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PubMed1989

Ascorbic acid absorption in Crohn's disease. Studies using L-[carboxyl-14C]ascorbic acid.

Total body pool and intestinal absorption of ascorbic acid were studied in 12 patients undergoing operation for Crohn's disease (six with fistulae and six without) and in six control patients undergoing operation for reasons other than Crohn's disease. L-[carboxyl-14C]Ascorbic acid, 0.19-0.40 megabecquerels (MBq), was given orally. After a period of equilibration, the labeled ascorbic acid was flushed out of the patient's body tissues using large doses of unlabeled ascorbic acid. Intestinal absorption of ascorbic acid, assessed from the total cumulative urinary 14C recovery, was found to be similar in patients with fistulizing Crohn's disease (73.9 +/- 8.45%), those without fistulas (72.8 +/- 11.53%), and in controls (80.3 +/- 8.11%). Total body pools of ascorbic acid, calculated using the plasma 14C decay curves, were similar in patients with Crohn's disease with fistulas (17.1 +/- 5.91 mg/kg), patients without fistulas (9.6 +/- 3.58 mg/kg), and in controls (13.3 +/- 4.28 mg/kg). The results indicate that ascorbic acid absorption is normal in patients with both fistulizing and nonfistulizing Crohn's disease. The results suggest that routine supplements of vitamin C are not necessary unless oral ascorbic acid intake is low.

Adult↗
PubMed1966

Effect of ascorbic acid on the serum folic acid estimation.

Ascorbic acid added to the basal medium increased the growth response of Lactobacillus casei in folic acid standards. The effect in the serum extracts was not marked, resulting in lowered serum folic acid estimations. However, results obtained on prolonged incubation were similar whether ascorbic acid was added or not. The presence or absence of ascorbic acid and variation of the incubation period may account for differences in reported normal ranges of serum folic acid levels.

Ascorbic Acid↗
PubMed1984

Simultaneous determination of uric and ascorbic acids in human serum by reversed-phase high-performance liquid chromatography with electrochemical detection.

A rapid, easy, and accurate method for the determination of uric acid and ascorbic acid in human serum by reversed-phase high-performance liquid chromatography with electrochemical detection has been developed. Human serum (0.5 ml) was mixed with 1.5 ml of an aqueous solution containing 2.0% metaphosphoric acid and the mixture was centrifuged at 3000g for 30 min. The supernatant was passed through a membrane filter to remove the particulate matter. Ten microliters of the filtrate was injected into the chromatographic system employed in this study. Complete separation of uric acid and ascorbic acid was achieved in about 2 min. The assay limit for quantitation was about 10 pg for uric acid and ascorbic acid under the present chromatographic conditions. The analytical recoveries of uric acid and ascorbic acid in human serum samples were found to be almost 100%.

Ascorbic Acid↗
PubMed1986

Effects of lipophilic derivatives of L-ascorbic acid and dehydro-L-ascorbic acid on the peroxidation of linoleic acid in neutral phosphate buffer containing alcohol.

6-O-Palmitoyl-AsA (AP) and -DHA (DHAP) suppressed LA peroxidation considerably in both 10% and 20% EtOH solutions. The duration of the suppression of LA peroxidation was longer with AP than with DHAP. But after the initial suppression of LA peroxidation, both derivatives showed an accelerating effect. 6-O-Acetyl-AsA (Ac-AsA) and -DHA (Ac-DHA) accelerated LA peroxidation from the start of the reaction in 10% EtOH, but suppressed it notably in 20% EtOH. 4-Phenyl-2,3-dihydroxy-2-buten-4-olide (PDHB) and 4-phenyl-2,3-dioxo-4-butenolide (PDOB) accelerated LA peroxidation in 10% EtOH. With 20% EtOH solution, PDHB suppressed LA peroxidation notably, as did AP, but PDOB showed only a short duration (about 1 h) of suppression. These results suggest the complexity of LA peroxidation catalyzed by lipophilic AsA or DHA in aqueous solution containing alcohol.

4-Butyrolactone↗
PubMed1991

L-ascorbyl-2-monophosphate has equal antiscorbutic activity as L-ascorbic acid but L-ascorbyl-2-sulfate is inferior to L-ascorbic acid for channel catfish.

Channel catfish (Ictalurus punctatus) fingerlings (13 g average initial weight) were fed semipurified diets supplemented with 0, 0.06, 0.12, 0.24 and 0.72 mmol/kg (0, 11, 22, 44 or 132 mg/kg) of ascorbic acid molar equivalent supplied by either L-ascorbic acid, L-ascorbyl-2-monophosphate (Mg salt) (AAP), or L-ascorbyl-2-sulfate (K salt) (AAS). After 14 wk, weight gains were equal for all fish fed diets containing L-ascorbic acid or AAP; however, growth rates were less for fish fed AAS at all dietary levels and for fish fed the ascorbic acid-free diet (control). There were no gross signs of vitamin C deficiency in any of the fish fed L-ascorbic acid or AAP, whereas spinal deformities were found in the controls and in fish fed all but the highest concentration of AAS. The percentage of spinal deformities decreased as dietary levels of AAS increased. Reduced bone collagen content and histopathology in liver and gill tissues also indicated ascorbic acid deficiency in the controls and in fish fed all but the highest concentration of AAS. Limited histopathology was found in fish fed the lowest level of L-ascorbic acid but not in those fed the lowest level of AAP. Regression analysis of weight gain data showed that the vitamin activity of ascorbic acid from AAS was only 5.2% of that from L-ascorbic acid for growth. This study indicates that AAP has equimolar activity to L-ascorbic acid as a vitamin C source for channel catfish and that AAS has vitamin activity for this species but at a much lower level than the other compounds.

Administration, Oral↗
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↗
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↗