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 109 records · Page 6Linked to original sources
PubMed1986

Effect of graded doses of erythorbic acid on ascorbic acid content of tissues of guinea pigs.

The effect of graded doses of erythorbic acid (ErA) on the content of ascorbic acid (AsA) in the tissues of guinea pigs administered AsA was studied. The guinea pigs were administered 5 mg AsA and 1, 5, 20, and 100 mg ErA; or 1 mg AsA and 1 and 20 mg ErA; or 20 mg AsA and 20 mg ErA for 16 days. The animals were then sacrificed, and the liver, adrenal glands, spleen, and kidneys were removed to determine the contents of AsA and ErA by using HPLC. The content of AsA in the tissues of the animals administered less than 5 mg ErA together with 5 mg AsA was not significantly different from that of the animals administered 5 mg AsA. The administration of 100 mg ErA together with 5 mg AsA caused a decrease in the amount of AsA in the tissues. The content of AsA in the tissues of the animals administered ErA together with 1 mg AsA was not significantly different from that of the animals administered 1 mg AsA. In the case of animals administered an equal amount of both AsA and ErA, the AsA tissue content was consistently much higher than that of ErA. These results indicated that the administration of relatively small amounts of ErA did not appear to reduce the availability of AsA.

Adrenal Glands↗
PubMed1986

Postmortem changes in uric acid and ascorbic acid in human cerebral cortex tissues excised after cardiac death.

There has been no report on the determination of uric acid (UA) in human brain and heart tissues. UA and ascorbic acid (AA) in human cerebral cortex and heart tissues excised after cardiac death have been studied by reversed-phase high-performance liquid chromatography (HPLC) with electrochemical detection (ECD). It has been found that the levels of AA and UA in the human cerebral cortex tissues tend to decrease and increase, respectively, after cardiac death as a function of time between death and forensic operation. In addition, it has been found that there is no special relationship between UA levels in human heart tissues and time after cardiac death, also that the UA levels in the heart are high as compared with those in human cerebral cortex tissues. We have emphasized that the HPLC-ECD method is useful in determining UA and AA in mammalian tissues by one-time chromatography to gain a better understanding of the relationship between disease and serum urate level.

Ascorbic Acid↗
PubMed2004

Effects of acetylsalicylic acid on ascorbic acid concentrations in plasma, gastric mucosa, gastric juice and urine--a double-blind study in healthy subjects.

OBJECTIVE: This study investigated concentrations of ascorbic acid (ASC) in gastric mucosa, gastric juice, urine and plasma in healthy subjects under steady state and fasted conditions with and without concomitant administration of acetylsalicylic acid (ASA). MATERIAL AND METHODS: This was a prospective, randomized, double-blind, parallel-group study in healthy subjects. It has assessed the effects of a 6-day administration of 0.8 g ASA or 0.48 g ASC, 3 times daily and the combination of both on concentrations of ASC in gastric mucosa, gastric juice, urine and plasma. Treatments were switched after 6 days without any washout for assessment of compartment sensitivity to changes in study medication resulting in an overall 14-day study period. Each of the 3 treatment groups consisted of 15 subjects. RESULTS: ASC concentrations were highest in the gastric mucosa (251+/-11 microg/g), followed by gastric juice (29+/-6 microg/ml), plasma (10+/-0.2 microg/ml), and urine (5+/-1 microg/ml). On day 7, ASC concentrations in gastric mucosa, plasma and urine had increased in those groups receiving ASC and decreased in the group receiving ASA only. All differences were statistically significant and indicate an interaction with ASA. In gastric juice, differences in ASC concentrations between the treatment groups were not statistically significant between baseline and day 7. ASC concentrations in plasma were strongly correlated with corresponding ASC concentrations in gastric mucosa (r = 0.34) and urine (r = 0.83), as were ASC concentrations in gastric mucosa with ASC in urine (r = 0.28). CONCLUSIONS: The gastric mucosa is the largest depot of ASC in the human body with ASC concentrations 25 times higher than in plasma. In healthy subjects, clinically relevant doses of ASA reduced ASC concentrations in gastric mucosa by about 10% within 6 days resulting from antioxidative defense mechanisms. In patients with long-term ASA treatment or conditions with additional risks such as elderly subjects with unfavorable dietary conditions and impaired antioxidative protection, a protective adjunct administration of ASC appears to be beneficial.

Adolescent↗
PubMed2000

Interconversion between dehydro-L-ascorbic acid and L-ascorbic acid.

L-Ascorbic acid (AA) plays an important role in biological systems as an electron donor. Erythorbic acid (EA) is the epimer of AA and has chemical characteristics very similar to those of AA. It is demonstrated in the present study by 1H-NMR that dehydro-L-ascorbic acid (DAA) was reduced by EA under neutral conditions but not acidic, and that dehydroerythorbic acid (DEA) was also reduced by AA under the same conditions. These reactions also occurred at a low concentration close to the concentration of AA in such biological tissue as the liver. Furthermore, the interconversion of DAA and AA at neutral pH and low concentration was also confirmed by radioluminography. These results suggest the interconversion between DAA and AA in vivo.

Ascorbic Acid↗
PubMed1995

Effect of pantothenic acid and ascorbic acid supplementation on human skin wound healing process. A double-blind, prospective and randomized trial.

This study aimed at testing human skin wound healing improvement by a 21-day supplementation of 1.0 g ascorbic acid (AA) and 0.2 g pantothenic acid (PA). 49 patients undergoing surgery for tattoos, by the successive resections procedure, entered a double-blind, prospective and randomized study. Tests performed on both skin and scars determined: hydroxyproline concentrations, number of fibroblasts, trace element contents and mechanical properties. In the 18 supplemented patients, it was shown that in skin (day 8) Fe increased (p < 0.05) and Mn decreased (p < 0.05); in scars (day 21), Cu (p = 0.07) and Mn (p < 0.01) decreased, and Mg (p < 0.05) increased; the mechanical properties of scars in group A were significantly correlated to their contents in Fe, Cu and Zn, whereas no correlation was shown in group B. In blood, AA increased after surgery with supplementation, whereas it decreased in controls. Although no major improvement of the would healing process could be documented in this study, our results suggest that the benefit of AA and PA supplementation could be due to the variations of the trace elements, as they are correlated to mechanical properties of the scars.

Adolescent↗
PubMed2000

Ascorbic acid stimulation of production of a highly branched ,beta-1,3-glucan by Aureobasidium pullulans K-1--oxalic acid, a metabolite of ascorbic acid as the stimulating substance.

The production of a highly branched beta-1,3-glucan by Aureobasidium pullulans K-1 in Czapek's medium has been found to be stimulated by ascorbic acid. When the culture supernatant, after removal of polysaccharide from the culture filtrate by ethanol precipitation, was concentrated, then added to a new medium and this strain was cultured in the medium, the polysaccharide production was stimulated the same as when L-ascorbic acid was added to the medium. The stimulating substance was partially purified from the supernatant, and was found to be oxalic acid; 0.03% oxalic acid was the most effective concentration for the stimulation of polysaccharide production. The stimulating substance, oxalic acid, was proved to be derived from ascorbic acid added to a medium in an experiment using L-[1-14C]ascorbic acid. We suggest that oxalic acid generated from the metabolism of ascorbic acid in cells of Aureobasidium pullulans K-1 participated in the stimulation of the polysaccharide production by ascorbic acid.

Ascorbic Acid↗
PubMed2002

Comparison of uric acid and ascorbic acid in protection against EAE.

Serum levels of uric acid (UA), an inhibitor of peroxynitrite- (ONOO-) related chemical reactions, became elevated approximately 30 million years ago in hominid evolution. During a similar time frame, higher mammals lost the ability to synthesize another important radical scavenger, ascorbic acid (AA), leading to the suggestion that UA may have replaced AA as an antioxidant. However, in vivo treatment with AA does not protect against the development of experimental allergic encephalomyelitis (EAE), a disease that has been associated with the activity of ONOO- and is inhibited by UA. When compared in vitro, UA and AA were found to have similar capacities to inhibit the nitrating properties of ONOO-. However UA and AA had different capacities to prevent ONOO- -mediated oxidation, especially in the presence of iron ion (Fe3+). While UA at physiological concentrations effectively blocked dihydrorhodamine-123 oxidation in the presence of Fe3+, AA did not, regardless of whether the source of ONOO- was synthetic ONOO-, SIN-1, or RAW 264.7 cells. AA also potentiated lipid peroxidation in vivo and in vitro. In conclusion, the superior protective properties of UA in EAE may be related to its ability to neutralize the oxidative properties of ONOO- in the presence of free iron ions.

Albumins↗
PubMed1998

Oxidation products of uric acid and ascorbic acid in preterm infants with chronic lung disease.

Allantoin, the oxidation product of uric acid (UA), can be used as an in vivo marker of free radical generation. The aims of the present study were to evaluate the allantoin changes in plasma and bronchoalveolar lavage fluid (BALF) as well as to examine plasma levels of ascorbic acid (AA) and its oxidation product, dehydroascorbic acid (DHAA), in infants with or without chronic lung disease (CLD) during the first week of life. The study population was 20 infants of 24-30 weeks gestation, comprising 10 who subsequently developed CLD and 10 without CLD. In the CLD infants, the plasma allantoin/UA ratio showed a significant increase after day 1 and continued to increase gradually to reach a peak on day 6 (6.5 +/- 4.1% for CLD and 2.1 +/- 0.9% for non-CLD infants). The allantoin/UA ratio in BALF was also higher in CLD infants and the difference reached significance on days 4-6 (41.2 +/- 15.8% for CLD and 11.7 +/- 9.9% for non-CLD infants). In contrast to allantoin, the plasma DHAA/AA ratio did not differ between the 2 groups throughout the study period. Our findings that the allantoin/UA ratios were significantly higher in CLD than non-CLD infants not only in plasma but also in BALF, and that the intergroup differences of this ratio in both plasma and BALF was more prominent in the latter half of the first week of life further confirm our previous speculation that oxygen radicals are involved in the development of neonatal CLD.

Allantoin↗
PubMed1997

Nitrogen dioxide depletes uric acid and ascorbic acid but not glutathione from lung lining fluid.

The aim of this study was to determine the kinetics of the reactions between the gaseous free-radical pollutant, nitrogen dioxide (NO2), and the water-soluble antioxidants present in respiratory tract lining fluid (RTLF). Samples of RTLF, recovered from 12 subjects (mean age 54.1+/-16.3 years; eight male, four female) as bronchoalveolar lavage (BAL) fluid were exposed ex vivo to NO2 [50-1000 parts per billion (ppb)] for 4 h. For comparison, similar exposures were carried out with single and composite solutions with relevant RTLF antioxidant concentrations. Ascorbic acid (AA), uric acid (UA), GSH depletion, and GSSG and malondialdehyde (MDA) formation were determined with time. In the three models, UA and AA were consumed in a time- and NO2-concentration-related fashion. In addition, their rate of depletion correlated positively with their initial concentration (UA, r=0.92, P<0.05; AA, r=0.94, P<0.05). Little difference was found between the rate of loss of AA (2.2+/-0. 2; 1.9+/-0.5; 1.4+/-0.3 nmol.l-1.h-1.ppb-1), and that of UA (2.4+/-0. 2; 2.1+/-0.6; 1.3+/-0.2 nmol.l-1.h-1.ppb-1) in the three RTLF models examined (single, composite, BAL fluid respectively). GSH loss from BAL fluid (0.2+/-0.1) was significantly less than that seen in either single (1.4+/-0.3) or composite (1.2+/-0.5 nmol.l-1.h-1. ppb-1) antioxidant solutions. In all cases, GSH consumption was significantly less than AA or UA. As model complexity increased, the rate of individual antioxidant loss decreased, such that in BAL fluid, AA, UA and GSH consumption rates were significantly less (P<0. 05) than in the pure or composite antioxidant mixtures. In BAL fluid, little GSSG production was observed at any NO2 concentration. MDA concentration, determined as a measure of lipid peroxidation, did not change following exposure to 50, 150 or 400 ppb NO2, but increased MDA was seen in BAL fluid from 8/12 subjects following exposure to 1000 ppb NO2 for 1 h or more. In conclusion, NO2, at environmentally relevant concentrations, depletes BAL fluid of the antioxidant defences, UA and AA, but not GSH.

Antioxidants↗
PubMed1981

Depletion and repletion of ascorbic acid in the Rhesus monkey: relationship between ascorbic acid concentration in blood components with total body pool and liver concentration of ascorbic acid.

Eight female monkeys (Macaca mulatta) were fed an ascorbic acid-free diet for 7 weeks, followed by repletion with a supplementation of 10 mg ascorbic acid per kg of body weight for 3 weeks. Once each week the ascorbic acid contents of blood components and liver samples, obtained by closed needle biopsy, were determined as the 2,4-dinitrophenylhydrazine derivative. In selected animals the size of the total body pool ascorbic acid was determined by isotope dilution after administration (i.v.) of 14C-ascorbic acid. At no time were the monkeys frankly scorbutic. Values for r2 were less than 0.10 between plasma, whole blood, and erythrocyte ascorbic acid contents compared with the total body pool of ascorbic acid. Leukocyte ascorbic acid content was positively related to the total body pool of ascorbic acid (P less than 0.001, r2 = 0.923). Values for r2 were less than 0.15 when whole blood and (erythrocyte) ascorbic acid content were each compared with liver ascorbic acid levels; however, there was a tendency for plasma ascorbic acid levels to be directly related to liver ascorbic acid levels (P less than 0.05, r2 = 0.477), when plasma ascorbic acid was greater than 0.1 micrograms/ml. The relationship between liver ascorbic acid and leukocyte ascorbic acid levels was statistically significant (P less than 0.01, r2 = 0.683). The high correlation of leukocyte ascorbic acid levels with liver ascorbic levels and with the total body pool of ascorbic acid suggests that leukocyte ascorbic acid values best represent the vitamin C status of the female Rhesus monkeys.

Animals↗
PubMed1998

Erythrocyte defenses against hydrogen peroxide: the role of ascorbic acid.

Ascorbate has been reported to increase intracellular hydrogen peroxide (H2O2) generation in human erythrocytes. In the present work, the basis for this prooxidant effect of the vitamin was investigated in the context of erythrocyte defenses against H2O2. Ascorbate added to erythrocytes caused a dose-dependent increase in intracellular H2O2, which was measured as inactivation of endogenous catalase in the presence of 3-amino-1,2,4-triazole (aminotriazole). Ascorbate-induced catalase inactivation was not observed when only the intracellular ascorbate concentration was increased, when cells were incubated with ascorbate in plasma, or when extracellular Fe3+ was chelated. Together, these results suggest that the observed ascorbate-induced H2O2 generation is due to Fe3+-catalyzed oxidation of extracellular, as opposed to intracellular, ascorbate by molecular oxygen. Rather than generate an oxidant stress in erythrocytes, ascorbate was one of the most sensitive intracellular antioxidants to H2O2 coming from outside the cells. On the other hand, intracellular ascorbate contributed little to the detoxification of H2O2, which was found to be mediated by both catalase and by the GSH system.

Ascorbic Acid↗
PubMed1980

Effects of ascorbic acid, vitamin E, and fatty acids on lipid composition in cockerels.

Serum, aorta, heart, and liver tissues of cockerels reflected numerous changes in cholesterol and triglyceride composition when 5 or 10% oleic or palmitic acid, ascorbic acid, and vitamin E were added to their diets. Heart cholesterol concentration and liver cholesteryl ester content increased with the 10% oleic acid diet. Heart and liver cholesterol increased when ascorbic acid was added to 5% fatty acid diets, and heart cholesterol increased when ascorbic acid was added to the 10% palmitic acid diet. Vitamin E exerted a cholesterol- or cholesteryl ester-lowering effect on both 10% palmitic and 10% oleic acid diets. Heart and liver triglycerides were lower with the 5% oleic acid diet than with the 5% palmitic acid diet. The opposite effect was observed with the 10% fatty acid diet. Dietary ascorbic acid appeared to have some triglyceride-lowering effect. Dietary fatty acid composition was reflected in cockerel aorta, heart, liver, and serum fatty acid distribution, with oleic acid having the greater influence.

Animals↗
PubMed1989

Effect of exogenous ascorbic acid intake on biosynthesis of ascorbic acid in mice.

The effect of exogenous ascorbic acid intake on biosynthesis of ascorbic acid in mice has been studied. After the mice were on diets containing added ascorbic acid for two months, the activities of ascorbic acid synthesizing enzymes in the mouse liver homogenates were measured using L-gulono-gamma-lactone as a substrate. Exogenous ascorbic acid intake (0.5, 1 or 5% in the diet) was able to increase the concentration of ascorbic acid in the blood and to decrease the activities of ascorbic acid synthesizing enzymes in mouse liver. The results suggest that ascorbic acid synthesis was controlled by local regulatory mechanism or by the concentration of ascorbic acid in the hepatic portal blood. Ingestion of dietary erythorbic acid, a stereoisomer of ascorbic acid, had no effect on the activities of ascorbic acid synthesizing enzymes.

Animals↗