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At least 19 recordsLinked to original sources
PubMed1978

Use of -l-ascorbic acid, ethocel coated ascorbic acid and ascorbate 2-sulfate in diets for channel catfish, Ictalurus punctatus.

Purified diets with five levels (25, 50, 75, 100, and 200 mg/kg) of supplemental L-ascorbic acid (LAA), and equimolar levels of ethylcellulose coated L-ascorbic acid (EAA) and dipotassium L-ascorbate 2-sulfate dihydrate (AS) were pelleted and fed to 7.9 +/- 0.2 g channel catfish fingerlings for 20 weeks. A dietary level of 23 mg/kg of all three forms of vitamin C prevented spinal abnormalities. Approximately 50 mg/kg diet of either LAA or EAA was sufficient for maximal growth and feed efficiency. Growth response to AS was similar to a Michaelis-Menten type curve and 200 mg/kg diet of AS was necessary to achieve maximal growth. Blood and liver ascorbic acid levels were positively correlated with supplemental levels of LAA, EAA, and AS up to 200 mg/kg; however, blood and liver ascorbic acid levels of fish fed AS were considerably less than those fed LAA and EAA. Weight gains were positively correlated with blood ascorbate levels up to 7 microgram/ml. No measurable level of AS was detected in blood or liver. These results suggest that the rate of enzymatic hydrolysis of AS to LAA or rapid excretion of AS may have been the limiting factor.

Animal Feed↗
PubMed1977

Interaction of erythorbic acid with ascorbic acid catabolism.

There exist altogether four stereoisomers of ascorbic acid. Erythorbic acid (D-isoascorbic acid) differs in the spatial configuration at carbon 5 and has less than 5 per cent of biological vitamin C activity. In guinea pigs, depending on an exogenous supply of ascorbic acid, a possible interaction of erythorbic acid with absorption, transport through the cell membranes at the tissue level, or with catabolism of ascorbic acid has been investigated. After oral administration, results suggest no difference in absorption of these two compounds from the intestine, whereas uptake by the tissues was approximately four to one in favour of ascorbic acid. Feeding experiments with erythorbic acid indicate the availability of ascorbic acid being diminished by 40-60% when administered together with erythorbic acid. Kinetic data on the catabolism of ascorbic acid showed a significant reduction in half-life (50% of the dose excreted) of the vitamin caused by administration of erythorbic acid. The results suggest the oxidative destruction of ascorbic acid in the liver being significantly accelerated. Thus, ingestion of erythorbic acid interacts with newly introduced ascorbic acid by enforcing the breakdown of ascorbic acid. Implications of these findings for the metabolism, availability and nutritional status of ascorbic acid in humans will be discussed.

Animals↗
PubMed1979

[The excretion of hippuric acid and ascorbic acid in the urine of liver-damaged rats (author's transl].

The authors investigated the effects of the administration of thioacetamide, carbon tetrachloride and aminophenazone on the excretion of ascorbic acid and hippuric acid in adult male and female Wistar rats. After a single application of thioacetamide and aminophenazone, the ascorbic acid content in the urine showed a dose-dependent increase, whereas that in the liver had decreased. This increase in the urinary ascorbic acid might be due to a release of stored ascorbic acid from the liver cells. When thioacetamide was given for a prolonged period, the ascorbic acid content in the urine increased at the beginning; later one, at the end of three weeks, it was slightly inferior to the control value. Both single and repeated applications of thioacetamide led to a decrease in the excretion of hippuric acid in the urine, which is attributed to an impairment of the mitochondrial hippuric acid synthesis. Long-term treatment with aminophenazone resulted in an increase of ascorbic acid in the urine, which is indicative of an induction effect, whereas the ascorbic acid content in the liver remained unchanged. There was no effect on the excretion of hippuric acid. In regard to their use in the toxicological evaluation of drugs, these two metabolic effects offer no decisive advantage over current liver function tests.

Aminopyrine↗
PubMed1975

Metabolism of ascorbic acid and ascorbic-2-sulfate in man and the subhuman primate.

Man does not catabolize ascorbate to CO2, whereas the monkey does catabolize ascorbate and ascorbate sulfate to CO2 when these compounds are given orally. However, it takes the same length of time to produce frank scurvy in both man and the monkey, thus indicating that the comparative storage, rate of use, and mode of metabolism of ascorbate is similar in both species. Preliminary feeding and isotope studies conducted on monkeys are in agreement with the fact that only a small amount of labeled ascorbate or ascorbate sulfate equilibrated with body stores. These results are in agreement with published ascorbic acid requirements of 10 mg/kg body weight. In our experiments, 250 mg/day had to be fed to a 10-kg monkey to completely clear all signs of scurvy and return blood ascorbate levels to normal. Ascorbic acid administered intravenously to monkeys appears to equilibrate completely with the ascorbate pool(s). Ascorbate sulfate was found to be a urinary metabolite of both ascorbic-1-14C acid and ascorbic-6-14C acid fed orally to monkeys.

Animals↗
PubMed1975

Automated single-column analysis of amino acids using ascorbic acid as reductant for air-stable ninhydrin.

The procedure for operation of a constant-temperature, single-column automated amino acid analyser in the sub-nanomole range is described. The cycle time for a complete analysis is 90 min including equilibration for next cycle. Eluting buffers can be made in the laboratory or commercially available concentrates (Pico-Buffers) can be used. A novel reducing agent, ascorbic acid, incorporated into the column buffers was used to reduce air-stable ninhydrin.

Amino Acids↗
PubMed1976

L-ascorbic acid, L-ascorbate 2-sulfate, and atherogenesis.

Rabbits on a high cholesterol diet were divided into three groups: one group received subcutaneous injections of physiological saline 3 times/day, 5 days/wk for 10 wk; another group received subcutaneous injections of L-ascorbic acid (0.37 mmole) according to the same timetable; and the third group was administered an equivalent amount of L-ascorbate 2-sulfate as outlined above. Each week the serum levels of total and free cholesterol and triglycerides were measured. At the end of 10 wk the animals were killed and the cholesterol content of the livers, spleens, and adrenal glands was measured. The aortas were examined for plaque deposition; the deposits were excised and pooled according to groups; and the total mass and cholesterol contents of the pooled plaques were determined. Administration of ascorbic acid or ascorbate 2-sulfate did not prevent hypercholesterolemia or elevated levels of serum triglycerides. No significant differences among the groups were found either in tissue cholesterol levels or in the extent or type of lesions found. Although plaque deposition appeared to be similar in the aortas of these animals, a marked difference was found in total mass and cholesterol content of the plaques: The plaques of the saline-treated group had a total mass and cholesterol content approximately 2.5 times that found in the group injected with ascorbic acid and about 1.5 times that found in the animals treated with ascorbate 2-sulfate. These results indicate that ascorbic acid, in particular, minimizes the total quantity of plaque deposition even though it is ineffective in preventing hypercholesterolemia, elevated serum triglycerides, and accumulation of cholesterol by several tissues.

Adrenal Glands↗
PubMed1979

Effects of ascorbic acid and sodium ascorbate on cyclic nucleotide metabolism in human lymphocytes.

L-ascorbic acid (LAA) augmented cGMP many-fold in highly purified human peripheral blood lymphocytes. The cGMP response occurred within 10 sec and persisted for at least 60 min. D-ascorbic acid (DAA) and dehydroascorbic acid (DHAA) were also equally active in enhancing cGMP concentrations but metabolic precursors of ascorbic acid and other inorganic acids did not increase cGMP levels. Determination of the amount of DHAA contaminating the LAA precluded the possibility that it was solely responsible for the enhanced cGMP levels. The sodium or calcium salts of ascorbic acid did not increase cGMP concentrations. If these neutralized preparations were acidified, increased cGMP concentrations were then noted. In broken cell preparations, LAA, DAA, and DHAA and to a lesser extent sodium ascorbate (NaA) enhanced guanylate cyclase activity while neither inhibited cAMP or cGMP phosphodiesterase (PDE) activity. The possible role of H2O2, fatty acid liberation, prostaglandin production, oxidizing-reducing agents, and free radical formation in mediating the effects of ascorbic acid on cGMP levels were evaluated, but none of these potential mechanisms were definitively proven to be a required intermediary for the cGMP enhancing activity of ascorbic acid. LAA, DHAA or NaA did not induce lymphocyte transformation or modulate lectin-induced mitogenesis.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1977

The effect of ascorbic acid on uric acid excretion with a commentary on the renal handling of ascorbic acid.

Under spontaneous conditions in man and dog, very little ascorbic acid is excreted in urine. Ascorbic acid clearance (C ascorbic acid) is promptly augmented when plasma ascorbic acid is increased by intravenous injection. No net tubular secretion of ascorbic acid is demonstrable in either man or dog when plasma ascorbic acid is elevated to levels as high as 12 mg/100 ml in man, and 28 mg/100 ml in the dog. Nevertheless, both in men and the Dalmatian dog, when the glomerular filtration rate (GFR) is decreased, excreted ascorbic acid in relation to the amount filtered is exaggerated so that C ascorbic acid:GFR approaches unity. It is possible that secreted ascorbic acid is masked under ordinary circumstances, with a more significant contribution of secreted ascorbic acid to total urinary ascorbic acid becoming apparent under conditions of low GFR. In man, when the plasma ascorbic acid level is raised to above 6 mg/100 ml, C urate:GFR rises from control value of 0.081 +/- 0.020, to 0.116 +/- 0.026. In both mongrel and Dalmatian dogs an effect of ascorbic acid on urate excretion is not conclusively shown. The uricosuric effect of ascorbic acid in man may be due to competition with uric acid for renal tubular reabsorptive transport. The difference in the metabolism of ascorbic acid in the dog as compared to man may help account for the inconsistent effect of ascorbic acid on uric acid excretion in the dog.

Aged↗
PubMed1975

The absorption of iron, with or without supplements of single amino acids and of ascorbic acid, in healthy and Fe-deficient children.

1. Studies were done on the effect of ascorbic acid and five amino acids (histidine, cystine, cysteine, valine and glutamic acid) on intestinal iron absorption in a group of ninety Egyptian infants and young children, of which fifty-seven were healthy controls and thirty-three were suffering from Fe-deficiency anaemia. 2. Supplements tested promoted Fe absorption in healthy controls in the following order: valine larger than histidine larger than ascorbic acid. Cysteine, glutamic acid and cystine were found to have no significant effect. 3. Supplementation with valine, ascorbic acid and histidine also increased intestinal Fe absorption in anaemic subjects, but to a lesser extent than in controls. 4. Supplementation of haematinic therapy with these compounds is recommended. Their use is also suggested to improve the availability of the Fe content of everday diets.

Amino Acids↗
PubMed1978

Intestinal ascorbic acid transport following diets of high or low ascorbic acid content.

Active transport of ascorbic acid in ileum is mediated by a carrier mechanism at the brush border membrane. This mechanism may show compensatory changes in activity in response to alterations of dietary ascorbic acid content. The unidirectional influx of ascorbic acid across the brush border into epithelial cells of guinea pig ileum was determined in vitro. Influx was significantly reduced in scorbutic animals and following 14 or 28 days of high doses (5 or 25 times normal) of ascorbic acid. The transport rate was reduced by intramuscular administration of ascorbic acid, suggesting that the transport mechanism may respond to circulating levels of the vitamin.

Animals↗
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↗