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PubMed1985

The effect of synovial fluid proteins in the degradation of hyaluronic acid induced by ascorbic acid.

The degradation of hyaluronic acid induced by ascorbic acid and the effect of synovial fluid proteins, such as ceruloplasmin, transferrin, and albumin, were investigated on the basis of the elution volume and the molecular weight of hyaluronic acid using high-performance gel permeation chromatography. Hyaluronic acid was degraded to less than one-third of the original molecular weight in the range of the physiological concentrations of ascorbic acid. Synovial fluid proteins protected against the ascorbate-dependent degradation of hyaluronic acid at their physiological concentrations. It is suggested that the inhibitory activity of ceruloplasmin mainly depends on the ferroxidase activity and that of transferrin is probably due to iron binding property.

Albumins↗
PubMed1975

Effect of oral administration of large quantities of ascorbic acid on blood levels and urinary excretion of ascorbic acid in healthy men.

The influence of the daily ingestion of 1, 2, 3, and 5 grams of ascorbic acid on whole blood and plasma ascorbic acid levels and on the urinary excretion of ascorbic acid has been investigated. The ingestion of one gram of ascorbic acid per day for one week significantly increases plasma and whole blood levels over presupplementation levels, but larger amounts of ascorbic acid do not further increase plasma and whole blood ascorbic acid levels. Urinary excretion increases with intake, up to intakes of 3 grams per day but does not increase further when 5 grams of ascorbic acid is ingested per day. Upon discontinuing ascorbic acid supplementation the plasma and whole blood levels decline rapidly and the urinary excretion of ascorbic acid falls to presupplementation values within a few days. The results suggest that there is need for a detailed study of the routes of excretion of ascorbic acid at high levels of intake and that the safety of ingesting large quantities of ascorbic acid may be questioned.

Adult↗
PubMed1988

Urinary ascorbic acid levels following the withdrawal of large doses of ascorbic acid in guinea pigs.

Male guinea pigs received sodium ascorbate solution [equivalent to 1 g ascorbic acid/(kg body weight.d)] by intraperitoneal injection for 4 wk. During the ascorbic acid treatment period, plasma and urinary ascorbic acid levels rose markedly. Three weeks after the ascorbic acid treatment was withdrawn, mean urinary ascorbic acid levels were significantly lower than their corresponding basal levels. At both 2 and 5 wk after withdrawal of ascorbic acid treatment, mean plasma ascorbic acid levels were below normal. The results indicate that these animals had experienced a transient withdrawal effect after administration of large doses of ascorbic acid that lasted about 1 wk. This, in turn, indicates that the rate of ascorbic acid turnover was probably increased during treatment, and this effect persisted even after the ascorbic acid was withdrawn. Examination of data from each individual experimental animal revealed that the pattern of urinary ascorbic acid excretion after the withdrawal of large doses of ascorbic acid varied from animal to animal. Among the twelve experimental guinea pigs, seven had abnormally low urinary ascorbic acid levels 2-4 wk after the withdrawal of the large doses of ascorbic acid.

Animals↗
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↗
PubMed1988

Enhanced prostaglandin synthesis as a mechanism for inhibition of melanoma cell growth by ascorbic acid.

Both ascorbic acid and the 1-series prostaglandins have been reported to be important regulators of cell growth and since ascorbic acid also increases the synthesis of the 1-series prostaglandins, it is possible that the effects of ascorbic acid on cell growth might be mediated by changes in 1-series prostaglandin synthesis induced by ascorbic acid. This study attempted to examine this possible relationship. The effects of ascorbic acid, prostaglandin E1 and the essential fatty acid precursors of the prostaglandins, linoleic acid and gamma-linolenic acid on the in vitro growth of transformed BL6 murine melanoma cells and untransformed monkey kidney (LLCMK) cells was determined. The effects of ascorbic acid addition on the growth inhibitory effect of the essential fatty acids and on the activity of delta-6-desaturase, a key enzyme in 1-series prostaglandin synthesis were also examined. Addition of ascorbic acid, prostaglandin E1 and both essential fatty acids was found to reduce BL6 growth while PGE1 and to a lesser extent the essential fatty acids reduced LLCMK cell growth. The growth inhibitory effect of the essential fatty acids was enhanced by ascorbic acid which was also found to stimulate delta-6-desaturase activity in BL6 cells. The growth inhibitory effect of ascorbic acid on BL6 cells may thus be mediated by changes in prostaglandin synthesis through an association with the metabolism of the essential fatty acid precursors of the prostaglandins.

Animals↗
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↗
PubMed1986

[Effect of the carcinogenic tyrosine metabolite p-hydroxyphenyllactic acid on the ascorbic acid concentration in the organs and blood of mice].

The effect of cancerogenic tyrosine metabolite, p-hydroxyphenyllactic acid, on the concentration of ascorbic acid in the organs and blood of mice has been studied. p-Hydroxyphenyllactic acid was demonstrated to decrease considerably ascorbic acid concentration in the liver, adrenal glands and blood of mice. The above phenomenon and the previous data on tyrosine aminotransferase induction by p-hydroxyphenyllactic acid suggest the existence of two interdependent mechanisms of cancerogenic tyrosine metabolite (p-hydroxyphenyllactic acid) accumulation.

Animals↗
PubMedDate not supplied

Interaction of vitamin E and ascorbic acid (review).

Ascorbic acid appears to have two opposite roles in animal tissues: to act as an antioxidant or to act as a prooxidant. The effects of ascorbic acid supplementation on the tissue antioxidant status seem to be dependent on the dose of ascorbic acid and the vitamin E status. Adequate doses of ascorbic acid supplementation to vitamin E-deficient subjects or animals help to partially maintain vitamin E levels, probably through sparing the degradative metabolism of vitamin E, and thus increase the antioxidant effectiveness. The sparing effect of ascorbic acid on vitamin E metabolism is also shown in the partial reversal of the manifestation of vitamin E deficiency. On the other hand, when the animals are marginally adequate in vitamin E status, ascorbic acid supplementation in large doses appears to promote lipid peroxidation and significantly decreases the antioxidant potential of animals. An increase of the level of vitamin E supplementation overcomes the prooxidant effect of large doses of ascorbic acid. This observation suggests that vitamin E requirement may be increased with a large dose of ascorbic acid supplementation.

Animals↗
PubMed1986

Effect of erythorbic acid administration on ascorbic acid content in guinea pig tissues.

The effect of erythorbic acid (ErA) on ascorbic acid (AsA) content in the tissues of normal and AsA-deficient guinea pigs was studied. The animals were sacrificed at varying intervals during the experimental period, and the liver, adrenal glands, spleen and kidneys were removed. The amounts of AsA and ErA in the tissues were measured by HPLC. The content of AsA in the tissues of the animals administered both AsA and ErA was lower than that of the animals administered only AsA. But the disappearance rate of AsA from the tissues of the AsA-deficient animals was similar to that of the animals administered only ErA. The amount of AsA in the tissues of the animals administered both AsA and ErA during the repletion period was lower than that of the animals administered only AsA. These results suggest that ErA administration may affect the amount of AsA in the tissues by inhibiting its tissue uptake or its storage in the tissues, and not by accerelating the catabolism of AsA in the tissues.

Adrenal Glands↗
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↗