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Results for “ASCORBIC ACID”

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At least 127 records · Page 7Linked to original sources
PubMed1987

Determination of ascorbic acid in human urine by high-performance liquid chromatography coupled with fluorimetry after post-column derivatization with benzamidine.

High-performance liquid chromatography on two Asahipak GS-320 hydrophilic gel columns (50 X 0.76 cm I.D.), connected in series, with 0.015 M tartrate buffer (pH 3.0), containing 2 mM ethylenediaminetetraacetate and 0.05% beta-thiodiglycol as eluent allowed the separation of glucose, diketogulonic acid + diketogluconic acid, dehydroisoascorbic acid, dehydroascorbic acid, ascorbic acid, and isoascorbic acid within 55 min. Ascorbic acid in a urine sample was stabilized by the addition of an equal volume of 5% metaphosphoric acid solution, containing 0.5% of beta-thiodiglycol. Filtration of the mixture through a column of Dowex 50W-X8 (H+) facilitated the determination of ascorbic acid and isoascorbic acid in human urine. Samples could be analyzed every 20 min.

Ascorbic Acid↗
PubMed1991

Role of exogenous ascorbic acid in tissue status of ascorbic acid-2-sulphate in guinea pigs.

Guinea pigs were given ascorbic acid orally in two doses; a low and a high dose. The tissue levels of ascorbic acid-2-sulphate was estimated in these animals after 15 days of feeding and a subsequent deprivation period of 15 days. The specific activity of the enzymes ascorbic acid sulphotransferase and ascorbic acid-2-sulphate sulphohydrolase was studied. During higher ascorbic acid intake, the activity of ascorbic acid sulphotransferase was increased, whereas ascorbic acid-2-sulphate sulphohydrolase showed a decreased activity. But when ascorbic acid intake was lowered or ceased, the activity of the above enzymes showed a reverse pattern. Possible reasons for the lack of antiscorbutic activity of ascorbic acid-2-sulphate in guinea pigs is discussed.

Animals↗
PubMed2002

Bioavailability of a series of novel acylated ascorbic acid derivatives, 6-O-acyl-2-O-alpha-D-glucopyranosyl-L-ascorbic acids, as an ascorbic acid supplement in rats and guinea pigs.

The bioavailability of a series of novel acylated ascorbic acid derivatives, 6-O-acyl-2-O-alpha-D-glucopyranosyl-L-ascorbic acids (6-Acyl-AA-2G), as an ascorbic acid (AA) supplement was investigated in rats and guinea pigs. Oral administration of 6-Acyl-AA-2G to rats resulted in an increase in the plasma AA level. However, the intact form was not detectable in the plasma by high-performance liquid chromatography, indicating its hydrolysis through the process of absorption. After an intravenous injection to rats of 6-Octa-AA-2G as a representative derivative, the intact form rapidly disappeared from the plasma, being followed by a prolonged and marked elevation of the plasma AA level. Various tissue homogenates from guinea pigs were examined for their releasing activity of AA, 2-O-alpha-D-glucopyranosyl-L-ascorbic acid (AA-2G) and 6-O-acyl-AA from 6-Acyl-AA-2G. High activity was observed in the small intestine. These hydrolytic activities to AA and 6-O-acyl-AA were completely inhibited by castanospermine, an alpha-glucosidase inhibitor, and AA-2G was observed as the only resulting hydrolysate, suggesting the participation of alpha-glucosidase and esterase in the in vivo hydrolysis of 6-Acyl-AA-2G. 6-Octa-AA-2G was found to exhibit an obvious therapeutic effect in scorbutic guinea pigs from its repeated oral administration. These results indicate that 6-Acyl-AA-2G is a readily available source of AA activity in vivo, and may be useful as an effective pharmacological agent and as a promising food additive.

Animals↗
PubMed1997

Liquid chromatographic measurement of L-ascorbic acid and D-ascorbic acid in biological samples.

D- and L-Ascorbic acids have been separated using liquid chromatography (LC) on a polymer-coated silica-based NH2 column and the L-isomer has been quantified in human serum, rat serum, rat lung, rat lung perfusate, infant formula (SRM 1846) and mixed food sample (SRM 2383). The D-isomer was observed only in trace amounts in the mixed food sample. The results demonstrate that ascorbic acid was stable on the column and completely recovered from supplemented samples of human serum and that this method of analysis is accurate, precise and has broad application exhibiting no dependence on the nature of the matrices evaluated herein.

Animals↗
PubMed1966

Ascorbic acid and aging in the rat. Uptake of ascorbic acid by teeth and concentration of various forms of ascorbic acid in different organs.

1. The uptake of ascorbic acid in vitro by the teeth of rats showed a gradual decrease with age, indicating that the uptake may be related to collagen synthesis as in bone. 2. The concentration of total free ascorbic acid in various organs declined with age, but the rate of decline was different in different organs. In the spleen, however, it increased until maturity and then declined. 3. This decrease may be due to one or both of the following reasons: (a) the permeability of different tissues may decrease at different rates for ascorbic acid, or (b) the requirement for ascorbic acid may decrease at different rates. 4. The bound ascorbic acid declined with age in the skin, kidney, liver and brain after the age of 10-12 weeks, and in the spleen after the age of 26 weeks. 5. The concentration of dehydroascorbic acid and dioxogulonic acid declined with age in the skin.

Aging↗
PubMed1981

Influence of chronic ascorbic acid deficiency and excessive ascorbic acid intake on bile acid metabolism and bile composition in the guinea pig.

The influence of chronic ascorbic acid (AA) deficiency and excessive ascorbate consumption on bile acid metabolism, liver and plasma cholesterol levels, hepatic microsomal cytochromes and biliary lipid composition was investigated. Male weanling guinea pigs were fed a cereal-based scorbutigenic diet supplemented with four levels of AA for 7 weeks: deficient, 15 and 30 mg/kg; control, 500 mg/kg; and excess, 20,000 mg/kg. Bile acid kinetic parameters were determined following the intraperitoneal administration of [24-14C] chenodeoxycholic acid. Dietary extremes of AA caused similar alterations in the parameters studied. Relative to the control group, the deficient and excess groups exhibited reduced cytochrome P-450 concentration, lower cholesterol 7 alpha-hydroxylase activity, lower bile acid turnover rate, prolonged bile acid half-life and increased plasma and liver cholesterol concentrations. Deficient and excess groups also exhibited lower biliary cholesterol saturation (i.e., increased bile acid-neutral sterol ratios) than controls. Urinary bile acid excretion was 2- to 3-fold higher in excess guinea pigs than in the other three groups. The data demonstrate the exceptional susceptibility of cholesterol 7 alpha-hydroxylase activity to alteration by dietary extremes of AA, resulting in marked inhibition of bile acid synthesis and elevation of cholesterol levels by both inadequate and excessive AA intake.

Animals↗
PubMed1985

Effects of ascorbic acid on blood pressure and ascorbic acid metabolism in spontaneously hypertensive rats (SH rats).

Spontaneously hypertensive rats (SH rats) were administered drinking water containing 0, 200 or 1000 ppm ascorbic acid with or without 0.5% NaCl and the usual laboratory stock diet for 130 days. The rats given ascorbic acid with or without 0.5% NaCl had a lower mean systolic blood pressure level than that of the respective control group. The difference in the mean blood pressure level from that of the control group was 18-19 mmHg for 200 ppm ascorbic acid group and 30-40 mmHg for 1000 ppm ascorbic acid group. The SH rats were shown to have some defects of ascorbic acid metabolism by lower tissue ascorbic acid levels in the liver, lung and adrenals, and by lower response of ascorbic acid synthesis to a xenobiotic than the Wistar Kyoto rats, which served as the normotensive control rats for SH rats. The abnormalities of ascorbic acid metabolism in the SH rats may be associated with, in part, their high blood pressure, because exogenous ascorbic acid prevented the blood pressure elevation of SH rats, but some other mechanism may also be involved in the effect of ascorbic acid on blood pressure.

Animals↗
PubMed1985

Transport of L-ascorbic acid and dehydro-L-ascorbic acid across renal cortical basolateral membrane vesicles.

The uptake of L-ascorbic acid and dehydro-L-ascorbic acid into renal cortical basolateral membrane vesicles has been characterized. The uptake systems for both solutes demonstrate saturation kinetics. The presence of structural analogs of L-ascorbic acid and dehydro-L-ascorbic acid results in cis-inhibition and trans-stimulation. Uptake of each substrate is Na+-independent, proceeding to an endpoint of substrate equilibrium across the vesicular membrane. The transport mechanism(s) for L-ascorbic acid and dehydro-L-ascorbic acid appears to be facilitated diffusion.

Animals↗