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PubMedDate not supplied

Ascorbic acid biosensor using ascorbate oxidase immobilized on alkylamine glass beads.

A biosensor for ascorbic acid based on enzyme kinetics of ascorbate oxidase (E.C.1.10.3.3) was developed. The enzyme was extracted from Cucurbita maxima, or jerimun and immobilized by covalent bounding, using glutaradehyde as a bifunctional agent, on alkylamine glass beads, with and without enzyme active site protection. A low-cost, home-made oxygen electrode was applied as a transducer. The system has sensitivity from 62.5 up to 500 microM of ascorbic acid with satisfactory operation for more than 2 mo.

Alkylation↗
PubMed1977

Effects of chronic vanadium pentoxide administration on L-ascorbic acid metabolism in rats: influence of L-ascorbic acid supplementation.

1. Rats toxicated with vanadium pentoxide showed drastic retardation in growth rate and supplementation of L-ascorbic acid to these rats could not reverse this effect. The urinary excretion of L-ascorbic acid and D-glucuronic acid was decreased in the toxicated group of rats. 2. Considerable lowering of L-ascorbic acid content of the liver tissues of rats was observed under vanadium toxicated conditions. Supplementation of L-ascorbic acid to this group raised the tissue Vitamin C reserve considerably. 3. The normal histological patterns of the liver and kidney tissues of rats were severely disturbed under vanadium toxicated conditions. L-ascorbic acid supplementation to this group of rats showed marked signs of restoration in this respect. 4. Vanadium pentoxide treatment brought about a significant reduction in the biosynthetic capacity of L-ascorbic acid, along with an enhanced utilization of this vitamin. Subsequent supplementation of L-ascorbic acid to the toxicated group of rats was found to be effective in reversing these effects almost to the basal level.

Animals↗
PubMed1975

Influence of lead administration on L-ascorbic acid metabolism in rats: effect of L-ascorbic acid supplementation.

1. Lead toxicated rats became severely anaemic which could be recovered to a considerable extent by simultaneous supplementation of L-ascorbic acid to these rats. 2. The concentrations of L-ascorbic acid in the liver tissues and in the urine of the toxicated rats were increased significantly while that in the kidney tissues was markedly reduced and supplementation of L-ascorbic acid to the toxicated rats could not raise appreciably this reduced L-ascorbic acid level in the kidney tissues. 3. The kidney of rats maintained on lead supplemented basal diet were enlarged significantly; the normal histological pattern of the kidney tissues was severely disturbed under the experimental condition exhibited by cellular necrosis and membrane rupture. 4. In the liver tissues of lead toxicated rats, the rate of L-ascorbic acid synthesis was enhanced and this was brought to the basal level by supplementation of L-ascorbic acid. Synthesis of L-xylulose in the kidney tissues of rats was drastically reduced under lead toxicosis and administration of L-ascorbic acid to the toxicated animals could not protect this effect.

Animals↗
PubMed1989

Effect of dietary ascorbic acid, cholesterol and PCB on cholesterol and bile acid metabolism in a rat mutant unable to synthesize ascorbic acid.

The effect of acute or chronic ascorbic acid deficiency on the activity of hepatic cholesterol 7 alpha-hydroxylase and fecal excretion of bile acids was investigated in ODS-od/od (OD) rats (a rat mutant unable to synthesize ascorbic acid) fed a purified basal diet or purified diets containing either cholesterol (2%) or polychlorinated biphenyl (PCB) (200 mg/kg). In OD rats, the dietary requirement of ascorbic acid to maintain normal growth and normal levels of cholesterol in serum and liver is about 300 mg of ascorbic acid/kg diet. In OD rats fed the basal diet, acute or chronic ascorbic acid deficiency did not affect the activity of hepatic cholesterol 7 alpha-hydroxylase and fecal excretion of bile acids. However, in OD rats fed diets containing either cholesterol or PCB, acute ascorbic acid deficiency caused a higher level of serum cholesterol, a lower activity of hepatic cholesterol 7 alpha-hydroxylase and a lower excretion of fecal bile acids than in OD rats fed a basal diet containing an adequate level of ascrobic acid. It is concluded that acute ascorbic acid deficiency causes a hypercholesterolemia due to the depression of bile acid synthesis in OD rats fed a purified diet with cholesterol or PCB.

Animals↗
PubMed1985

Requirement for ascorbic acid in a rat mutant unable to synthesize ascorbic acid.

The activities of several enzymes involved in hepatic ascorbic acid synthesis and the requirement of dietary ascorbic acid were investigated in the OD (osteogenic disorder) rat, which has a hereditary defect in ascorbic acid-synthesizing ability. No activity of hepatic L-gulonolactone oxidase was detected in OD rats. However, OD rats maintained the normal activities of hepatic UDPglucose dehydrogenase, UDPglucuronyl transferase and beta-glucuronidase. Hemorrhage in muscle and leg joints, lower hepatic content of cytochrome P-450 and lower activities of hepatic drug-metabolizing enzymes, higher serum and adrenal levels of corticosterone and lower urinary excretion of hydroxyproline were observed in ascorbic acid-deficient OD rats than in OD rats fed 300 mg ascorbic acid/kilogram diet. Consequently, we conclude that OD rats cannot synthesize ascorbic acid because of the lack of activity of hepatic L-gulonolactone oxidase and that the dietary addition of about 300 mg ascorbic acid (per kilogram diet) is enough to prevent signs of vitamin C deficiency and to achieve maximum growth, and that more than 300 mg ascorbic acid per kilogram diet may be required for the maximum activity of hepatic drug-metabolizing enzymes.

Adrenal Glands↗
PubMed1991

Relationship in humans between ascorbic acid consumption and levels of total and reduced ascorbic acid in lens, aqueous humor, and plasma.

The relationships between plasma, aqueous humor and lens ascorbic acid levels are examined in 131 samples from 127 patients. Mean ascorbate intake for nonsupplemented individuals was 148 mg/day or over two times the recommended daily allowance. A subset of 44 patients participated in a trial to assess the impact of vitamin C supplementation of 2 grams per day on aqueous and lens ascorbic acid levels. Such supplementation significantly increased both total and reduced ascorbic acid levels in plasma and aqueous and total ascorbic acid in the lens. Correlation coefficients relating total and reduced ascorbic acid levels in the three tissues ranged from 0.42 to 0.19 (p less than 0.05 for all correlation coefficients). Over 60% of the ascorbate was present in the reduced form in plasma and aqueous, and about 50% of the lens ascorbate was in the reduced form.

Adult↗
PubMed1984

[Recent knowledge concerning the biochemistry and significance of ascorbic acid].

The ascorbic acid plays an important part by activation of hydroxylation reactions in various biosyntheses, such as in that of tropocollagen, bile acids and carnitine. It also considerably participates in the detoxication of compounds by hydroxylation and in the maintenance of the cytochrome P 450 contents in the liver. A sufficient supply is of importance for the absorption and accumulation of iron as well as for the efficiency of the immune system. After application of 14C-labelled ascorbic acid the compound is retained mainly in the brain, the salivary glands, the adrenal glands, the testes and in the eye lens. The largest contents of ascorbic acid lies in the pituitary gland, in the adrenal glands and in the eye lens. The need of ascorbic acid varies in man in dependence upon the state of development and the loads between 30 and 60 mg/die. In great smokers, after operations and traumas as well as when infections are present the intake of 100 to 200 mg a day are recommended. When more 1 g a day are taken the utilization decreases, the decomposition and the excretion, respectively, increase. A dose of more than 2 g a day inhibits the phagocytosis activity of leucocytes.

Age Factors↗
PubMed1990

Effect of ascorbic acid supplementation on haematological response and ascorbic acid status of young female adults.

Haematological response and ascorbic acid (AA) status were evaluated in 32 young adult females (age 20-34 years) 8 weeks after supplementation with two levels of AA (50 and 100 mg). Both levels of AA intake produced a similar response marked by significant elevation (p less than 0.01) in Hb concentration, Hct level, RBC count, serum and leucocyte ascorbate concentrations. Ten weeks after withdrawal of the supplements, values for all parameters evaluated decreased significantly (p less than 0.01) to presupplementation levels. Haemoglobin concentration and leucocyte ascorbate remained relatively higher (p less than 0.01) than initial values in subjects who received 100 mg AA. This study showed that AA supplementation improved erythropoietic activity and AA status of our female population. However, the higher dose of AA (100 mg) sustained Hb concentration and tissue ascorbate longer after withdrawal of supplementation.

Adult↗
PubMed1975

Automated constant-current coulometric assay system for ascorbic acid and sodium ascorbate.

The performance of an automated constant-current coulometric system for the assay of ascorbic acid and sodium ascorbate is described. After loading, it is capable of analyzing 25 samples and printing out the titer values with no operator attention for 2.5 hr. Under optimum conditions, ascertained by evaluating various electrochemical parameters, the accuracy and precision (95% ts) were found to be +/- 0.3%.

Ascorbic Acid↗
PubMed1987

Effect of dietary ascorbic acid, cholesterol and PCB on cholesterol concentrations in serum and liver in a rat mutant unable to synthesize ascorbic acid.

The effect of ascorbic acid deficiency and excessive ascorbic acid intake on serum and liver levels of cholesterol and lipids was investigated in ODS-od/od (OD) rats fed a normal diet, a cholesterol-containing diet or a polychlorinated biphenyl (PCB)-containing diet. The OD rat is a rat mutant unable to synthesize ascorbic acid. In OD rats, the dietary requirement of ascorbic acid to maintain normal growth and normal levels of cholesterol in serum and liver is about 300 mg of ascorbic acid/kg diet. In control (ODS-+/+) rats that can synthesize ascorbic acid, dietary addition of 0.5% cholesterol and 0.25% cholic acid caused elevation of cholesterol concentrations in serum and liver, elevation of total lipids in liver and reduction of the ratio of high density lipoprotein (HDL) cholesterol to total cholesterol in serum. Dietary addition of PCB (200 mg/kg diet) caused elevation of serum concentration of cholesterol and of the ratio of HDL-cholesterol to total cholesterol in serum. In OD rats fed a normal diet, ascorbic acid deficiency slightly elevated serum concentration of cholesterol, elevated liver concentration of cholesterol and reduced the ratio of HDL-cholesterol to total cholesterol in serum; and ascorbic acid excess did not affect serum and liver concentrations of cholesterol and the ratio of HDL-cholesterol to total cholesterol in serum. In OD rats fed a cholesterol-containing diet, ascorbic acid deficiency elevated serum and liver concentrations of cholesterol, and did not affect the ratio of HDL-cholesterol to total cholesterol in serum; and ascorbic acid excess did not affect serum and liver concentrations of cholesterol and the ratio of HDL-cholesterol to total cholesterol in serum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Ascorbic acid absorption in Crohn's disease. Studies using L-[carboxyl-14C]ascorbic acid.

Total body pool and intestinal absorption of ascorbic acid were studied in 12 patients undergoing operation for Crohn's disease (six with fistulae and six without) and in six control patients undergoing operation for reasons other than Crohn's disease. L-[carboxyl-14C]Ascorbic acid, 0.19-0.40 megabecquerels (MBq), was given orally. After a period of equilibration, the labeled ascorbic acid was flushed out of the patient's body tissues using large doses of unlabeled ascorbic acid. Intestinal absorption of ascorbic acid, assessed from the total cumulative urinary 14C recovery, was found to be similar in patients with fistulizing Crohn's disease (73.9 +/- 8.45%), those without fistulas (72.8 +/- 11.53%), and in controls (80.3 +/- 8.11%). Total body pools of ascorbic acid, calculated using the plasma 14C decay curves, were similar in patients with Crohn's disease with fistulas (17.1 +/- 5.91 mg/kg), patients without fistulas (9.6 +/- 3.58 mg/kg), and in controls (13.3 +/- 4.28 mg/kg). The results indicate that ascorbic acid absorption is normal in patients with both fistulizing and nonfistulizing Crohn's disease. The results suggest that routine supplements of vitamin C are not necessary unless oral ascorbic acid intake is low.

Adult↗