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Results for “Ascorbic Acid”

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PubMed1990

Electrokinetic energy conversion by aqueous oxalic acid, citric acid, ascorbic acid, hippuric acid, and acetyl salicylic acid across urinary bladder membranes.

Efficiency of energy conversion for electro-osmosis and streaming potential and the degree of coupling of acids across urinary bladder membranes of goat have been computed using non-equilibrium thermodynamic theory. The energy conversion maxima and degree of coupling for acids responsible for the formation of urinary calculi are found to be much low as compared to urea and urine.

Animals↗
PubMed1990

A relationship between vitamin B12, folic acid, ascorbic acid, and mercury uptake and methylation.

Ingestion of megadoses of certain vitamins appears to influence the in vivo methylation of mercuric chloride in guinea pigs. The addition of megadoses of vitamin B12 fed either singularly or in combination with folic acid resulted in increased methylmercury concentrations in the liver. Moreover, percent methylmercury levels were significantly increased with B12 treatment in the liver (B12 only and B12/folic acid) and brain (B12/vitamin C). Incorporation of high levels of folic acid into the dietary regime also increased the methylmercury concentration particularly in the liver and hair tissues. The addition of vitamin C in the diet, particularly in combination with B12 (brain) or folic acid (muscle) resulted in increased methylmercury levels in these tissues and percent methylmercury values with B12 in the muscle and brain tissue.

Animal Nutritional Physiological Phenomena↗
PubMed2000

Ascorbic acid and ascorbic acid 6-palmitate induced oxidation in egg yolk dispersions.

The oxidation in aqueous dispersions of egg yolk powder and the influence of addition of the proposed antioxidants ascorbic acid and ascorbic acid 6-palmitate indicate that both ascorbic acid and ascorbic acid 6-palmitate propagated the oxidation of egg yolk powder dispersions. Ascorbic acid 6-palmitate was found to be more prooxidative than ascorbic acid. Moreover, it was found that addition of ascorbic acid or ascorbic acid 6-palmitate gave rise to an increase in the amount of free iron Fe(II) in the egg yolk dispersions. It is proposed that ascorbic acid and ascorbic acid 6-palmitate react with the phosvitin-Fe(III) complex found in egg yolk and release Fe(II), which subsequently propagates lipid oxidation. It appears that less oxidation occurs in egg yolk dispersions exposed to high concentrations of peroxy radicals with added ascorbic acid than egg yolk dispersions with added ascorbic acid without exposure to peroxy radicals.

Ascorbic Acid↗
PubMed2000

Intracellular accumulation of ascorbic acid is inhibited by flavonoids via blocking of dehydroascorbic acid and ascorbic acid uptakes in HL-60, U937 and Jurkat cells.

In HL-60, U937 and Jurkat cells, the intracellular accumulation of ascorbic acid occurred via uptakes of both dehydroascorbic acid (an oxidized metabolite of ascorbic acid) and ascorbic acid (vitamin C). Dehydroascorbic acid and ascorbic acid were transported into cells by sodium-independent glucose transporters (GLUT 1 and GLUT 3) and sodium-dependent ascorbic acid transporters, respectively. Flavonoids inhibited the intracellular accumulation of ascorbic acid by blocking dehydroascorbic acid and ascorbic acid uptakes in the transformed cells. At flavonoid concentrations of 10-70 micromol/L, approximately 50% of dehydroascorbic acid uptake was inhibited in the cells. In Jurkat cells, two potent flavonoids (myricetin and quercetin) competitively inhibited dehydroascorbic acid uptake, and K(i) values were approximately 14 and 15 micromol/L, respectively. Because GLUT 1 and GLUT 3 transport dehydroascorbic acid, the inhibition of dehydroascorbic acid uptake by flavonoids was investigated by using Chinese hamster ovary cells overexpressing rat GLUT 1 or human GLUT 3. Myricetin at concentrations of 22 and 18 micromol/L, respectively, inhibited half of dehydroascorbic acid uptake in the cells overexpressing GLUT 1 and GLUT 3. Myricetin also inhibited ascorbic acid uptake; inhibition was noncompetitive with K(i) = 14 micromol/L in Jurkat cells. These data indicate that flavonoids inhibit both ascorbic acid and dehydroascorbic acid uptake but do so by different mechanisms. These data may contribute to new understanding of the biological effect of flavonoids on the intracellular accumulation of ascorbic acid in human cells.

Animals↗
PubMed1992

Comparison of ascorbic acid and ascorbic acid 2-O-alpha-glucoside on the cytotoxicity and bioavailability to low density cultures of fibroblasts.

Ascorbic acid 2-O-alpha-glucoside (AA-2G) is a stable ascorbate derivative which has vitamin C activity in vivo and in vitro. We studied whether AA-2G exerts a prooxidant action in cultured fibroblasts from chick embryo and human skin, as does ascorbic acid. At concentrations of 0.1-1.0 mM, ascorbic acid markedly reduced the viable cell number of low density cultures within 24 hr, whereas AA-2G had no such effect. The ascorbate cytotoxicity was dependent on the cell density at the time of its addition and it was characteristic of low density cultures. This cytotoxicity was completely prevented by catalase and partially by an Fe3+ ion chelator, desferrioxamine. In the early culture stage at which a morphological change in the fibroblasts began to occur, intracellular ascorbate concentrations in low density cultures after addition of ascorbic acid were much higher than in high density cultures. However, at the same concentrations, AA-2G did not cause an elevation even in low density cultures and it was also effective on collagen synthesis at high and medium densities. These results suggest that the abnormally accumulated ascorbic acid in the cells cultured at low density possibly amplifies the generation of oxygen radicals through the reduction of Fe3+ ions and subsequent oxidative reactions, leading to cell death. Therefore, it is concluded that AA-2G which supplies an adequate amount of ascorbic acid during culture period is a bioavailable ascorbate source without cytotoxicity.

Animals↗
PubMed2004

Effects of ascorbic acid and ascorbic acid 2-phosphate, a long-acting vitamin C derivative, on the proliferation and differentiation of human osteoblast-like cells.

In order to investigate the effect of ascorbic acid (AsA) and ascorbic acid 2-phosphate (Asc 2-P), a long-acting vitamin C derivative, on the growth and differentiation of human osteoblast-like cells, we supplemented the culture medium of MG-63 cells with various concentrations (0.25 to 1 mM) of these factors. Asc 2-P significantly stimulated nascent cell growth at all concentrations in the presence of fetal bovine serum (FBS). On the other hand, AsA showed a growth repressive effect depending on its concentration, and that of FBS. Asc 2-P also increased expression of osteoblast differentiation markers, such as collagen synthesis and alkaline phosphatase (ALP) activity. These stimulative activities of Asc 2-P were attenuated by inhibitors of collagen synthesis, indicating that these effects were dependent on collagen synthesis. Electron micrographs of the cells showed the formation of a three-dimensional tissue-like structure endowed with a mature extracellular matrix in the presence of Asc 2-P.

Alkaline Phosphatase↗
PubMed2006

Attenuation of abnormalities in the lipid metabolism during experimental myocardial infarction induced by isoproterenol in rats: beneficial effect of ferulic acid and ascorbic acid.

The present study aims at evaluating the effect of the combination of ferulic acid and ascorbic acid on isoproterenol-induced abnormalities in lipid metabolism. The rats were divided into eight groups: Control, isoproterenol, ferulic acid alone, ascorbic acid alone, ferulic acid+ascorbic acid, ferulic acid+isoproterenol, ascorbic acid+isoproterenol and ferulic acid+ascorbic acid+isoproterenol. Ferulic acid (20 mg/kg b.w.t.) and ascorbic acid (80 mg/kg b.w.t.) both alone and in combination was administered orally for 6 days and on the fifth and the sixth day, isoproterenol (150 mg/kg b.w.t.) was injected intraperitoneally to induce myocardial injury to rats. Induction of rats with isoproterenol resulted in a significant increase in the levels of triglycerides, total cholesterol, free fatty acids, free and ester cholesterol in both serum and cardiac tissue. A rise in the levels of phospholipids, lipid peroxides, low density lipoprotein and very low density lipoprotein-cholesterol was also observed in the serum of isoproterenol-intoxicated rats. Further, a decrease in the level of high density lipoprotein in serum and in the phospholipid levels, in the heart of isoproterenol-intoxicated rats was observed, which was paralleled by abnormal activities of lipid metabolizing enzymes: total lipase, cholesterol ester synthase, lipoprotein lipase and lecithin: cholesterol acyl transferase. Pre-cotreatment with the combination of ferulic acid and ascorbic acid significantly attenuated these alterations and restored the levels to near normal when compared to individual treatment groups. Histopathological observations were also in correlation with the biochemical parameters. These findings indicate the synergistic protective effect of ferulic acid and ascorbic acid on isoproterenol-induced abnormalities in lipid metabolism.

Adrenergic beta-Agonists↗
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↗