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PubMed1986

Ascorbic acid specifically enhances dopamine beta-monooxygenase activity in resting and stimulated chromaffin cells.

Ascorbic acid enhancement of norepinephrine formation from tyrosine in cultured bovine chromaffin cells was characterized in detail as a model system for determining ascorbate requirements. In resting cells, ascorbic acid increased dopamine beta-monooxygenase activity without changing tyrosine 3-monooxygenase activity. [14C]Norepinephrine specific activity was increased by ascorbic acid, while [14C]dopamine specific activity was unchanged. Dopamine content, dopamine biosynthesis, tyrosine content, and tyrosine uptake were also unaffected by ascorbic acid. Furthermore, increased norepinephrine formation could not be attributed to changes in norepinephrine catabolism. Enhancement of dopamine beta-monooxygenase activity was specific for ascorbic acid, since other reducing agents with higher redox potentials were unable to increase norepinephrine formation. The specific effect of ascorbic acid on enhancement of norepinephrine formation was also observed in chromaffin cells stimulated to secrete with carbachol, acetylcholine, veratridine, and potassium chloride. In stimulated cells with and without ascorbate, there were no differences in dopamine content, tyrosine uptake, dopamine specific activity, and norepinephrine catabolism. These data indicate that, under a wide variety of conditions, only one catecholamine biosynthetic enzyme activity, dopamine beta-monooxygenase, is specifically stimulated by ascorbic acid alone in cultured chromaffin cells. This model system exemplifies a new approach for determining ascorbic acid requirements in cells and animals.

Animals↗
PubMed2006

Ascorbic acid deficiency stimulates hepatic expression of inflammatory chemokine, cytokine-induced neutrophil chemoattractant-1, in scurvy-prone ODS rats.

ODS rat has a hereditary defect in ascorbic acid biosynthesis and is a useful animal model for elucidating the physiological role of ascorbic acid. We previously demonstrated by using ODS rats that ascorbic acid deficiency changes the hepatic gene expression of acute phase proteins, as seen in acute inflammation. In this study, we investigated the effects of ascorbic acid deficiency on the production of inflammatory chemokine, cytokine-induced neutrophil chemoattractant-1 (CINC-1), in ODS rats. Male ODS rats (6 wk of age) were fed a basal diet containing ascorbic acid (300 mg/kg diet) or a diet without ascorbic acid for 14 d. Obvious symptoms of scurvy were not observed in the ascorbic acid-deficient rats. Ascorbic acid deficiency significantly elevated the serum concentration of CINC-1 on d 14. The liver and spleen CINC-1 concentrations in the ascorbic acid-deficient rats were significantly elevated to 600% and 180% of the respective values in the control rats. However, the lung concentration of CINC-1 was not affected by ascorbic acid deficiency. Ascorbic acid deficiency significantly elevated the hepatic mRNA level of CINC-1 (to 480% of the value in the control rats), but not the lung mRNA level. These results demonstrate that ascorbic acid deficiency elevates the serum, liver and spleen concentrations of CINC-1 as seen in acute inflammation, and suggest that ascorbic acid deficiency stimulate the hepatic CINC-1 gene expression.

Animals↗
PubMed2006

Antagonistic activity of ascorbic acid (vitamin C) on dopaminergic modulation: apomorphine-induced stereotypic behavior in mice.

Among the various neurotransmitter systems implicated in the mechanism of action of ascorbic acid (vitamin C), the relationship between the dopaminergic system and ascorbic acid is not particularly clear. Ascorbic acid is speculated to have an antagonistic effect on dopaminergic modulation. With this background in mind, in the present study we have seen the effect of ascorbic acid per se and in combination with typical and atypical antipsychotic agents against apomorphine-induced stereotypic behavior in mice. Male Laka mice weighing 20-25 g were used in the present study. Apomorphine-induced stereotypic behavior was used as an animal model. Various dopaminergic modulators were used. Ascorbic acid dose-dependently inhibited stereotypic behavior produced by apomorphine in mice. It potentiated the antipsychotic activity of haloperidol (0.1 mg/kg i.p.), a typical antipsychotic agent. When administered along with atypical antipsychotics, clozapine (1-2 mg/kg i.p.), sulpiride (10-20 mg/kg i.p.) and risperidone (0.0025 mg/kg i.p.), ascorbic acid also potentiated their activity. Also when given along with SCH-23390, a selective D(1) antagonist, an additive effect was observed. Ascorbic acid also inhibited the supersensitization response of apomorphine on reserpinization (2 mg/kg i.p.). Interestingly, at a lower dose (100 mg/kg i.p.), ascorbic acid potentiated the dopaminergic activity of apomorphine (0.5 mg/kg) and BHT-920 (0.25 mg/kg i.p.). However, when given concomitantly with SKF-38393, it failed to alter the response of SKF-38393. The data substantiate the hypothesis that ascorbic acid potentiated the activity of typical as well as atypical antipsychotics and that the effect of ascorbic acid on the dopaminergic system is markedly dose dependent; a low dose (100 mg/kg i.p.) potentiated the dopaminergic action while higher doses (400-1,600 mg/kg i.p.) blocked it.

Animals↗
PubMed1989

Ascorbic acid as a factor controlling "in vivo" its biosynthetic pathway.

The capacity of ascorbic acid biosynthesis in potato tuber tissue is closely correlated with the ascorbic acid content of the cells: the lower the endogenous content of ascorbic acid, the greater its biosynthesis. At the highest level of ascorbic acid found in the cells, the biosynthetic capacity is virtually zero. In these conditions, adding glucose (the first precursor of ascorbic acid) has no effect whatsoever, whereas adding galactono-gamma-lactone (the last precursor) induces a high rate of ascorbic acid synthesis. It is suggested that AA biosynthesis is subject to a regulatory mechanism "in vivo" which controls an initial step in the biosynthetic pathway. The last step in this pathway, catalyzed by galactone oxidase, is never blocked and, moreover, its activity is greater than that of the preceding steps.

Ascorbic Acid↗
PubMed1965

REGULATION OF ASCORBIC ACID AND OF XYLULOSE SYNTHESIS IN RAT-LIVER EXTRACTS. THE EFFECT OF STARVATION ON THE ENZYMES OF THE GLUCURONIC ACID PATHWAY.

1. The synthesis of ascorbic acid in rat-liver extracts is impaired during starvation, and more from glucuronolactone and glucuronate than from gulonate and gulonolactone. 2. The formation of xylulose from gulonate and from gulonolactone is greatly enhanced during starvation, whereas it is decreased from glucuronolactone and from glucuronate. 3. The activity of the enzymes of the glucuronic acid pathway during starvation has been determined in rat-liver preparations. Gulonolactone oxidase is decreased, NAD-linked gulonate dehydrogenase is enhanced, and uronolactonase, aldonolactonase and NADP-linked hexonate dehydrogenase are unchanged. 4. The impairment of ascorbic acid synthesis from gulonate observed during starvation can be accounted for by the depressed activity of gulonolactone oxidase. 5. The cause of the enhanced formation of xylulose has been located in the sedimentable fraction of liver homogenate. 6. The hypothesis is formulated of an increased utilization of the glucuronic acid pathway during starvation.

Alcohol Oxidoreductases↗
PubMed1995

Ascorbic acid transport and distribution in human B lymphocytes.

Ascorbic acid (vitamin C) transport was investigated in human B lymphocytes. The vitamin was transported by two components. The first was a high-affinity activity with an apparent Km of 7-10 microM and Vmax of 0.14 mM/h (3.11 x 10(-4) mumol x h-1 x mg protein-1). The activity was concentration and temperature dependent, saturable, and inhibited by carbonylcyanide-p-trifluoromethoxyphenylhydrazone and ouabain and generated ascorbic acid accumulation against a concentration gradient. Kinetics for the second component were indeterminate because ascorbate was not accumulated against a concentration gradient. Subcellular fractionation revealed that intracellular ascorbic acid in human B lymphocytes was > 90% localized to the cytosol and not protein bound. Kinetic parameters of high-affinity ascorbic acid transport could operate effectively with plasma concentrations normally found in humans.

Ascorbic Acid↗
PubMed1987

Influence of ascorbic acid dose on N-nitrosoproline formation in humans.

A relationship between ascorbic acid intake and N-nitrosoproline (NPRO) excretion in humans on a controlled diet was established. Seven healthy males were placed on a low nitrate, low ascorbic acid diet for 12 consecutive days. On days 3-12, a 5.24 mmol oral dose of sodium nitrate was administered in mid-afternoon, at least 2 h after the subject's last meal. On days 4-12, a 4.35 mmol oral dose of L-proline was administered 30 min after the nitrate dose. Ascorbic acid was given in amounts which increased daily from day 5 to day 10 (0.01-5.68 mmol; 1.76-1000 mg) with the proline. Total 24 h urines were assayed for nitrate, NPRO and total ascorbic acid. Nitrate balance was monitored using [15N]nitrate. Average endogenous nitrate synthesis was 1.28 +/- 0.43 mmol/day/person. NPRO excretion was reduced by 6 nmol/day when 0.05 mmol of ascorbic acid was administered. However, as much as 5.68 mmol ascorbic acid did not return NPRO excretion to levels observed before the nitrate and proline were administered. More than 10 times the ascorbic acid required to completely inhibit NPRO formation in vitro did not return NPRO excretion to baseline levels. These data indicate that endogenous nitrosation may be more facile than predicted by the in vitro chemistry.

Adult↗
PubMed2003

Ascorbic acid recycling in human erythrocytes is induced by smoking in vivo.

Tobacco smoke contains large numbers of radicals that burden the antioxidant defense and, thus, lower plasma antioxidants, in particular vitamin C or ascorbic acid, is commonly observed among smokers. Ascorbic acid recycling describes the process in which ascorbic acid is oxidized to dehydroascorbic acid by various pathways and subsequently reduced back to ascorbic acid intracellularly, e.g., in erythrocytes, thereby preserving the ascorbic acid pool. In humans who are unable to synthesize ascorbic acid, and in smokers in particular, who are prone to oxidation, this process must be very efficient and of great importance. It has previously been reported that isolated erythrocytes subjected to tobacco smoke in vitro had significantly lower ascorbic acid recycling as compared to controls. In contrast to these findings, we now report that freshly isolated erythrocytes from long-term smokers (n = 39) display a significantly increased rate of ascorbic acid recycling in vivo as compared to those isolated from nonsmokers (n = 31; p <.0001). Preliminary data suggests that the increase results from induction of dehydroascorbic acid reductase activity rather than from differences in energy status, glutathione content, or altered transport capacity. The induction of ascorbic acid recycling as a potential adaptation mechanism of the antioxidant defense to oxidative insults is discussed.

Antioxidants↗
PubMed1977

Phagocytosis and leukocyte enzymes in ascorbic acid deficient guinea pigs.

Enzymes related to bactericidal activities of leukocytes were studied in ascorbic acid deficient guinea pig leukocytes. The activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase were not affected either under resting or phagocytizing conditions in ascorbic acid deficiency. Granule bound NADPH-oxidase activity of resting leukocytes also was not altered in ascorbic acid deficiency. However, the extent of stimulation in NADPH-oxidase activity under phagocytizing condition was found to be significantly lower in ascorbic acid deficient leukocytes than that in control leukocytes. Similary, the extent of release of acid phosphatase from lysosomes during phagocytosis was also low in ascorbic acid deficient leukocytes. Ascorbic acid deficiency did not influence the activities of glutathione reductase and myeloperoxidase of leukocytes. The significance of these enzyme changes is discussed in relation to the decreased phagocytic and bactericidal activities of leukocytes in ascorbic acid deficiency.

Acid Phosphatase↗
PubMed1993

Effect of ascorbic acid on pituitary prolactin secretion in the non-ascorbate synthesizing Osteogenic Disorder Shionogi (ODS) rat.

We examined the secretion of prolactin (PRL) in the hereditary scurvy-prone Osteogenic Disorder Shionogi (ODS) rat to investigate the role of ascorbic acid (AsA) in pituitary lactotroph and hypothalamic function. Plasma PRL concentrations of conscious AsA-deficient or control ODS rats were measured before and after the administration of metoclopramide (MCP), 5-hydroxy-L-tryptophan (5-HTP) or saline. The basal plasma PRL levels did not differ between the two groups. However, the AsA-deficient rats exhibited significantly larger changes in plasma prolactin concentration in response to MCP or 5-HTP than the control ODS rats. Thus, AsA deficiency enhanced the stimulated, but not the basal, secretion of PRL in ODS rats. Our findings suggest that AsA may have an inhibitory effect on PRL secretion.

5-Hydroxytryptophan↗
PubMed2005

Determination of ascorbic acid and carotenoids in food commodities by liquid chromatography with mass spectrometry detection.

Two methods, one to determine ascorbic acid and one to determine lycopene and beta-carotene, in vegetables and fruits by liquid chromatography coupled with mass spectrometry (LC-MS) have been established. The chromatographic separation of the studied compounds and their MS parameters were optimized to improve selectivity and sensitivity. In both methods, separation was carried out with two coupled columns, first a C(18) and then a dC(18), using as mobile phase 70% methanol (0.005% acetic acid) and 30% acetic acid 0.05% for ascorbic acid determination and a mixture of methanol, tetrahydrofuran, and acetonitrile (60:30:10 v/v/v) for carotenoid analysis in isocratic mode. The molecular ion was selected for the quantification in selective ion monitoring (SIM) mode. Ascorbic acid was detected with electrospray ionization probe (ESI) in negative mode, while chemical ionization atmospheric pressure (APCI) in positive mode was used for the target carotenoids. The methodology for ascorbic acid analysis is based on an extraction with polytron using methanol and a mixture of methaphosphoric acid and acetic acid. Extraction of the carotenoids was carried out with tetrahydrofuran/methanol (1:1) (v/v). The proposed methods were applied, after their corresponding validations, to the analysis of four varieties of tomatoes, tomato in tin enriched and dried tomato, and to the analysis of mango and kiwi fruits, to compare the content in these compounds. Moreover, the influence of the process of freezing and the effect that the manipulation/preservation has in the content of ascorbic acid in tomato have also been studied.

Actinidia↗
PubMed1991

Regulation of collagen synthesis by ascorbic acid: characterization of the role of ascorbate-stimulated lipid peroxidation.

Recently, we have described the ability of traditional lipid peroxidation inhibitors to inhibit ascorbate-stimulated collagen synthesis. In order to characterize further this effect, we have tested the ability of known and potential inhibitors of lipid peroxidation for their effects on ascorbate-stimulated collagen synthesis and lipid peroxidation. In our experiments, mannitol, a water soluble antioxidant, had no effect on ascorbate-induced collagen synthesis nor on lipid peroxidation. However, alpha-tocopherol, which is a lipophilic antioxidant, inhibited both effects of ascorbate. Superoxide dismutase, catalase, and their polyethylene glycol conjugate forms did not inhibit the ascorbate-stimulated collagen synthesis or lipid peroxidation. In addition, no effect was seen with the oxygen radical scavengers isopropanol, ethanol, or dimethyl sulfoxide. Two iron chelators, o-phenanthroline and alpha,alpha-dipyridyl, both inhibited ascorbate-induced lipid peroxidation and collagen synthesis, consistent with the previously described iron-dependence of lipid peroxidation by ascorbate. These results support a correlation between collagen synthesis and lipid peroxidation and provide a theory for the mechanism of ascorbic acid regulation of collagen synthesis.

Antioxidants↗
PubMed1985

Blood ascorbic acid and histamine levels in patients with placental bleeding.

Concentrations of histamine and total ascorbic acid (L-ascorbic acid plus dehydroascorbic acid) in the antecubital vein blood of women in abruptio placentae (normally situated placentae) and placenta praevia have been measured. The results show that blood ascorbic acid in abruptio placentae is significantly (P less than 0.05) lower than the values found in placenta praevia. This may reflect impaired absorption and/or increased breakdown of ascorbic acid in abruptio placentae. Histamine levels in the two conditions are similar to one another.

Abruptio Placentae↗
PubMed1980

Effect of ascorbic acid on urine pH in patients with injured spinal cords.

The ability of ascorbic acid to lower urinary pH in patients with spinal cord injury and neurogenic bladder was studied. Ascorbic acid (1 g four times daily) or placebo was administered for five days in a double-blind, crossover study to 20 patients with spinal cord injury and neurogenic bladder. Urine pH was measured for two days before and during administration of placebo or ascorbic acid. The mean decrease in urinary pH with ascorbic acid was 0.58, but this reduction was not statistically or clinically significant. Only 7 of 20 patients showed a mean urine pH of 5.5 or less (acidic) during treatment with ascorbic acid. The study suggests that an ascorbic acid dosage of 1 g four times daily should not be used to maintain an acidic urinary pH for control of urinary tract infections in patients with spinal cord injuries.

Adolescent↗
PubMed1993

Chemo-immunotherapeutical studies on Dalton's lymphoma in mice using cisplatin and ascorbic acid: synergistic antitumor effect in vivo and in vitro.

Combined effects of ascorbic acid (vitamin C) and cisplatin on the growth of Dalton's lymphoma in C3H/He mice was investigated. Chemotherapy with sub-therapeutical dose (3 mg/kg) enabled to increase the survival time of the tumor bearing mice without any tumor free survivors. Ascorbic acid enhances the antitumor effect of cisplatin in vivo resulting in 60/70 day survivors along with tumor free survivors. Ascorbic acid also enhances the efficacy of low dose of cisplatin (5 micrograms/ml) in vitro. Tumor cells incubated with cisplatin and ascorbic acid, when injected into normal mice, exhibited inhibited growth resulting in an increased life span of tumor bearing mice and tumor free survivors. Inoculation of tumor cells incubated with cisplatin (5 micrograms/ml) and different concentrations (25 or 50 micrograms/ml) of ascorbic acid resulted in 30% tumor free mice which was not observed when concentration of cisplatin increased to 10 micrograms/ml in the medium. A possible cause of the enhancement of cisplatin-induced tumor growth inhibition may be the modulation of permeability of tumor cell membrane by ascorbic acid which increases the uptake of cisplatin into tumor cells, making less efficient the DNA repair machinery due to increased efficiency of adduct formation in DNA molecule. Possibly, this effect of ascorbic acid renders cisplatin more effective as an antitumor agent.

Animals↗
PubMed1995

Sperm quality and ascorbic acid concentration in rainbow trout semen are affected by dietary vitamin C: an across-season study.

High concentrations of ascorbic acid occur in scurvy-prone, teleost fish plasma. We quantified seasonal relationships between 1) dietary level of vitamin C and level of seminal plasma ascorbic acid, and 2) seminal plasma ascorbic acid concentration and sperm quality, in rainbow trout (Oncorhynchus mykiss). We maintained six groups of 2-yr-old rainbow trout on diets supplemented with 0, 30, 110, 220, 440, and 870 ppm ascorbyl monophosphate beginning in May 1992. Sperm were produced during the end of October 1992 through April 1993; we collected milt 13 times from 3-8 fish per treatment. We quantified ascorbic acid concentration in seminal plasma, and sperm concentration, motility, and weight. Seminal plasma ascorbic acid concentrations were affected directly by the ascorbyl monophosphate level in the diet. Seminal plasma ascorbic acid concentrations also were affected by season. Ascorbic acid deficiency did not influence semen quality (sperm concentration and motility) at the beginning of the spawning season. However, sperm concentration and motility in a group fed an ascorbic acid-free diet declined during the period of study. Ascorbic acid deficiency reduced both sperm concentration and motility, and thus fertility, of rainbow trout. These results indicate that vitamin C is important for male fish reproduction; the dietary requirement for seminal plasma ascorbic acid saturation exceeds that for optimum growth.

Animals↗
PubMed1990

Cellular functions of ascorbic acid.

It has long been suspected that ascorbic acid is involved in many cellular reactions. This is evident from the multitude of seemingly unrelated symptoms seen in scurvy. However, until recently, our understanding of its involvement was confined to its role in the synthesis of collagen. Studies in the past few years have unveiled mechanisms of its actions in collagen formation and many other enzymatic reactions. In addition, numerous physiological responses are reportedly affected by ascorbic acid. From the well-characterized enzymatic reactions involving ascorbic acid, it has become clear that in animal cells the ascorbate does not seem to be directly involved in catalytic cycles. Rather its major function seems to keep prosthetic metal ions in their reduced form. The role of ascorbate as a reductant in these enzymatic reactions complements its other antioxidant functions which have been recently appreciated, including that as a scavenger of free radicals. Therefore, it seems that the major function of ascorbate is to protect tissues from harmful oxidative products and to keep certain enzymes in their required reduced forms. However, it remains unclear how the deficiency of ascorbate leads to the pathological symptoms found in scurvy.

Animals↗
PubMed1986

Ascorbic acid levels in the aqueous humor of nocturnal and diurnal mammals.

Ascorbic acid concentration is known to be very high in the aqueous humor of humans and most animals. The role it might play in ocular function is a subject of conjecture. Some have proposed that it might protect the eye against light-induced damage. We examined the aqueous humor from 22 species of mammals to determine the range of levels and to see if there was a correlation with behavior. A wide range of ascorbic acid levels in the aqueous humor was found. Most of the animals considered to be diurnal had higher ascorbic acid levels than the nocturnal animals. This would suggest that ascorbic acid in the aqueous humor may play a protective role in those animals who are most exposed to light. Regardless, any theory proposing a role for ascorbic acid in the eye in mammals must take the wide range of ascorbic acid levels into account.

Animals↗