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PubMed1991

Modifying effect of ascorbic acid and sodium ascorbate on the promoting stage of uterine sarcomogenesis induced in CBA mice by 1,2-dimethylhydrazine and estradiol-dipropionate.

Administration of estradiol-dipropionate (EP) after the cessation of 1,2-dimethylhydrazine (DMH) treatment increased the incidence of uterine sarcomas in CBA mice from 32.5 (DMH alone) to 62.5%. Ascorbic acid (AA) (0.3% in drinking water) given simultaneously with EP decreased the tumour incidence to 35%. Sodium ascorbate did not exert an inhibiting effect. AA inhibited the increase of uterine weight produced in mice by EP and did not influence the growth of mouse transplantable uterine sarcomas. The mechanisms of the antiestrogenic effects of AA are discussed.

1,2-Dimethylhydrazine↗
PubMed1988

[Modifying effect of ascorbic acid and sodium ascorbate on uterine carcomogenesis induced by 1,2-dimethylhydrazine in CBA mice].

Administration of ascorbic acid (0.3% in drinking water) inhibited the promoting effect of estradiol dipropionate on the 1,2-dimethylhydrazine-induced uterine sarcomogenesis in CBA mice. However administration of sodium ascorbate intensified the promoting effect of estradiol on the uterine sarcomogenesis, as evidenced by the shortening of the periods of tumour incidence.

1,2-Dimethylhydrazine↗
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↗
PubMed1980

Attachment of Entamoeba histolytica to glass in a defined maintenance medium: specific requirement for cysteine and ascorbic acid.

Cysteine and ascorbic acid were previously shown to be required by Entamoeba histolytica trophozoites for attachment to glass, elongation, and ameboid movement as well as for short-term (12-24 h) survival in a balanced salt solution containing bovine serum albumin and a vitamin solution (Maintenance Medium 1). If the only function of cysteine and ascorbate was to decrease the redox potential, other reducing agents should be effective. However, the requirement for cysteine in the presence of ascorbic acid was highly specific. Equally effective were D- and L-cysteine; however, of many other compounds tested, only thioglycolic acid, ascorbic acid, or L-cystine (in decreasing order) were somewhat active. Under N2 atmosphere, cysteine and ascorbic acid were still required, although their concentrations could be halved. The ability to attach in the maintenance medium was irreversibly lost after only 5 min of cysteine-ascorbic acid deprivation; however, there was no decrease in viability when the amebae were transferred to growth medium within 30 min. Cysteine thiol groups in the medium were oxidized rapidly regardless of the concentration of ascorbic acid or the presence of amebae; however, ascorbic acid prolonged attachment of amebae.

Animals↗
PubMed1991

Ascorbic acid deficiency elevates serum level of LDL-cholesterol in a rat mutant unable to synthesize ascorbic acid.

The effect of ascorbic acid deficiency on serum levels of high density lipoprotein- (HDL-), low density lipoprotein- (LDL-), very low density lipoprotein- (VLDL-) and chylomicron-cholesterol was examined in ODS-od/od rat (ODS rat), that is a rat mutant unable to synthesize ascorbic acid. Male ODS rats were fed an ascrobic acid-free diet for 20 days. In another two groups, the diet supplemented with 300 mg ascorbic acid/kg diet was fed either ad libitum (ad libitum control) or in pair-feeding (pair-fed control). Pair-fed rats received the same amount of diet as rats fed the ascorbic acid-free diet. Serum level of total cholesterol in the ad libitum control rats, ascorbic acid-deficient rats, and the pair-fed control rats were 100.1 +/- 8.4 mg/dl, 92.8 +/- 6.2 mg/dl and 72.2 +/- 4.8 mg/dl, respectively. The level of LDL-cholesterol in ascorbic acid-deficient rats was significantly higher than that in the ad libitum control or that in the pair-fed control. The level of HDL-cholesterol in ascorbic acid-deficient rats was lower than that in the ad libitum control, but was not changed as compared with that in the pair-fed control. Ascorbic acid deficiency did not affect serum level of VLDL-cholesterol or chylomicron-cholesterol as compared with those in the controls. These results demonstrate that ascorbic acid deficiency causes the elevation of serum level of LDL-cholesterol both in ad libitum feeding condition and pair feeding condition.

Animals↗
PubMed1982

Effect of amino acids imbalance and ascorbic acid deficiency on carcinogenic action of N-nitrosopiperidine in guinea pigs.

The long-term maintenances of guinea pigs on diets with (a) lack of vitamin C, (b) lack of lysine, methionine and threonine or (c) with a deficiency of all the above nutrients led to the development of oesophageal hyperplasia and atrophic gastritis. These dietary insufficiences were found to favour oesophageal and gastric cancer production by NPIP with a greatly shortened tumour induction time. It seems likely that the observed features of NPIP carcinogenesis depend on the alteration of the chemistry and biochemistry of these organs provoked by the low intake of the above-mentioned nutrients.

Amino Acids↗
PubMed1989

Ascorbic acid in a New World monkey family: species difference and influence of stressors on ascorbic acid metabolism.

Like other simian primates, the New World monkey Callithrix jacchus, marmoset, and Saguinus fuscicollis, tamarin, require ascorbic acid as an essential nutrient. For adult marmosets, a daily intake of 15 mg/kg metabolic body weight was found to be necessary to obtain a serum level above the kidney threshold. A survey of the serum ascorbic acid level of marmosets and tamarins in a breeding colony resulted in a vast divergence between the two species, indicating a higher ascorbic acid requirement for tamarins. Unaccustomed trial conditions or additional stressors resulted in a higher catabolism of ascorbic acid to CO2 in both species, measured with 14C labeled material, compared to a higher rate of renal excretion when the animals were accustomed to the metabolic cage. These isotope excretion studies suggest a different metabolic behavior of ascorbic acid in the two species. This is supposedly caused by a higher sensitivity of the tamarins when subjected to the same conditions as marmosets.

Animals↗
PubMed1984

Structure of ascorbic acid and its biological function. Determination of the conformation of ascorbic acid and isoascorbic acid by infrared and ultraviolet investigations.

The four O-H bands of ascorbic acid could be assigned by means of infrared investigations. It could be shown by electron spin resonance and nuclear magnetic resonance measurements that the radical sodium ascorbate is formed by a cyclic side-chain structure resulting in a loss of C(6)-OH and C(3)-OH. The C(2) = C(3) double bond is still maintained as could be shown by infrared and ultraviolet absorption spectroscopy. In the case of complete oxidation of ascorbic acid to dehydroascorbic acid, C(6)-OH is reestablished (indicating the reopening of the furanoid ring), while C(2)-OH as well as the C(2) = C(3) double bond have disappeared due to the deprotonation of C(2)-OH and C(3)-OH. In the case of isoascorbic acid and its radical potassium isoascorbate similar results are obtained with one distinct difference: in the case of isoascorbic acid, C(2)-OH does not appear while C(3)-OH exhibits a shoulder.

Ascorbic Acid↗
PubMed1969

Studies on the structure of hyaluronic acid. Characterization of the product formed when hyaluronic acid is treated with ascorbic acid.

Physical and chemical methods were used to characterize hyaluronic acid before (fraction HAIIBI) and after (fraction HA-AA) treatment with ascorbic acid. Fraction HA-AA was recovered with an almost quantitative yield and was shown to be chemically identical with fraction HAIIBI by all the methods used. These two materials, however, differed markedly in their molecular sizes and degree of polydispersity. By using sedimentation, diffusion and sedimentation-equilibrium analyses, weight-average molecular weights of about 1.2x10(6) and 6.5x10(4) respectively were obtained for fractions HAIIBI and HA-AA. It is concluded from these results that hyaluronic acid has a molecular weight of about 65000 and that the polysaccharide chain of this molecule is not depolymerized by ascorbic acid. It is further proposed that hyaluronic acid molecules in the matrix of connective tissues are present either in an aggregated form or as subunits of heterogeneous macromolecules, and that it is the linkages responsible for the organization of these structures which are broken by ascorbic acid.

Animals↗
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↗