that aspirin impairs the gastrointestinal absorption of ascorbic acid in guinea pigs, possibly by interfering with its active transport.

Animals↗
PubMed1983

The effect of ascorbic acid on the conjugation of 4-hydroxybiphenyl in rat isolated hepatocytes.

Ascorbic acid at high non-physiological levels inhibited the sulphation of 4-hydroxybiphenyl by rat isolated hepatocytes. Glucuronylation of 4-hydroxybiphenyl, formed from 4-methoxybiphenyl, was increased at ascorbic acid levels which inhibited sulphation. The glucuronylation of 4-hydroxybiphenyl added directly to the cells was enhanced at concentrations of ascorbic acid which did not inhibit sulphation. Ascorbic acid did not influence the cytochrome P-450-dependent O-demethylation of 4-methoxybiphenyl or the level of cellular lipid peroxidation.

Animals↗
PubMed1987

Effect of ascorbic acid on the absorption of zinc and calcium in man.

The effect of ascorbic acid on the absorption of zinc and calcium, was studied in healthy subjects by a radionuclide technique with 65Zn and 47Ca and whole body retention measurements. Addition of 100 mg of ascorbic acid to a water solution of 40 or 200 mumol zinc and 1 g of ascorbic acid to a high phytate meal with wholemeal bread had no effect on zinc absorption. Neither did 1 g of ascorbic acid added to 6.4 mmol of calcium influence the retention and calculated absorption of calcium. The results suggest that ascorbic acid does not affect the absorption of normal dietary levels of zinc and calcium.

Absorption↗
PubMed1991

Use of ascorbic acid to prevent the decline in eggshell quality observed with saline drinking water.

Three experiments were carried out to determine the value of ascorbic acid in overcoming the poor eggshell quality problem associated with the use of saline drinking water. Laying hens were supplied with either town water or town water supplemented with NaCl, ascorbic acid, or a combination of NaCl and ascorbic acid. Supplementing the drinking water lf laying hens with NaCl (2 g/L) significantly increased the incidence of eggshell defects and significantly decreased eggshell quality. Simultaneous supplementation of the saline drinking water with ascorbic acid (1 g/L) prevented these detrimental effects. This response to ascorbic acid was dependent upon concentration. Ascorbic acid acted as a preventive rather than a remedial treatment: hens producing eggs with defective shells as a result of receiving saline drinking water failed to show any improvement in eggshell quality or any reduction in the incidence of eggshell defects when the saline water was supplemented with ascorbic acid.

Animals↗
PubMed1979

Appraisal of ascorbic acid for acidifying the urine of methenamine-treated geriatric patients.

A study was made of 73 elderly patients receiving methenamine and ascorbic acid concurrently. Each patient had an indwelling Foley catheter. Urinary pH was assessed in relation to the dosage of ascorbic acid, duration of therapy, formulation, and dosing intervals for ascorbic acid and methenamine. Statistical analysis revealed a significant increase in urinary pH when the dosage of ascorbic acid was increased. No significant relationships were found between urinary pH and the dosage forms of ascorbic acid, the salt of methenamine used, or the duration of methenamine therapy. Changes in urinary pH at different dosing intervals for ascorbic acid were found to be significant, at the 10 percent level only, for the three-times-daily dose schedule. These data raise a question as to the value of ascorbic acid for acidifying the urine of catheterized patients receiving methenamine therapy.

Aged↗
PubMed1988

Stabilization of ascorbic acid in human plasma, and its liquid-chromatographic measurement.

We describe two independent HPLC procedures for the rapid, accurate analysis for ascorbic acid in human plasma. No sample extraction or phase separation is required. We also describe a procedure for preparing a human plasma reference material for use in clinical laboratory analysis for ascorbic acid. The ascorbic acid in plasma can be determined in 15 min, with as little as 50 microL of sample. Analytical recoveries are near 100% with direct injection of deproteinized plasma. Extensive stability data under several conditions, with dithiothreitol as a preservative (antioxidant), indicate that ascorbic acid remains stable in stored plasma for as long as 57 weeks. CVs for round-robin analysis of 11 normal human blood samples by two independent methods were between 0.1% and 5.3%. These clinical samples appear to be stable for at least 50 days under the described conditions of stabilization and sample treatment. Finally, because ascorbic acid prepared by the described procedures is stable at room temperature for at least 18 h, these methods can be readily adapted to clinical laboratory automation at room temperature.

Ascorbic Acid↗
PubMed2006

Effect of smoking on seminal plasma ascorbic acid in infertile and fertile males.

This work aimed to assess the relationship of seminal ascorbic acid levels with smoking in infertile males. One hundred and seventy men were divided into four groups: nonobstructive azoospermia [NOA: smokers (n = 20), nonsmokers (n = 20)]; oligoasthenozoospermia [smokers (n = 30), nonsmokers (n = 20)]; asthenozoospermia [smokers (n = 20), nonsmokers (n = 20)] and normozoospermic fertile men [smokers (n = 20), nonsmokers (n = 20)]. The patients underwent medical history, clinical examination, conventional semen analysis and estimation of ascorbic acid in the seminal plasma calorimetrically. There was a significant decrease in the mean seminal plasma ascorbic acid levels in smokers versus nonsmokers in all groups (mean +/- SD; 6.03 +/- 2.18 versus 6.62 +/- 1.29, 7.81 +/- 1.98 versus 9.44 +/- 2.15, 8.09 +/- 1.98 versus 9.95 +/- 2.03, 11.32 +/- 2.15 versus 12.98 +/- 12.19 mg dl(-1) respectively). Fertile subjects, smokers or not, demonstrated significant higher seminal ascorbic acid levels than any infertile group. Seminal plasma ascorbic acid in smokers and nonsmokers was correlated significantly with sperm concentration (r = 0.59, 0.60, P < 0.001), sperm motility (r = 0.65, 0.55, P < 0.001) and negatively with sperm abnormal forms per cent (r = -0.53, -0.50, P < 0.001). Nonsignificant correlations were elicited with semen volume (r = 0.2, 0.09) or liquefaction time (r = 0.03, 0.06). It is concluded that seminal plasma ascorbic acid decreased significantly in smokers and infertile men versus nonsmokers and fertile men, and is significantly correlated with the main sperm parameters: count, motility and normal morphology. Also, cigarette smoking is associated with reduced semen main parameters that could worsen the male fertilizing potential, especially in borderline cases.

Ascorbic Acid↗
PubMed1986

Effect of dietary ascorbic acid and vitamin E on metabolic changes in rats and guinea pigs exposed to PCB.

The effect of the addition of dietary ascorbic acid and/or vitamin E (all-rac-alpha-tocopheryl acetate) in rats and guinea pigs exposed to PCB (polychlorinated biphenyls) was studied. Rats were fed diets containing one of three levels of vitamin E (30, 500 or 1000 mg/kg diet) with or without PCB (200 mg/kg diet). Guinea pigs were fed diets containing PCB (40 mg/kg diet) with 200 or 1000 mg ascorbic acid/kg diet and/or 70 or 2000 mg vitamin E/kg diet. For rats fed PCB, ascorbic acid in urine was 40-fold higher and in liver, 2-fold higher than for rats fed no PCB, and thiobarbituric acid-reactive substances (TBA-RS, indicators of lipid peroxidation) in liver was 1.5-fold higher. In rats fed PCB, high dietary vitamin E significantly lowered the urinary ascorbic acid and TBA-RS. Liver ascorbic acid was lowered by high dietary vitamin E only in control rats. In guinea pigs, feeding PCB caused severe growth retardation and the liver TBA-RS was 1.8-fold higher than in guinea pigs not fed PCB. Feeding high levels of both ascorbic acid and vitamin E was more effective in reversing the growth depression and in lowering TBA-RS level (due to PCB) than feeding the vitamins separately. Ascorbic acid metabolism in rats was affected by high dietary vitamin E. The possibility of a higher requirement for ascorbic acid and vitamin E in guinea pigs exposed to PCB was indicated. Interaction of ascorbic acid and vitamin E in animals exposed to PCB was suggested.

Animals↗
PubMed2004

Pulmonary epithelial lining fluid and plasma ascorbic acid concentrations in horses affected by recurrent airway obstruction.

OBJECTIVE: To determine the pulmonary epithelial lining fluid (ELF) concentrations and degree of oxidation of ascorbic acid in horses affected by recurrent airway obstruction (RAO) in the presence and absence of neutrophilic airway inflammation. ANIMALS: 6 RAO-affected horses and 8 healthy control horses. PROCEDURE: Nonenzymatic antioxidant concentrations were determined in RBC, plasma, and ELF samples of control horses and RAO-affected horses in the presence and absence of airway inflammation. RESULTS: ELF ascorbic acid concentration was decreased in RAO-affected horses with airway inflammation (median, 0.06 mmol/L; 25th and 75th percentiles, 0.0 and 0.4 mmol/L), compared with RAO-affected horses without airway inflammation (1.0 mmol/L; 0.7 and 1.5 mmol/L) and control horses (2.2 mmol/L; 1.4 and 2.2 mmol/L). Epithelial lining fluid ascorbic acid remained significantly lower in RAO-affected horses without airway inflammation than in control horses. Moreover, the ELF ascorbic acid redox ratio (ie, ratio of the concentrations of dehydroascorbate to total ascorbic acid) was higher in RAO-affected horses with airway inflammation (median, 0.85; 25th and 75th percentiles, 0.25 and 1.00), compared with RAO-affected horses without airway inflammation (0.04; 0.02 and 0.22). The number of neutrophils in bronchoalveolar lavage fluid was inversely related to the ELF ascorbic acid concentration (r = -0.81) and positively correlated with the ascorbic acid redox ratio (r = 0.65). CONCLUSIONS AND CLINICAL RELEVANCE: Neutrophilic inflammation in horses affected by RAO is associated with a reduction in the ELF ascorbic acid pool. Nutritional supplementation with ascorbic acid derivatives in horses affected by RAO is an area for further investigation.

Animals↗
PubMed1997

Ascorbic acid deficiency in porphyria cutanea tarda.

Porphyria cutanea tarda (PCT), the most common form of porphyria, is manifested as skin photosensitivity caused by excess hepatic production of uroporphyrin and heptacarboxylporphyrin. In experimental animal models, ascorbic acid modulates chemically induced uroporphyrin accumulation. The purpose of this study was to determine whether ascorbic acid is decreased in the plasma of patients with PCT. Plasma was obtained after an overnight fast from 21 PCT patients, 16 of whom were infected with hepatitis C virus (HCV), and from a separate group of 9 patients with HCV infection but not PCT. Thirteen PCT patients were studied when they had active disease and 8 after treatment-induced remission. Plasma ascorbic acid was low (<23 micromol/L) in 11 (85%) of the 13 untreated PCT patients and deficient (<11 micromol/L) in 8 (62%). Two patients with normal ascorbic acid levels (45 and 62 micrommol/L) had consumed multivitamins. In 2 patients with deficient ascorbic acid, plasma levels returned to normal after phlebotomy treatment. Of the 8 patients studied during remission, 4 had normal ascorbic acid values and 4 were deficient (5 to 8 micromol/L). Plasma ascorbic acid values were normal for all patients who had HCV but no PCT. These data suggest that plasma ascorbic acid concentrations are commonly low in PCT, but this decrease is unrelated to HCV infection. Ascorbic acid deficiency may be one of the factors that contributes to the pathogenesis of PCT.

Adult↗
PubMed1976

Effect of ascorbic acid on rate of heat acclimatization.

There is some indication in the literature that ascorbic acid (vitamin C) may reduce the physiological responses to heat stress. Consequently, the effect of ascorbic acid ingestion on heat-strain indicators has been studied on a group of 60 mining recruits undergoing climatic room acclimatization. Of the 60 men, 19 received a daily dose of 250 mg ascorbic acid; 21 a daily dose of 500 mg ascorbic acid; and 20 received a placebo daily. Measurements of rectal temperature, heart rate, and hourly sweat rate were made on all subjects during the 4 h of heat exposure per day for 10 days. The wet bulb temperature was 32.2 degrees C, the dry bulb 33.9 degrees C, the air movement 0.4 m/s, and the work rate 35 W. The results indicate that the rate and degree of acclimatization, as assessed by 4th-h rectal temperature, is enhanced by ascorbic acid supplementation and that no differences in response could be shown between daily dosages of 250 and 500 mg of vitamin C.

Acclimatization↗
PubMed2005

Chondrocyte transport and concentration of ascorbic acid is mediated by SVCT2.

Collagen II is the major protein component of articular cartilage and forms the collagen fibril network, which provides the tensile strength of cartilage. Collagen II synthesis is enhanced by ascorbic acid (vitamin C) at both a transcriptional and post-transcriptional level. While the importance of ascorbic acid in the synthesis of collagen has been established, the mechanism by which this essential nutrient is transported into chondrocytes has not been investigated previously. We have characterized the transport of the reduced form of ascorbic acid in passaged primary human chondrocytes to discern the physiologically relevant pathways of ascorbic acid transport in cartilage. We have found that chondrocytes are robust concentrators of ascorbic acid, capable of transporting the reduced form, and concentrating total ascorbic acid, in the reduced form and its metabolites, 960-fold over the concentration in the extracellular milieu. Chondrocyte transport of ascorbic acid was sodium and temperature dependent, stereoselective for the L-forms, and inhibited by the anion transport inhibitor, sulfinpyrazone. Chondrocytes preferentially expressed the full-length and functional isoform of sodium-dependent vitamin C transporter 2 (SVCT2). When this transcript was suppressed with sequence-specific siRNAs, the active transport component of ascorbic acid was abolished. Thus, we provide the first evidence that SVCT2 mediates the secondary active and concentrative transport of ascorbic acid in human chondrocytes.

Amino Acids↗
PubMed1984

Ascorbic acid in thyroidectomized rats. I) Biosynthesis and catabolism.

Thyroidectomized rats showed a decrease in ascorbic acid and dehydroascorbic acid, with almost no alterations in the diketogulonic acid in liver and kidney. Total ascorbic acid in urine was found to be increased, whereas glucuronic acid in urine decreased significantly. There were no significant changes in the activities of ascorbic acid synthesizing enzymes. Activities of the degrading enzymes were found to increase significantly in the liver, with no remarkable change in their activities in kidney. Daily administration of thyroxine for 10 days to thyroidectomized rats normalized the activities of dehydroascorbatase and 2,3 diketoaldonate decarboxylase in the liver, whereas single administration of thyroxine on the 7th day after thyroidectomy could not bring about such restoration. It seems that thyroxine has no direct role on ascorbic acid metabolism in rats.

Animals↗
PubMed1994

Improved method for the analysis of ascorbic acid in plasma by high-performance liquid chromatography with electrochemical detection.

We improved the analytical method for the detection of ascorbic acid in plasma by high-performance liquid chromatography (HPLC) with an electrochemical detector (ECD) to be more selective and rapid than the protocol previously used. Main improvements are as follows. Applied potential of ECD to obtain the maximal response for ascorbic acid was +450 mV versus Ag/AgCl, but it was reduced to +350 mV. In that condition, uric acid did not respond to ECD, and only ascorbic acid was detected. EDTA contained in sample extraction/stabilizing solution gave the peak after the ascorbic acid. The addition of EDTA (0.2 mM) to the mobile phase eliminated the EDTA peak. These two improvements gave the chromatogram in which the peak that appeared from the plasma sample was only ascorbic acid, and shorten the sample run time. Ascorbic acid in plasma was unstable even though the plasma was treated with methanol/EDTA: it decreased from 1.5 h at 4 degrees C. However, the treated sample, which was placed at -14 degrees C until the analysis was performed, gave the reliable ascorbic acid value at least up to 6 h. The data obtained from the HPLC-ECD method was consistent with those from the hydrazine method.

Ascorbic Acid↗
PubMed2001

L-ascorbic acid potentiates endothelial nitric oxide synthesis via a chemical stabilization of tetrahydrobiopterin.

Ascorbic acid has been shown to stimulate endothelial nitric oxide (NO) synthesis in a time- and concentration-dependent fashion without affecting NO synthase (NOS) expression or l-arginine uptake. The present study investigates if the underlying mechanism is related to the NOS cofactor tetrahydrobiopterin. Pretreatment of human umbilical vein endothelial cells with ascorbate (1 microm to 1 mm, 24 h) led to an up to 3-fold increase of intracellular tetrahydrobiopterin levels that was concentration-dependent and saturable at 100 microm. Accordingly, the effect of ascorbic acid on Ca(2+)-dependent formation of citrulline (co-product of NO) and cGMP (product of the NO-activated soluble guanylate cyclase) was abolished when intracellular tetrahydrobiopterin levels were increased by coincubation of endothelial cells with sepiapterin (0.001-100 microm, 24 h). In contrast, ascorbic acid did not modify the pterin affinity of endothelial NOS, which was measured in assays with purified tetrahydrobiopterin-free enzyme. The ascorbate-induced increase of endothelial tetrahydrobiopterin was not due to an enhanced synthesis of the compound. Neither the mRNA expression of the rate-limiting enzyme in tetrahydrobiopterin biosynthesis, GTP cyclohydrolase I, nor the activities of either GTP cyclohydrolase I or 6-pyruvoyl-tetrahydropterin synthase, the second enzyme in the de novo synthesis pathway, were altered by ascorbate. Our data demonstrate that ascorbic acid leads to a chemical stabilization of tetrahydrobiopterin. This was evident as an increase in the half-life of tetrahydrobiopterin in aqueous solution. Furthermore, the increase of tetrahydrobiopterin levels in intact endothelial cells coincubated with cytokines and ascorbate was associated with a decrease of more oxidized biopterin derivatives (7,8-dihydrobiopterin and biopterin) in cells and cell supernatants. The present study suggests that saturated ascorbic acid levels in endothelial cells are necessary to protect tetrahydrobiopterin from oxidation and to provide optimal conditions for cellular NO synthesis.

Ascorbic Acid↗
PubMed1994

Effect of ascorbic acid on apparent iron absorption by women with low iron stores.

The effect of ascorbic acid supplementation on apparent iron absorption was tested in women with low iron stores. For 10 wk, 25 healthy nonpregnant women, aged 20-45 y with low serum ferritin (3.5-17.7 micrograms/L), consumed either a diet with predicted poorly bioavailable iron or a typical Western diet, classified according to dietary meat and ascorbic acid contents. Meals were supplemented with ascorbic acid (500 mg, three times a day) for 5 of the 10 wk, in a double-blind, crossover design. Ascorbic acid did not affect most biochemical indexes of iron status, the biological half-life of 59Fe, or apparent iron absorption (diet-feces) from either diet, but slightly increased serum ferritin (11.9 vs 10.7 micrograms/L, P < 0.06) when data from both diets were combined. These results support other evidence that ascorbic acid has less effect on iron bioavailability than has been predicted from tests with single meals.

Adult↗