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At least 235 records · Page 13Linked to original sources
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↗
PubMed2004

Effect of cadmium on free amino acid, glutathione and ascorbic acid concentrations in two barley genotypes (Hordeum vulgare L.) differing in cadmium tolerance.

Hydroponic experiment was carried out to study the effect of three Cd levels on glutathione (GSH), free amino acids (FAA), and ascorbic acid (ASA) concentration in the different tissues of 2 barley cultivars with different Cd tolerance. Cadmium concentration in both roots and shoots increased with external Cd level, while biomass and ASA concentration declined, and Wumaoliuling, a Cd-sensitive genotype was more affected than ZAU 3, a Cd-tolerant genotype. The effect of Cd on GSH concentration was dose- and time-dependent. In the 5 d exposure, root GSH concentration increased in 0.5 microM Cd treatment compared with control, but decreased significantly in 5 microM Cd treatment, irrespective of genotypes. However, in the 10 d exposure, GSH concentration in all plant tissues decreased with increasing Cd levels in the culture medium, and Wumaoliuling was much more affected than ZAU 3. Cadmium treatment greatly altered FAA concentration and composition in plants. The effect of Cd on glutathione (Glu) concentration in roots varied with genotypes. ZAU 3 showed a steady increase in root Glu concentration in both 0.5 and 5 microM Cd treatments, while Wumaoliuling was decreased by 38.0% in 5 microM Cd treatment, compared with the control. The results indicate that GSH and ASA are attributed to Cd tolerance in barley plants, and the relative less reduction in GSH concentration in ZAU 3 under Cd stress relative to the control may account for its higher Cd tolerance.

Amino Acids↗
PubMed1997

Ascorbic acid and 6-deoxy-6-chloro-ascorbic acid: potential anticancer drugs.

The role of ascorbic acid (AA) in prevention and suppression of carcinogenesis has been known for a long time. It was also found that AA may inhibit the growth of some tumor cells in vitro and in vivo. We examined the influence of ascorbic acid and 6-chloro-6-deoxy ascorbic acid (6-Cl-AA) on the growth of various human cell lines: lung fibroblasts (Hef), ovarian adenocarcinoma (OVCAR), colon adenocarcinoma (HT-29), laryngeal carcinoma (HEp2) cells, HEp2 cells resistant to vincristine (HEp2VA3), cervical carcinoma (HeLa) cells, HeLa cells resistant to cisplatin (Helacis), breast adenocarcinoma (SK-BR-3) cells, and SK-BR-3 resistant to doxorubicin (SK-BR-3-Dox), as well as mouse fibroblasts L929, mouse melanoma B16 (Mel B16) cells and Chinese hamster fibroblasts (V79). Both drugs arrested the growth of: HeLa, SK-BR-3, SK-BR-3-Dox, L929, and Mel B16 cells, but did not influence the growth of others: Hef, OVCAR, HEp2, HEp2VA3 and V79. 6-Cl-AA suppressed more the proliferation of HeLacis, SK-BR-3-Dox and Mel B16 cells than AA, while AA was active only against HT-29 cells. Inhibitory effect of 6-Cl-AA was confirmed by the in vivo experiments on solid melanoma B16 tumors. Our results indicate that AA and 6-Cl-AA could serve as potential antitumor agents, especially against some tumor cells resistant to chemotherapy.

Animals↗
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↗
PubMed2000

Simultaneous analysis of tea catechins, caffeine, gallic acid, theanine and ascorbic acid by micellar electrokinetic capillary chromatography.

A micellar electrokinetic capillary chromatography (MEKC) method for the simultaneous analysis of five tea catechins, theanine, caffeine, gallic acid and ascorbic acid has been developed. The catechins are (-)-epicatechin, (+)-catechin, (-)-epigallocatechin, (-)-epicatechin gallate and (-)-epigallocatechin gallate. p-Nitrophenol serves as both reference and internal standard. All the components are separated within 13 min with a 57 cm uncoated fused-silica column. On-column detection was carried out at 200 nm. This method has been used to measure these compounds in fresh tea leaves and tea liquor. The limit of detection for all analytes ranged from 1 to 20 microg/ml.

Ascorbic Acid↗
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↗
PubMed1980

Interrelationship of dietary ascorbic acid and iron on the tissue distribution of ascorbic acid, iron and copper in female guinea pigs.

Female guinea pigs were fed diets varied in ascorbic acid and iron concentration for 21 days. Tissue concentrations of ascorbic acid, iron (total, ferritin and hemosiderin) and copper were determined in blood, liver and spleen. High dietary ascorbic acid (10 times control) increased tissue ascorbic acid levels and produced a decrease in liver ferritin and hemosiderin, without altering liver or plasma total iron. Conversely, splenic total iron increased with no changes in ferritin and hemosiderin iron. The increased ascorbic acid did lower copper levels in blood and liver, 39% and 52%, respectively. In guinea pigs maintained on an ascorbic acid-free diet for 21 days, a decrease in hepatic ferritin and total iron was observed, as well as an increase in splenic hemosiderin and total iron. No change in plasma iron was observed nor were any of the copper pools altered. Intake of high dietary iron (10 times control) increased hepatic iron stores and produced a reciprocal decrease in hepatic copper. Even though splenic iron increased, no significant change in copper resulted. The significance of these nutrient interactions is discussed.

Animals↗
PubMed1998

Age-associated decline in ascorbic acid concentration, recycling, and biosynthesis in rat hepatocytes--reversal with (R)-alpha-lipoic acid supplementation.

Ascorbic acid recycling from dehydroascorbic acid and biosynthesis from gulono-1,4-lactone were used as measures of cellular response capacity to increased oxidative stress induced by tert-butylhydroperoxide. The hepatic ascorbic acid concentration was 54% lower in cells from old rats when compared to cells isolated from young rats (P<0.0005). Freshly isolated hepatocytes from old rats exhibited a significantly decreased ascorbic acid recycling capacity in response to oxidative stress (P<0.005) compared to cells from young rats. Ascorbic acid synthesis in these cells from old animals was unaffected by various concentrations of tert-butylhydroperoxide, but amounted to only approximately half of the biosynthetic rate when compared to cells from young animals (P<0.001). Cells from young animals were not significantly affected by the tert-butylhydroperoxide treatments. The results demonstrate a declining ability with age to respond to increased oxidative stress. (R)-alpha-Lipoic acid, a mitochondrial coenzyme, is a powerful antioxidant. A two-week dietary supplementation of old animals with 0.5% (R)-alpha-lipoic acid prior to cell isolation almost completely reversed the age-associated effects on ascorbic acid concentration (P<0.0001), recycling (P<0.05) and biosynthesis after oxidative stress. These results provide further evidence for the potential of alpha-lipoic acid in treatment of diseases related to oxidative stress. Furthermore, the study extends the value of ascorbic acid as a biomarker of oxidative stress.

Aging↗
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↗
PubMed1994

Ascorbic acid deficiency in guinea pigs: contrasting effects of tissue ascorbic acid depletion and of associated inanition on status indices related to collagen and vitamin D.

To investigate the sensitivity of guinea pig tissues to ascorbic acid depletion, as distinct from inanition, young male guinea pigs were maintained with either ascorbic acid restriction or total diet restriction for 8 weeks. One group (A) received no ascorbic acid for 3 weeks, then 0.5 mg/d for 5 weeks; one group (B) was weight-matched by restricted food intake to the first group; a third (marginally deficient) group (C) received 1 mg ascorbic acid/d throughout; a fourth was weight-matched to this group (D); and a fifth group received the control diet ad lib. (E). Both of the groups with restricted ascorbic acid intakes (A and C) developed very low tissue ascorbic acid contents, but only the first group (severely deficient group A) also exhibited a severely reduced growth rate. This group also exhibited reduced femur calcium and hydroxyproline contents and reduced skin hydroxyproline content. These changes were not seen in the corresponding weight-matched group (B). Neither plasma alkaline phosphatase (EC 3.1.3.1) activity, nor a variety of indices of vitamin D status exhibited changes which could be attributed specifically to reduced ascorbic acid intake and hence to lowered tissue ascorbic acid content. It is concluded that low tissue ascorbic acid levels in guinea pigs clearly alter the connective tissue composition of growing femur and skin, but do not necessarily produce a major, specific effect on vitamin D status. Moreover, the control of inanition is crucial to permit interpretation of the changes in metabolism that are caused by ascorbic acid deficiency.

Alkaline Phosphatase↗
PubMed1997

Bilirubin oxidation provoked by endotoxin treatment is suppressed by feeding ascorbic acid in a rat mutant unable to synthesize ascorbic acid.

We examined the possibility that bilirubin oxidation is provoked in vivo by using scurvy-prone ODS-od/od rats treated with endotoxin (lipopolysaccharide). Recently, bilirubin oxidative metabolites were isolated from human urine and named biotripyrrin-a and biotripyrrin-b. In ODS-od/od rats fed an ascorbic-acid-free diet, the concentration of bilirubin metabolites in urine was increased 7.0-fold at 3 h after injection of lipopolysaccharide and 4.4-fold at 10 h compared to the control rats injected with saline. The dietary supplement of ascorbic acid, the physiological antioxidant, suppressed the increase in bilirubin metabolites in urine after lipopolysaccharide injection: concentrations of biotripyrrin-a and biotripyrrin-b in urine collected 6.5-10 h after the injection were lower in rats fed an ascorbic-acid-supplemented diet than in rats fed an ascorbic-acid-free diet. Moreover, feeding of ascorbic acid suppressed the hepatic mRNA level of heme oxygenase-1, the rate-limiting enzyme of bilirubin biosynthesis, in rats injected with lipopolysaccharide. These findings indicate that bilirubin oxidation is markedly stimulated in lipopolysaccharide-treated rats and suggest that bilirubin and ascorbic acid have physiologically protective effects against oxidative stress.

Animals↗