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 505 records · Page 28Linked to original sources
PubMed1975

Pulmonary edema and ascorbic acid loss.

Loss of ascorbic acid from lung and pulmonary edema were produced in mice by intravenous injection of either adrenaline or noradrenaline (5 mumol/kg). While adrenalectomy performed before noradrenaline administration reduced the degree of pulmonary edema, a prior dose of hexamethonium accentuated this effect. Given alone, hexamethonium caused both loss of ascorbic acid and pulmonary edema. The results show that although endogenous catecholamines can potentiate the pulmonary edema produced by either adrenaline or noradrenaline, they play no specific role in the ascorbic acid loss. The evidence suggests that lung ascorbic acid levels are decreased following the development of pulmonary edema, irrespective of how it was caused.

Adrenal Glands↗
PubMed2000

Nonenzymatic elimination of ascorbic acid in clinical samples.

OBJECTIVES: Ascorbic acid interferes significantly in the oxidative reaction of chromogenic reagents by peroxidase and hydrogen peroxide. Currently, ascorbate oxidase is commonly utilized for eliminating the interference of ascorbic acid in the oxidative colorimetric reaction. This enzyme, however, displays several disadvantages, such as high cost, variation from lot to lot, and low stability. We applied a series of commercially available and stable radicals (ascorbic acid quenchers [AAQs]) for nonenzymatic quenching of ascorbic acid in the uricase-based uric acid determination in serum and urine. DESIGN AND METHODS: In order to evaluate the quenching activity of AAQs, a commercially available uric acid detection kit was used. TBA-80FR.NEO biochemical analyzer was utilized for the assay. RESULTS: 4-Hydroxy-2,2,6,6-tetramethyl-1-piperidinyloxy free radical (AAQ-2) was the most effective ascorbic acid quencher among the four stable radicals, and the uric acid assay suffered no interference by AAQ-2. The ascorbic acid quenching ability of 2 mmol/L of AAQ-2 in reagent solution (reagent-I) was > or = 2 U/ml ascorbate oxidase in reagent solution. CONCLUSIONS: AAQ-2 was proven to be a suitable quencher of ascorbic acid in clinical samples.

Ascorbate Oxidase↗
PubMed1991

Concerted proton-electron transfer between ascorbic acid and cytochrome b561.

Ascorbic acid is an essential reductant in biology but its reducing power is paradoxical. At physiological pH the predominant form of ascorbate (the monoanion) is a poor electron donor because it oxidizes to the energetically unfavorable neutral free radical. The ascorbate dianion forms the relatively stable semidehydroascorbate radical anion and is a powerful electron donor but its concentration at neutral pH is insufficient to produce the reaction rates observed. For example, ascorbate rapidly reduces cytochrome b561 from adrenal medullary chromaffin vesicles. This fast reaction rate may be rationalized by a mechanism involving concerted proton-electron transfer rather than electron transfer alone. This would permit reduction of the cytochrome by the abundant ascorbate monoanion but would circumvent formation of unfavorable intermediates. This may be a general mechanism of biological ascorbic acid utilization: enzymes using ascorbic acid may react with the ascorbate monoanion via concerted proton-electron transfer.

Ascorbic Acid↗
PubMed1995

Requirement for Na(+)-dependent ascorbic acid transport in osteoblast function.

Ascorbic acid is necessary for expression of the osteoblast phenotype. We examined whether Na(+)-dependent transport is required for MC3T3-E1 preosteoblast cells to respond to vitamin C and investigated the role of membrane transport in the intracellular accumulation and function of ascorbate. MC3T3-E1 cells were found to possess a saturable, stereoselective, Na(+)-dependent ascorbic acid transport activity that is sensitive to the transport inhibitors sulfinpyrazone, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, and phloretin. Transport activity showed no competition with glucose or 2-deoxyglucose and was not inhibited by cytochalasin B, indicating that it is distinct from known hexose transporters. On addition of 100 microM ascorbic acid to the extracellular medium, intracellular concentrations of 10 mM were reached within 5-10 h and remained constant for up to 24 h. A good correlation was observed between intracellular ascorbic acid concentration and rate of hydroxyproline synthesis. Although ascorbic acid was transported preferentially compared with D-isoascorbic acid, both isomers had equivalent activity in stimulating hydroxyproline formation once they entered cells. Marked stereoselectivity for extracellular L-ascorbic acid relative to D-isoascorbic acid was also seen when alkaline phosphatase and total hydroxyproline were measured after 6 days in culture. Moreover, ascorbic acid transport inhibitors that prevented intracellular accumulation of vitamin blocked the synthesis of hydroxyproline. Thus Na(+)-dependent ascorbic acid transport is required for MC3T3-E1 cells to achieve the millimolar intracellular vitamin C concentrations necessary for maximal prolyl hydroxylase activity and expression of the osteoblast phenotype.

3T3 Cells↗
PubMed1976

Formation in vitro of ascorbic acid 2-sulfate.

The sulfation of ascorbic acid by an ascorbic acid sulphotransferase was investigated using rat liver and colon homogenates. When Na2 35 SO4 or 3'-phosphoadenylyl [35S]sulfate (P-Ado-P-35S) and ascorbic acid were used as substrates, chromatographic behavior of the reaction products on thin-layer cellulose suggested that ascorbic acid 2-[35S]sulfate was formed. With Na2 35SO4 as the source of radioactive sulfate in the assay system, ATP was found to be an obligatory cofactor. Incorporation of [35S]sulfate frofrom Na2 35SO4 into ascorbic acid 2-[35S]sulfate was also decreased when ATP sulfurylase inhibitors were added to the system. P-Ado-O35S alone in the assay without ATP was an extemely effective sulfating agent. In addition, liver and colon homogenates from vitamin A deficient and sufficient rats were used in one of the studies. Vitamin A deficiency appeared to have little effect on ascorbic acid 2-sulfate formation.

Animals↗
PubMed1979

Studies on the bioavailability of zinc in man. III. Effects of ascorbic acid on zinc absorption.

As ascorbic acid is known to enhance the absorption of dietary iron and to inhibit the absorption of dietary copper, studies were undertaken to examine the effect of ascorbic acid on the bioavailability of zinc in human subjects. The index of absorption was the change in plasma zinc concentration after a 110-mg aqueous dose of ZnSO4.7H2O (containing 25 mg of elemental zinc). Doses of 0.5, 1.0, and 2.0 g of ascorbic acid, representing a spectrum of Zn:ascorbic acid molar ratios from the dietary to the pharmacological range, failed to produce any significant change in the pattern of zinc absorption. Moreover, 2.0 g of ascorbic acid, equivalent to a Zn:ascorbic acid ratio of 0.145 failed to improve the absorption of 108 mg of elemental zinc incorporated into 120 g of black bean gruel. Ascorbic acid over a range of dosages commonly consumed by man had no demonstrable effect on the absorption of inorganic zinc.

Absorption↗
PubMed1984

Evidence of rebound effect with ascorbic acid.

The urinary excretion pattern of ascorbic acid in two subjects who had been taking a large amount of ascorbic acid (10 g per day) and later reverted to a small intake (125 mg per day) is described. The ascorbic acid concentration in the 24-hour urine samples was measured over a 40-day collection of this period. The mean urinary ascorbic acid excretion during the loading period of the two subjects was about 2 g per day. Upon termination of the high intake of ascorbic acid, urinary ascorbic acid excretion dropped to presupplementation levels within 6 days. Urinary ascorbic acid of the two subjects continued to decrease to below basal level, and remained at abnormally low levels for 10 and 12 days respectively. We hypothesize that the high intake of ascorbic acid has induced the formation of increased amounts of enzymes that help convert the ascorbic acid into other substances and that these substances are valuable. Some possible physiological actions of these ascorbic acid metabolites are discussed.

Adult↗
PubMed1968

Effects of iron overload on ascorbic acid metabolism.

Studies of the ascorbic acid status in two subjects with idiopathic haemochromatosis and in 12 with transfusional siderosis showed that all had decreased levels of white cell ascorbic acid. The urinary excretion of ascorbic acid was also diminished in those subjects in whom such measurements were made. The administration of ascorbic acid was followed by only a small rise in the urinary ascorbic acid output, while the oxalic acid levels (measured in two subjects) showed a significant rise. These findings resemble those described in siderotic Bantu, and support the thesis that increased iron stores lead to irreversible oxidation of some of the available ascorbic acid.

Adolescent↗
PubMed1991

Further investigations into the relationship between the dopaminergic system, ascorbic acid and uric acid in the rat striatum.

Levels of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), ascorbic acid (AA), dehydroascorbic acid (DHAA), and uric acid were determined in the rat striatum following single apomorphine (1 mg/kg), scopolamine (0.6 mg/kg), pilocarpine (4 mg/kg), or pilocarpine + scopolamine (4 and 0.6 mg/kg, respectively) injections. The decrease in DOPAC levels and in the DOPAC/DA ratio, induced by the pharmacological manipulation, was linearly correlated with the increase in DHAA levels (r = -0.9060, P less than 0.05) and with the increase in the DHAA/AA ratio (r = -0.9004, P less than 0.05), respectively. It is concluded that dopaminergic activation or cholinergic inhibition both increase striatal AA oxidation, which is correlated with a decrease in DA turnover.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

Cortical ablation and drug-induced changes in striatal ascorbic acid oxidation and behavior in the rat.

Rats whose frontoparietal cortex had been bilaterally ablated were allowed 21 days for recovery and then treated with apomorphine (APO), 1 mg/kg SC or scopolamine (SCOP), 0.6 mg/kg SC. Soon after a behavioral test, dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), ascorbic acid (AA), and dehydroascorbic acid (DHAA) levels were determined by HPLC/EC in striatal synaptosomes (left side) and whole striatum (right side). SCOP behavioural effects were attenuated by cortical ablation, while those of APO were affected to a lesser extent. In the striatum of unoperated and sham-operated rats DHAA contents and DHAA/AA ratio resulted increased after drugs administration. No change in AA oxidation was observed in the striatum of ablated rats. In the synaptosomes of unoperated and sham-operated rats both drugs led to a decrease in DHAA contents and DHAA/AA ratio. In unoperated and sham-operated rats APO and SCOP caused a decrease of the DOPAC/DA ratio in the whole striatum and striatal synaptosomes. In ablated rats APO caused a decrease of DOPAC/DA ratio in the whole striatum and synaptosomes, while SCOP effects on DA turnover resulted attenuated in the whole striatum and abolished in synaptosomes. We conclude that drug-induced AA oxidation is likely to occur in the extracellular space and requires intact corticostriatal glutamatergic pathways. The latter may play an enabling role in SCOP behavioral effects.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2005

Interference of ascorbic acid with chemical analytes.

BACKGROUND: Ascorbic acid can interfere with methodologies involving redox reactions, while comprehensive studies on main chemistry analysers have not been reported. We therefore attempted to determine the interference of ascorbic acid with analytes on the Beckman Synchron LX20. METHODS: Various concentrations of ascorbic acid were added to serum, and the serum analytes were measured on the LX20. RESULTS: With a serum ascorbic acid concentration of 12.0 mmol/L, the values for sodium, potassium, calcium and creatinine increased by 43%, 58%, 103% and 26%, respectively (P<0.01). With a serum ascorbic acid concentration of 12.0 mmol/L, the values for chloride, total bilirubin and uric acid decreased by 33%, 62% and 83%, respectively (P<0.01), and were undetectable for total cholesterol, triglyceride, ammonia and lactate. There was no definite influence of ascorbic acid on analytical values for total CO(2), urea, glucose, phosphate, total protein, albumin, amylase, creatine kinase, creatine kinase-MB, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total iron, unbound iron-binding capacity or magnesium. CONCLUSIONS: Ascorbic acid causes a false increase in sodium, potassium, calcium and creatinine results and a false decrease in chloride, total bilirubin, uric acid, total cholesterol, triglyceride, ammonia and lactate results.

Ascorbic Acid↗
PubMed1982

Cholesterol-ascorbic acid interactions in guinea pig liver homogenates, and in the in situ perfused liver: relationship between ascorbic acid status and cholesterol and bile acid synthesis from mevalonate.

Cell free homogenates, and in situ perfused livers were used to study cholesterol synthesis and catabolism in control and latently scorbutic guinea pigs. In the homogenate studies, cholesterol synthesis from (2-14C) mevalonate was significantly depressed in latently scorbutic guinea pigs when compared to controls (0.02 less than p less than 0.05). Synthesis of cholesterol from (1-14C) acetate and n (1-14C) octanoate was minimal in guinea pigs. In the in situ liver perfusions, the synthesis of cholesterol from (2-14C) mevalonate was 40% lower in latently scorbutic guinea pigs than in control animals (p less than 0.005). The synthesis of cholesterol from (1-41C) acetate did not show the same clear cut effect. Bile acid production in the in situ perfused liver was unexpectedly higher in the latently scorbutic animals than in control animals (p = 0.005), although the incorporation of the label from (2-14C) mevalonate into the bile acids from the two groups was not significantly different. This finding led to the latently scorbutic group having a far lower specific activity in the bile acid fraction than the replete group.

Animals↗
PubMed1978

Ascorbic acid requirements in postoperative patients.

The postoperative ascorbic acid requirements of 63 surgical patients were assessed by measurements of buffy layer leukocyte ascorbic acid and the ascorbic acid content of leukocytes. There was a significant reduction in ascorbic acid levels following operation. The postoperative changes were unrelated to the extent of surgical trauma or the volume of blood transfused during operation, but there was a significant correlation between postoperative ascorbic acid measurements and white blood counts. It appears that postoperative leukocytosis and release by the bone marrow of leukocytes with a low ascorbic acid content may partly account for the postoperative changes in buffy layer and leukocyte ascorbic acid measurements. However, surgical operations were followed by an authentic increase in ascorbic acid requirements, and there was a 42 per cent reduction in circulating leukocyte ascorbic acid levels on the third postoperative day. The findings of this study create an argument for the use of ascorbic acid supplements in surgical patients, although it is unlikely that postoperative changes in leukocyte ascorbic acid have pathologic significance in wound repair.

Aged↗