Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ASCORBIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMed1986

Some behavioural and EEG effects of ascorbic acid in rats.

Ascorbic acid (50-200 mg/kg IP) activated gross behaviour and EEG of rats. The behavioural excitation induced by d-amphetamine (2.5 mg/kg SC) was significantly potentiated by ascorbic acid (100-200 mg/kg IP). Catalepsy induced by haloperidol (0.25 mg/kg IP) was attenuated by ascorbic acid (50-200 mg/kg IP) while pentobarbitone (20 mg/kg IP)-induced sleep in rats was dose-dependently antagonised by ascorbic acid (50-400 mg/kg IP). Ascorbic acid (50-400 mg/kg IP) desynchronized the EEG of the frontal cortex and optic cortex while the EMG activity was slightly enhanced in the rat. Ascorbic acid (100 mg/kg IP) potentiated d-amphetamine (2.5 mg/kg SC)-induced EEG desynchronization and EMG activation in the rat. These results indicate that ascorbic acid exerts stimulatory effects in rats. The results also suggest that dopaminergic mechanism may contribute indirectly or directly to the observed behavioural and EEG effects of ascorbic acid.

Animals↗
PubMed1997

Lack of promotion of urinary bladder carcinogenesis by sodium bicarbonate and/or L-ascorbic acid in male ODS/Shi-od/od rats synthesizing alpha 2 mu-globulin but not L-ascorbic acid.

The study was designed to investigate whether sodium bicarbonate (NaHCO3) and/or L-ascorbic acid (AsA) promote urinary bladder carcinogenesis in male ODS/Shi-od/od (ODS) rats, which, unlike male F344 rats, are resistant to sodium L-ascorbate (Na-AsA)-promoting effects. Whereas F344 rats can synthesize AsA and alpha 2 mu-globulin (A2 mu-G), only A2 mu-G in produced in ODS rats. The two strains were given 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in their drinking water for 2 wk and then were fed basal CA-1 diet supplemented with 3% NaHCO3 plus 5% AsA (NaHCO3 + AsA), 3% NaHCO3, 5% AsA, or no chemicals for 32 wk. ODS rats given BBN-NaHCO3 or BBN-(NaHCO3 + AsA) had only a few small carcinomas in the urinary bladder, like those receiving BBN alone or BBN-AsA. In contrast, F344 rats administered BBN-NaHCO3 or BBN-(NaHCO3 + AsA) had many more, larger, carcinoma than animals of the same strain given BBN alone or BBN-AsA. AsA alone did not have any effect in either strain. Administration of NaHCO3 alone or NaHCO3 + AsA was associated with significant elevation of urinary pH and Na+ concentration to the same extent in both strains but, again, AsA alone was without effect. NaHCO3 + AsA and AsA alone increased the urinary concentration of total ascorbic acid in both strains but the observed levels wer lower in ODS rats. The results indicate that ODS rats are resistant to the modifying effects of NaHCO3 and/or AsA on two-stage urinary bladder carcinogenesis, and thus that the susceptibility to the promotional activity of sodium-salt-type compounds may be regulated by factors other than A2 mu-G-synthesizing ability and urinary levels of pH, Na+ and total ascorbic acid.

Animals↗
PubMed1994

Chromium and chronic ascorbic acid depletion effects on tissue ascorbate, manganese, and 14C retention from 14C-ascorbate in guinea pigs.

Chromium (Cr) potentiates the effects of insulin and a role for insulin in ascorbic acid transport has been reported. Therefore, the effects of Cr and ascorbate depletion on tissue ascorbic acid and 14C distribution and excretion after a 14C ascorbate dose were investigated in guinea pigs. As utilization of dietary Cr is affected by interaction with other minerals, tissue manganese (Mn), zinc (Zn), copper (Cu), and iron (Fe) were examined. For 20 wk, 40 weanling animals were fed either a Cr-deficient (< 0.06 micrograms Cr/g diet, -Cr) or a Cr-adequate (2 micrograms Cr from CrCl3/g diet, +Cr) casein-based diet and were given 1 mg ascorbate/d (-C) or 10 mg ascorbate/d (+C) for 20 wk. Animals fed the Cr-depleted diet had decreased weight at 20 wk (p < 0.01). Six hours before necropsy, animals were dosed by micropipette with 1.8 microCi of L-[carboxyl-14C] ascorbic acid and placed in metabolic cages. Ascorbate supplementation increased Fe concentrations in most analyzed tissues, hepatic 14C, tissue ascorbate and Mn concentration in the adrenal and testes, but decreased the concentrations of Cu in the kidney and Mn in the spleen. Liver Mn concentration was higher and kidney Mn concentration was lower in +Cr animals. Interactions between Cr and ascorbic acid affected Mn concentrations in bone and brain. These results indicate that ascorbate and Cr may affect Mn distribution. Chromium supplementation decreased plasma cortisol, brain 14C and the amount of 14C expired as carbon dioxide. These findings suggest that dietary Cr may affect ascorbic acid metabolism and the metabolic response to stress.

Adrenocorticotropic Hormone↗
PubMed1990

Glutathione and ascorbic acid concentrations in the duodenum of rats with cysteamine-induced ulcers: influence of cysteine and ascorbic acid pretreatments.

Duodenal ulceration in rats was induced by a single subcutaneous injection of cysteamine at doses of 7, 28, 42 and 65 mg/100 g body weight 24 h before killing. Duodenal ulceration induced by cysteamine was dose-dependent. However, at 65 mg/100 g body weight, 5 of 6 animals died within 24 h. The concentrations of reduced glutathione (GSH) and ascorbic acid were measured in the duodenal homogenates of cysteamine-treated rats. The ulcerogen, at doses of 28 and 42 mg/100 g body weight, significantly reduced the GSH concentration. At a dose of 28 mg/100 g body weight, however, it did not significantly affect the duodenal ascorbic acid concentration. Pretreatment of rats with daily intramuscular injections of cysteine at 25, 50 and 100 mg/kg or ascorbic acid at 50, 100 and 200 mg/kg for 7 days had no significant effect on the duodenal ulceration produced by cysteamine (28 mg/100 g body weight), although each pretreatment significantly raised the duodenal concentrations of GSH and ascorbic acid respectively, in control rats, and to a lesser extent in cysteamine-treated animals.

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↗
PubMed1998

The influence of amino acid source on the stability of ascorbic acid in TPN mixtures.

This study was undertaken to investigate the stability of ascorbic acid and its primary degradation product, dehydroascorbic acid, in total parenteral nutrition (TPN) mixtures. The influence of the type of bag and the commercial source of amino acid on ascorbate degradation was examined, using a stability-indicating high-pressure liquid chromatography (HPLC) method. Ascorbic acid was most stable in multilayered bags, compared with ethylvinyl acetate (EVA) bags. Results indicated that, in multilayered bags, the initial rapid ascorbic acid degradation was greatest in TPN mixtures containing amino acid infusions without reducing activity. In contrast, degradation in TPN mixtures containing amino acids with reducing compounds (Vamin 14 and Freamine III 8.5%) was less than 10% of the added amount. Dehydroascorbic acid degraded approximately in parallel with ascorbic acid, and it contributed to the total available ascorbate activity. The addition of air to TPN mixtures in multilayered bags caused accelerated degradation of both ascorbic acid and dehydroascorbic acid. It is concluded that TPN mixtures compounded in multilayered bags can be safely assigned extended shelf lives, especially if compounded using an amino acid with reducing activity. This is principally due to the protective effect of the bag wall in preventing oxygen transmission, the cause of ascorbic acid oxidation, because oxygen transmission through the bag wall is minimized during storage. TPN mixtures stored in EVA bags should be administered within 2-4 d of compounding, depending on the amino acid infusion used.

Air↗
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↗
PubMed1988

Growth, ascorbic acid and iron contents of tissues of young guinea-pigs whose dams received high or low levels of dietary ascorbic acid or Fe during pregnancy and suckling.

1. Guinea-pig dams were fed on purified diets containing high (5 g/kg diet plus 1 g/l drinking water) or moderate (0.5 g/kg diet) levels of ascorbic acid, in combination with high (1 g/kg diet) or moderate (0.043 g/kg diet) levels of iron, during pregnancy and suckling. Their offsprings' diets contained 0.1 g ascorbic acid/kg and 0.04 g Fe/kg. 2. High ascorbic acid intake clearly enhanced both tissue ascorbate and Fe storage in the dams, and high Fe intake increased both the dams' and the pups' tissue Fe stores. 3. In the animals receiving high Fe intake, a co-existing high ascorbate intake by the dams reduced the growth rate of the offspring, but only during the early stages of development, not during the later stages of post-weaning growth. All the pups' tissue ascorbate levels fell after weaning, but those born of the dams receiving the high ascorbic acid diets did not fall to levels lower than those of the other pups. 4. Thus, although certain disadvantages to the offspring resulting from very-high ascorbic acid intake by pregnant guinea-pig dams were detected, these did not include permanently increased ascorbate requirements, and hence a progression to scurvy as the pups grew and matured.

Animals↗
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↗
PubMed1987

Isolation and characterization of rat hepatic ascorbic acid-2-sulfatases.

Ascorbic acid-2-sulfatase was isolated from rat liver by a multistep procedure. DEAE Sephacel ion-exchange chromatography resolved crude ascorbic acid-2-sulfatase into cationic and anionic fractions. These fractions were purified 75- and 230-fold, respectively. The comparative biochemical properties suggest that arylsulfatase B is responsible for the cationic ascorbic acid-2-sulfatase activity, while arylsulfatase A appears to be responsible for the anionic ascorbic acid-2-sulfatase activity. Partially purified arylsulfatase A hydrolyzed ascorbic acid-2-sulfate at 4% the rate of p-nitrocatechol sulfate hydrolysis, while arylsulfatase B hydrolyzed ascorbic acid-2-sulfate at 0.6% the p-nitrocatechol sulfate rate.

Animals↗