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At least 37 records · Page 2Linked to original sources
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

Automated constant-current coulometric assay system for ascorbic acid and sodium ascorbate.

The performance of an automated constant-current coulometric system for the assay of ascorbic acid and sodium ascorbate is described. After loading, it is capable of analyzing 25 samples and printing out the titer values with no operator attention for 2.5 hr. Under optimum conditions, ascertained by evaluating various electrochemical parameters, the accuracy and precision (95% ts) were found to be +/- 0.3%.

Ascorbic Acid↗
PubMed1975

Metabolism of L-ascorbic acid in rats under in vivo administration of mercury: effect of L-ascorbic acid supplementation.

1. Rats toxicated with mercury showed drastic fall in growth rate and supplementation of L-ascorbic acid to these rats could not reverse this effect. The contents of L-ascorbic acid and of D-glucuronic acid in the urine of the toxicated animals were decreased which could be counteracted by subsequent L-ascorbic acid supplementation. 2. The concentration of L-ascorbic acid in the liver tissues of mercury toxicated rats was decreased markedly and administration of L-ascorbic acid to this group could raise the tissue reserve considerably. 3. Severe damages of the normal histological pattern of the kidney tissues of rats viz. cellular and glomerular degeneration were observed under mercury toxicity. 4. In the liver tissues of the mercury toxicated rats, the rate of L-ascorbic acid synthesis was reduced along with increased catabolism of L-ascorbic acid. Subsequent supplementation of L-ascorbic acid to these toxicated rats was, however, found to be effective in reversing these alterations almost to the basal level.

Animals↗
PubMed1977

Ascorbic acid metabolism and the clinical factors which affect tissue saturation with ascorbic acid.

The factors which give rise to tissue desaturation of ascorbic acid are classified and discussed. Nutritional deprivation, normal physiological factors and metabolic factors, and pathophysiological factors may all give rise to acute and continuing ascorbic acid tissue desaturation while the factors continue to operate. Nutritional desaturation can easily be rectified by providing supplementary Vitamin C in adequate dosage. The other factors can only be rectified when the causative mechanism is arrested. Iatrogenic desaturation may be produced by aspirin and several other drugs. While causative factors excluding that of nutrition are operating, it is very difficult if not impossible to restore normal tissue values of ascorbic acid. In consequence side effects which arise from supplementary Vitamin C administration do not arise in these circumstances. The supplementary Vitamin C administration is defined as compensatory administration of Vitamin C. In healthy individuals administration of supplementary Vitamin C can be defined as (large doses). Such large doses may give rise to side effects. The mechanism by which ascorbic acid is involved in the inflammatory response is discussed.

Ascorbic Acid↗
PubMed1977

Effect of PCB (polychlorobiphenyls) on on L-ascorbic acid, pyridoxal phosphate and riboflavin contents in various organs and on hepatic metabolism of L-ascorbic acid in the rat.

Effects of continuous oral administration of PCB (polychlorobiphenyls, 10-100 mg/kg/day, 4 weeks) on tissue levels of L-ascorbic acid (vitamin C), pyridoxal phosphate and riboflavin (vitamin B2) in various organs and on hepatic metabolism of L-ascorbic acid were examined in male Wistar rats weighing 150-250 g. Riboflavin contents in the liver, kidney, brain, heart and testis were not altered by PCB treatments, whereas the hepatic level of pyridoxal phosphate, a biologically active form of vitamin B6, was significantly reduced by PCB administration. Under the same experimental conditions, L-ascorbic acid contents in the liver, kidney, lung and testis showed a significant increase. Histochemical studied revealed that in the adrenal gland, increase of L-ascorbic acid was localized in the fasciculate and reticular zones of cortex, respectively. It was found that increase of L-ascorbic acid in the liver is caused predominantly by activation of biosynthesis at the steps of galactose to D-glucuronic acid and is not due to changes in the catabolic processes of L-ascorbic acid per se. Possible significance of these changes in tissue levels and/or metabolism of vitamins in the occurrence of PCB intoxication is briefly discussed.

Administration, Oral↗
PubMed1975

Ascorbic acid requirements and metabolism in relation to organochlorine pesticides.

Those organochlorine pesticides which possess both high lipoid solubility and high resistance to biodegradation are prone to accumulation in animal tissues and produce relatively long-term effects as toxicants. Such compounds, typified by DDT, Dieldrin, and Lindane, are profound inducers of hepatic microsomal enzymes, including parts of the glucuronic acid and ascorbic acid biosynthetic pathways. Consequently, administering such pesticides to rats in accompanied by enhanced formation and excretion of D-glucuronic acid and L-ascorbic acid, or D-glucaric acid in the case of guinea pigs. Secondarily, the efficiency in biodegrading the pesticides is reduced in ascorbic-acid-deficient guinea pigs with correspondingly greater residue accumulation in tissue. This would aggravate chronic toxic effects of the compounds. Finally, the capacity of the liver to adapt to the presence of such toxicants through enhanced microsomal enzymatic levels appears to be sensitive to its ascorbate status. Impaired enzyme induction is apparent quite early during ascorbic acid depletion in guinea pigs. The enhanced turnover of ascorbate produced by such pesticides, the poor enzymatic adaptation to them during ascorbate depletion and the dependency of the oxidase system upon adequate ascorbate, all point to the central significance of ascorbate status in the liver, and possibly other tissues, as a determinant of their chronic toxicity.

Animals↗
PubMed1979

On the possible involvement of ascorbic acid and copper proteins in leukemia. III. ESR investigations on the interaction between ascorbic acid and some transition metal ions.

The interaction between lyophilized samples of ascorbic acid and Cu2+, Fe3+ or Mn2+ has been investigated by means of ESR spectroscopy. All of the three transition metal ions form complexes with vitamin C, but only in the case of Cu2+ and Fe3+ the interaction results in a reduction of the metal ions. Cu2+ and ascorbic acid seem to form 2 : 1 complexes with an equilibrium constant of about K = 1 X 10(7) mol-1. None of these metal ion complexes exhibits, however, the ESR spectrum obtained with leukemic blood.

Ascorbic Acid↗
PubMed1978

Studies on the cholesterol synthesis in the human adipose tissue. II. Mechanism of metabolic shifts and regulation of cholesterol through ascorbic acid.

Ratios of yields of cholesterol in different media with different metabolites (200 estimations) show that if the initial normal quantity in a system is X, glucose makes it 4X which is then reduced by the amino acids and ascorbic acid. Alanine, Serine, Threonine, Cysteine, Cystine and Lysine reduce it to 2X. Glycine, Valine, Leucine, Aspartic, Phenylalanine, Tyrosine, Tryptophan roughly increase it to 6X. Other amino acids are intermediate between the above sets. Balanced amino acids and fatty acids keep up the glucose value 4X but the individual amino acids behave as above. Ascorbic acid reduces the quantity of cholesterol everywhere from one third to one half bringing it back to normal X. Since it is not directly involved in the cholesterol synthesis, it must be acting through the pyridine nucleotides. The interesting feature is that the C/H ratio in the amino acids corresponds to the yield of cholesterol with respect to glucose saline yield = 1. Mechanism of metabolic shifts has been discussed on the empirical basis as also on the basis of the change in ratios of NAD+ (NADP+) to NADH2 (NADPH2) through ascorbic acid.

Acetates↗
PubMed1975

Alleviating mortality associated with a vitamin E-selenium deficiency by dietary ascorbic acid.

Adding ascorbic acid to a practical ration deficient in vitamin E and selenium for the growing duck substantially reduced associated mortality. The continued appearance of various myopathies but absence of vascular faults supported implication of a reduced de novo ascorbate synthesis as part of the syndrome. Presumably, alleviation of this induced secondary inadequacy with its more lethal pathology was the primary reason for the lower death rate.

Animal Feed↗
PubMed1979

On the possible involvement of ascorbic acid and copper proteins in leukemia. IV. ESR investigations on the interaction between ascorbic acid and some copper proteins.

The interaction between lyophilized samples of ascorbic acid and some copper proteins (ceruloplasmin, cytochrome-c-oxidase, ascorbate-oxidase) has been investigated by means of ESR spectroscopy. The spectra obtained are identical to the one obtained with leukemic blood. The consequences of this for the molecular events occurring in cancer are discussed. The model proposed can explain the experimental findings reported thus far (such as change in spin concentration with the development of cancer, the presence of a high concentration of antioxidants etc.) as well as reconsile the two existing and seemingly contradictory hypothesis. Possible implications for lipid peroxidation and for the respiratory process are discussed.

Ascorbate Oxidase↗
PubMed1978

Effect of ascorbic acid on oxygen consumption, glycolysis and lipid metabolism of diabetic rat testis. Ascorbic acid and diabetes, I.

Alloxan diabetes caused a marked stimulation of endogenous oxygen uptake by rat testis tissues. However, the oxygen uptake in the presence of added glucose or pyruvate as substrate was significantly reduced. The ability of the testis tissues to utilize these substrates and to produce lactate was significantly inhibited in the diabetic animals. Alloxan diabetes also increased the levels of cholesterol, cholesterol esters, non-esterified fatty acids, triglycerides and phospholipids in rat testis tissues. Treatment of the diabetic rats with ascorbic acid caused more or less a normalization of all the parameters tested.

Animals↗
PubMed1978

Studies on L-ascorbic acid metabolism in rats under chronic toxicity due to organophosphorus insecticides: effects of supplementation of L-ascorbic acid in high doses.

The effects of chronic administration of two organophosphorus insecticides, parathion and malathion on the growth rate, ascorbic acid metabolism and some other nutritional and physiological parameters in rats were studied. Both parathion and malathion toxicity retarded the growth rate of rats. Inhibition of brain acetylcholinesterase was taken as an index of organophosphorus insecticide toxicity. Haemoglobin concentration of blood and organ weights were not affected under the toxic conditions. Parathion and malathion administration stimulated the activity of L-gulonolactone oxidase along with a simultaneous increase in the tissue storage and urinary excretion of vitamin C. The activities of other enzymes of ascorbic acid metabolism, dehydroascorbatase, uronolactonase, and L-gulonate dehydrogenase and decarboxylase were altered under the experimental conditions. Only minor histological changes of the liver and kidney tissues were noted under parathion and malathion toxicities. Excess intake of vitamin C under the toxic conditions was found to be very effective in counteracting the growth retardation and also the alterations produced by parathion and malathion both at the enzymatic and histological levels.

Animals↗
PubMed1979

Effects of ascorbate on leucocytes: Part II. Effects of ascorbic acid and calcium and sodium ascorbate on neutrophil phagocytosis and post-phagocytic metabolic activity.

The effects of ascorbic acid and calcium and sodium ascorbate at a concentration range of 10(-6)M - 10(-1)M on polymorphonuclear leucocyte (PMN) phagocytosis of Candida albicans and post-phagocytic nitroblue tetrazolium (NBT) reduction, hexose monophosphate shunt (HMS) activity and myeloperoxidase-mediated iodination of ingested protein were investigated. Phagocytosis of C. albicans was unaffected by ascorbate concentrations of 10(-6)M - 10(-2)M; however, progressive inhibition was observed at concentrations of 10(-2)M upwards. Enhancement of resting and stimulated HMS activity and NBT reduction was evident at ascorbate concentrations of 10(-5) M - 10(-2)M. The stimulations of HMS activity and NBT reduction was independent of myeloperoxidase iodination of ingested protein and this latter function was strongly inhibited by ascorbate. Concentrations of ascorbic acid and calcium and sodium ascorbate which caused inhibition of phagocytosis and HMS activity were the same as those which mediated stimulation of cell motility, indicating that independent cellular mechanisms may govern motility and phagocytosis.

Ascorbic Acid↗
PubMed1976

Effects of tetraacetyl-bis-dehydroascorbic acid, a derivative of ascorbic acid, on Ehrlich cells and HeLa cells (human carcinoma cells).

Derivatives of ascorbic acid were synthesized, and the studies were made on their effects in Ehrlich ascites carcinoma cells, in regard to the inhibition and the prolongation of survival time as well as on the morphological degeneration in HeLa cells. In a model infection study carried out by using tetraacetyl-bis-dehydroascorbic acid in dd mice infected with Ehrlich cells, it was proved that the prolongation of survival time was nearly double in comparison to the control group mice. Also, it was noted that hypertrophy due to abdominal dropsy and body weight were reduced much more than in the control group. From these results, the inhibiting effect of tetraacetyl-bis-dehydroascorbic acid was confirmed. While in the case of DHA and other derivatives, almost no inhibition and prolongation of survival time were observed. As for HeLa cells in a tissue culture, tetraacetyl-bis-DHA, in a dosage of 125-250 mug/ml, demonstrated definitely its morphological degeration. After 125 mug/ml of tetraacetyl-bis-DHA was added to a tissue culture solution of HeLa cells, the cells were washed and recultured. No growth of the cells was observed. Consequently, this substance was confirmed to be anti-HeLa substance with a low toxicity.

Animals↗