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PubMed1986

Ascorbic acid requirement for the induction of microsomal drug-metabolizing enzymes in a rat mutant unable to synthesize ascorbic acid.

We investigated the requirement of ascorbic acid for the induction by polychlorinated biphenyls (PCB) of hepatic drug-metabolizing enzymes in ODS-od/od rat (OD rat) which is a rat mutant unable to synthesize ascorbic acid. ODS- +/+ rats (+/+ rat), which can synthesize ascorbic acid, were used as controls. In OD rats, the dietary requirement of ascorbic acid to maintain normal growth and prevent any signs of scurvy is about 300 mg of ascorbic acid per kilogram diet. In this study, dietary levels of ascorbic acid tested were 0, 50, 300, 1000 and 3000 mg ascorbic acid per kilogram diet with or without 200 mg of PCB per kilogram diet. Feeding PCB did not affect growth in rats of either genotype. When statistical analysis was done within groups fed diets without PCB, ascorbic acid deficiency caused significant decreases in body weight gain, hepatic activities of drug-metabolizing enzymes and level of hepatic cytochrome P-450. When OD rats were fed a diet without PCB, the supplementation of about 300 mg ascorbic per kilogram diet was sufficient to maintain normal activities of hepatic aminopyrine N-demethylase, aniline hydroxylase, cytochrome c reductase and reduction of cytochrome P-450 and a normal level of hepatic cytochrome P-450. However, when OD rats were fed a diet supplemented with 200 mg PCB per kilogram of diet, significantly higher activities of hepatic aminopyrine N-demethylase and aniline hydroxylase and significantly higher level of hepatic cytochrome P-450 were observed in OD rats fed a diet supplemented with 1000 mg or 3000 mg ascorbic acid per kilogram of diet than in rats fed a diet supplemented with 300 mg of ascorbic acid. It is concluded that the dietary requirement of ascorbic acid is increased severalfold by the administration of xenobiotics, such as PCB, for the maximum induction of hepatic drug metabolism.

Aminopyrine N-Demethylase↗
PubMedDate not supplied

[Effect of amino acid imbalance and ascorbic acid deficit on the carcinogenic effect of N-nitrosopiperidine].

A study was made of the effect of ascorbic acid deficiency and low levels of lysine, methionine and threonine on the cancerogenic effect of nitrosopiperidine which was fed to guinea-pigs with drinking water in a single dose of 4.25 mg/kg bw. Deficiency of the nutrients given alone or especially in combination speeded up the growth tumors induced by the cancerogenic agent. A possibility of inducing esophageal tumors in guinea-pigs has been demonstrated for the first time.

Amino Acids↗
PubMed1987

Activation of serum complement leads to inhibition of ascorbic acid transport.

Ascorbic acid is transported into 3T6 fibroblasts by a carrier-mediated, energy-dependent saturable active process with a Km of 112 microM and Vmax of 158 pmole/min/mg protein. The transport is dependent on extracellular Na+ concentration which reduces the Km. It was recently observed in this laboratory that bovine serum contained a heat-labile factor which, after interaction with bacterial endotoxin (lipopolysaccharides), inhibited ascorbic acid transport (J.J. Alleo and H. Padh, Proc Soc Exp Biol Med 179:128-131, 1985). We report here that the inhibition of ascorbic acid transport by endotoxin is mediated by the activation of serum complement. This was done by examining the activation of complement by other activators like zymosan and immunocomplexes (e.g., albumin and antibodies to albumin). Ascorbate transport was inhibited by the mixture of unheated serum and the activators. No inhibition was observed with serum devoid of C3 (component 3 of the complement). When C3-deficient serum was reconstituted by the addition of purified C3, the endotoxin-induced inhibition of ascorbate transport was restored. The implication of these findings is that in spite of a normal intake and blood level of the vitamin, tissues may not be getting adequate vitamin C during disease states when the complement in serum is activated. In other words, what may be considered an adequate intake of vitamin C under health conditions may not be adequate under disease conditions.

Animals↗
PubMed1991

L-ascorbic acid 2-phosphate, a phosphate derivative of L-ascorbic acid, enhances the growth of cultured rabbit keratocytes.

We examined the effect of L-ascorbic acid 2-phosphate (P-Asc) on the proliferation of cultured rabbit keratocytes. P-Asc is a phosphate derivative of L-ascorbic acid and has more prolonged vitamin C activity in solution than does L-ascorbic acid. The proliferation of cultured keratocytes was promoted by the presence of P-Asc in culture medium. Transmission electron microscopic observations revealed that cells were more multi-layered after culture in the presence of P-Asc (0.1 mM) for 30 days than were those cultured in the absence of P-Asc. The effect of P-Asc was abrogated by L-azetidine 2-carboxylic acid, which is an analogue of proline that inhibits the production and secretion of collagen. Our observations support a therapeutic role for P-Asc in the repair of corneal stromal damage such as that caused by a corneal chemical burn.

Animals↗
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↗
PubMed1982

Ascorbic acid sulfate sulfohydrolase (C2 sulfatase): the modulator of cellular levels of L-ascorbic acid in rainbow trout.

The enzyme L-ascorbic acid 2-sulfate sulfohydrolase (C2 sulfatase) was purified from rainbow trout liver. The enzyme catalyzes the hydrolysis of L-ascorbic acid 2-sulfate and has a pH optimum at 6.0. It has a molecular weight of about 117,500 at pH 5.0 and is inhibited by a number of sulfhydryl blocking agents including L-ascorbic acid. C2 sulfatase activity was observed in most metabolic organs of rainbow trout. These findings suggest that the physiologic role of the enzyme is to maintain adequate cellular concentrations of L-ascorbic acid in the fish. The activity of the enzyme is controlled by L-ascorbic acid through feedback inhibition. Comparison of kinetic constants and inhibition patterns suggests that C2 sulfatase is structurally identical to human arylsulfatase A. However, unlike C2 sulfatase, human arylsulfatase A may not be involved in ascorbate metabolism. Its physiologic substrate is reported to be cerebroside-3-sulfate, not L-ascorbic acid 2-sulfate. A scheme is proposed to account for the functional divergence of these two structurally identical enzymes.

Animals↗
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↗
PubMed2003

Diverse effects of ascorbic acid and palmitoyl ascorbate on Helicobacter pylori survival and growth.

Among many antioxidants used in the food, pharmaceutical and cosmetic industries, ascorbic acid (AA) is one of the most important. AA has been suggested to decrease the risk of gastric disease (gastritis, duodenal ulcer, and carcinoma) by direct action on Helicobacter pylori. However, there are limited studies on the possible role of AA and its derivatives such as palmitoyl ascorbate (PA) on the growth and survival of H. pylori. In the present study it was demonstrated in vitro that AA in the concentration range 10-20 mg x ml(-1) (50-100 mM) inhibited H. pylori growth in liquid medium under microaerophilic conditions. In contrast, under aerobic conditions AA in the concentration range 2-20 mg x ml(-1) (10-100 mM) significantly increased the survival of H. pylori presumably eliminating the toxic effect of reactive oxygen species on bacterial cells. The hydrophobic derivative of AA, PA (a food antioxidant), demonstrated a strong antibacterial effect, under both aerobic and microaerophilic conditions in the concentration range 0.04-0.4 mg x ml(-1) (0.1-1.0 mM). This effect was also tested on other bacterial strains: Escherichia coli, Proteus vulgaris, Proteus mirabilis, Pseudomonas aeruginosa, Enterococcus faecalis, Bacillus cereus, Bacillus subtilis, Staphylococcus aureus, Staphylococcus epidermidis, Clostridium sporogenes and Campylobacter jejuni. Among these bacterial strains, PA showed a similar inhibitory effect on B. cereus and B. subtilis as observed with H. pylori. The results suggest that PA may be considered an important AA derivative in eradication of H. pylori in vitro and in vivo and to decrease the risk for gastric diseases.

Aerobiosis↗
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↗
PubMed2000

Synthesis and antitumor activities of novel pyrimidine derivatives of 2,3-O,O-dibenzyl-6-deoxy-L-ascorbic acid and 4,5-didehydro-5,6- dideoxy-L-ascorbic acid.

The new pyrimidine derivatives of 2,3-O, O-dibenzyl-6-deoxy-L-ascorbic acid (8-10) were synthesized by condensation of uracil and its 5-fluoro- and 5-trifluoromethyl-substituted derivatives with 4-(5,6-epoxypropyl)-2, 3-O,O-dibenzyl-L-ascorbic acid (7), while pyrimidine derivatives of 4,5-didehydro-5,6-dideoxy-L-ascorbic acid (14-17) with free C-2' and C-3' hydroxy groups in the lactone ring were obtained by debenzylation of 11-13 with boron trichloride. Z-Configuration of the C4'=C5' double bond and position of the benzyl group in the lactone ring of 14 were deduced from their (1)H and (13)C NMR spectra and connectivities in COSY, ROESY, and HMBC spectra. The exact stereostructure of 13 was confirmed by its X-ray crystal structure analysis. Of all the compounds in the series, compound 16 containing a 5-fluoro-substituted uracil ring showed the most significant antitumor activities against murine leukemia L1210/0 (IC(50) = 1.4 microg/mL), murine mammary carcinoma FM3A/0 (IC(50) = 0.78 microg/mL), and, to a lesser extent, human T-lymphocyte cells Molt4/C8 (IC(50) = 31.8 microg/mL) and CEM/0 cell lines (IC(50) = 20.9 microg/mL).

Animals↗