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PubMed1990

Effect of vitamin C depletion on serum cholesterol and lipoprotein levels in ODS (od/od) rats unable to synthesize ascorbic acid.

The effect of ascorbic acid deficiency on serum and liver cholesterol, phospholipid and triglyceride levels, serum lipoprotein levels and serum lipoprotein cholesterol levels were examined in male rats with a hereditary defect in ascorbic acid synthesis (ODS rats). Male homozygotes (od/od) and male rats of their parent strain (+/+) were each divided into four treatment groups and were fed vitamin C-deficient or vitamin C-replete diets containing either 0 or 0.5% cholesterol. During the 3-wk feeding-period the ODS (od/od) rats fed the vitamin C-deficient diet gradually decreased food intake, resulting in a lower body weight than that of od/od rats given ascorbic acid. The serum cholesterol level was significantly higher in the vitamin C-deficient od/od rats fed the cholesterol diet, and it tended to be higher in those fed the control (0% cholesterol) diet, whereas the liver lipid levels remained unchanged relative to those in od/od rats fed the vitamin C-replete diet. The serum very low density lipoprotein and high density lipoprotein (HDL) cholesterol levels were lower in od/od rats fed the vitamin C-deficient diet without cholesterol, but intermediate density lipoprotein and low density lipoprotein cholesterol levels were markedly higher in the vitamin C-deficient od/od rats than in od/od rats given ascorbic acid, regardless of dietary cholesterol level. The ratio of HDL2 cholesterol to HDL3 cholesterol was also higher in the vitamin C-deficient od/od rats. The parent strain of the od/od rats (+/+) showed no change due to vitamin C deficiency. These results suggest that vitamin C deficiency delays low density lipoprotein metabolism and produces hypercholesterolemia in male od/od rats.

Animals↗
PubMed1992

The effects of cortical ablation on d-amphetamine-induced changes in striatal dopamine turnover and ascorbic acid catabolism in the rat.

Dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), ascorbic acid (AA) and dehydroascorbic acid (DHAA) levels were determined by HPLC in the striatal synaptosomal fraction and in the whole striatum of rats, whose fronto-parietal cortex had been bilaterally ablated, after a single injection of d-amphetamine (2.0 mg/kg i.p.). d-Amphetamine significantly increased the DHAA/AA ratio in unoperated and sham-operated rats, but failed to increase it in ablated rats, as compared to pertinent saline-treated groups. In the synaptosomal fraction, d-amphetamine significantly decreased the DHAA/AA ratio in unoperated, sham-operated and ablated rats. d-Amphetamine significantly decreased the DOPAC/DA ratio in the whole striatum and significantly increased it in the striatal synaptosomal fraction in all experimental groups. Cortical ablation greatly increased d-amphetamine-induced motor hyperactivity. We conclude that the d-amphetamine-induced increase in AA striatal oxidation requires integrity of the cortico-striatal glutamatergic pathways. Further, AA oxidation occurs in the extracellular space. The cortico-striatal glutamatergic pathways exert an inhibitory modulation on d-amphetamine behavioral effects.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1993

Correlation between 1-methyl-4-phenylpyridinium ion (MPP+) levels, ascorbic acid oxidation and glutathione levels in the striatal synaptosomes of the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated rat.

In 6-month-old male Wistar rats, levels of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), ascorbic acid (AA), dehydroascorbic acid (DHAA), uric acid, glutathione (GSH) and 1-methyl-4-phenylpyridinium ion (MPP+) were determined by HPLC in the crude striatal synaptosomal fraction after single injections of MPTP 35 mg/kg i.p. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced a 32.5% death rate within 15 min to 10 h. Groups of surviving rats were sacrificed 1, 3, 8 and 24 h after MPTP. MPTP significantly increased levels of DHAA and uric acid and decreased levels of DOPAC and GSH. Individual synaptosomal levels of MPP+ were correlated inversely with DOPAC (r = -0.601, P < 0.002) and GSH levels (r = -0.496, P < 0.02) and directly with levels of uric acid (r = +0.627, P < 0.001); these latter, in turn, were correlated with DHAA (r = +0.418, P < 0.05) and GSH levels (r = -0.357, P = 0.07). In conclusion, the response of the endogenous antioxidant system (increase in AA oxidation, decrease in GSH levels) correlates well with the MPTP-induced increase in uric acid levels and provides further evidence for a mechanism of MPTP neurotoxicity involving oxidative stress produced by xanthine oxidase.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1993

Effect of L-ascorbic acid pretreatment on cadmium toxicity in the male Fischer (F344/NCr) rat.

Some studies have indicated that cadmium-induced lethality and selective injurious effects to specific tissues, such as testes or liver, can be prevented by pretreatment with the antioxidant L-ascorbic acid (ascorbic acid). However, the basis of this tolerance is unclear. We examined the effects of ascorbic acid pretreatment on cadmium toxicity in male Fischer (F344/NCr) rats. Cadmium treatment alone (25 mumol CdCl2/kg, s.c.) proved lethal, causing a 93% mortality within 72 h, but in rats pretreated with ascorbic acid (2 g/kg, s.c. 24, 12 and 1 h) cadmium-induced lethality was nearly prevented. Hepatic lesions, including hepatocellular necrosis, induced by cadmium were at least partially ameliorated by ascorbic acid pretreatment. Ascorbic acid pretreatment had no effect on cadmium-induced testicular lesions nor on cadmium content in testes, liver, kidney and urine. Ascorbic acid alone modestly increased hepatic metallothionein (MT), but not renal MT and had no effect on induction of hepatic or renal MT by cadmium. In contrast to liver and kidney, testicular cadmium-binding protein (TCBP) in rats exposed to cadmium alone decreased markedly. Moreover, the level of TCBP decreased unexpectedly in ascorbic acid pretreated rats as compared with control. These results indicate that ascorbic acid pretreatment decreases the toxicity of cadmium in the rat without markedly modifying its toxicokinetics or markedly stimulating MT synthesis.

Animals↗
PubMed1975

Oral contraceptives and ascorbic acid.

Plasma, leukocyte, and platelet ascorbic acid levels are decreased in women ingesting oral contraceptive steroids. Studies have shown that it is the estrogenic component of the oral contraceptive agents that is associated with the decresased ascorbic acid concentrations. Urinary excretion of ascorbic acid does not appear to be increased by the steroids. Although serum levels of copper are increased by estrogens and oral contraceptives, ascorbic acid catabolism does not appear to be increased (unpublished). Our preliminary data on tissue uptake of ascorbic acid suggest that changes in tissue distribution are one possible answer for the observed effects of the steroids on blood levels of ascorbic acid.

Adrenal Glands↗
PubMed1971

Relationship between leucocyte and plasma ascorbic acid concentrations.

Leucocyte and plasma ascorbic acid values were measured in healthy students, adult factory employees, and old people not receiving supplementary vitamin C and in healthy old people receiving 500 mg of vitamin C daily. Significant positive correlations between leucocyte and plasma ascorbic acid were found in all the groups. The regression lines differed significantly between one another within the sexes, but the pooled lines for each sex did not differ significantly in the unsupplemented groups. The relationship between plasma and leucocyte ascorbic acid values in the supplemented group differed significantly from that in the pooled unsupplemented groups.There was a limited range of variation in leucocyte ascorbic acid values compared with the range in plasma values in the supplemented group, whereas there was a wider range of variation in the leucocyte values in the unsupplemented groups. Leucocytes can therefore achieve a saturation level of ascorbic acid. Measurement of leucocyte ascorbic acid concentrations alone does not provide a reliable guide for the estimation of tissue status of ascorbic acid in normal individuals. Leucocyte concentrations provide a measure of the availability of ascorbic acid for storage, and plasma levels give an indication of its metabolic turnover rate. When these values are related the regression lines provide information about the storage and metabolism of ascorbic acid in normal individuals.

Adult↗
PubMed1993

Endothelial potentiation of relaxation response to ascorbic acid in rat and guinea pig thoracic aorta.

The role of the endothelium was evaluated in the relaxation of rat and guinea pig aortic rings induced by ascorbic acid. Ascorbic acid relaxed rat and guinea pig aortic rings that were previously contracted with submaximal dose of phenylephrine (PE), in a concentration dependent manner. Removal of the endothelium significantly reduced the sensitivity but not the magnitude of the response to ascorbic acid. Methylene blue, but not propranolol, blocked the endothelial augmentation of vascular relaxation to ascorbic acid. Vessels precontracted with potassium chloride (high K+) were also relaxed by ascorbic acid. Methylene blue also inhibited the response to ascorbic acid in the intact vessels precontracted with high K+. A23187 and acetylcholine, but not ADP, variably caused endothelium dependent component relaxation in guinea pigs, whereas all of these three probes constantly caused it. In Ca(2+)-free medium, Ca(2+)-induced contraction of high K(+)-depolarized rat aorta was inhibited by the presence of ascorbate, which was more pronounced in endothelium intact rings than in endothelium denuded ones. PE-induced contraction in the presence of different concentrations of ascorbate reduced both the sensitivity and the maximal contractile force in rat aorta. Ascorbic acid (0.125-32 mM) did not change the pH in the medium. From these findings, it is speculated that 1) receptor- and potential-operated Ca2+ channels may be modulated by ascorbate, 2) endothelium has a significant role in promoting relaxation induced by ascorbic acid.

Animals↗
PubMed1977

Ascorbic acid and melanogenesis.

The ascorbic acid contents of skin, plasma and urine were estimated in 12 vitiligo cases, one albino and 10 normal subjects. All the estimations were repeated after saturation with ascorbic acid. There was no difference between the two groups with regard to the ascorbic acid contents of their plasma or urine. The ascorbic acid level of vitiliginous skin was decreased; however, this difference just falls short of significance at the level P = 0-05. Further investigations with a larger group of patients are indicated.

Albinism↗
PubMed1985

Enhancement of norepinephrine biosynthesis by ascorbic acid in cultured bovine chromaffin cells.

Ascorbic acid donates electrons to dopamine beta-monooxygenase during the hydroxylation of dopamine to norepinephrine in vitro. However, the possible role of ascorbic acid in norepinephrine biosynthesis in vivo has not been defined. We therefore investigated the effect of newly accumulated ascorbic acid on catecholamine biosynthesis in cultured bovine adrenal chromaffin cells. Cells supplemented for 3 h with ascorbic acid accumulated 9-fold more ascorbic acid than found in control cells. Under these conditions, the cells loaded with ascorbate were found to double the rate of norepinephrine biosynthesis from [14C]tyrosine compared to control. By contrast, the amounts present of [14C] 3,4-dihydroxyphenylalanine and [14C]dopamine synthesized from [14C]tyrosine were unaffected by the preloading of ascorbic acid. Ascorbate preloaded cells incubated with [3H]dopamine also showed a similar increase in the rate of norepinephrine formation, without any change in dopamine transport into the cells. Thus, these data were consistent with ascorbate action at the dopamine beta-monooxygenase step. In order to determine if ascorbate could interact directly with dopamine beta-monooxygenase localized within chromaffin granules, we studied whether isolated chromaffin granules could accumulate ascorbic acid. Ascorbic acid was not transported into chromaffin granules by an uptake or exchange process, despite coincident [3H]dopamine uptake which was Mg-ATP dependent. These data indicate that ascorbic acid does augment norepinephrine biosynthesis in intact chromaffin cells, but by a mechanism that might enhance the rate of dopamine hydroxylation indirectly.

Adrenal Medulla↗
PubMedDate not supplied

[Formation of complexes of ascorbic acid and biological ligands].

Ascorbic acid has wide usage in medical practice for treatment some diseases caused by degeneration of connective tissue. Ascorbic acid has strong reduce properties. This article is dedicated to investigating complexation properties of ascorbic acid with components of biomembrans-bioligands: the most widespread aminoacids of connective tissue, phosphatidylholine, ATP, calcium salts, proteins. The investigations realised give the opportunity to make the conclusion that ascorbic acid has some complexation properties with different bioligands. But the stability of these complex products is different. And these stability variationes are described in this article.

Ascorbic Acid↗
PubMed2004

Voltammetric peak separation of dopamine from uric acid in the presence of ascorbic acid at greater than ambient solution temperatures.

Peak overlap in voltammetry poses challenges for the quantitative analysis of electroactive species. Dopamine and uric acid are typically challenging to determine voltammetrically because of their very similar oxidation peak potentials. We report preliminary results of the use of a screen-printed carbon electrode for the determination of dopamine and uric acid in an electrolyte solution maintained above ambient temperatures. Higher temperatures resulted in dramatic shifting of the dopamine oxidation peak toward lower potentials, while the uric acid peak was essentially stationary. Ascorbic acid, an interference in voltammetric uric acid determinations, is effectively suppressed at higher temperatures. This resulted in a greater peak separation of dopamine from uric acid at higher temperatures, which is desirable for better peak integration. In addition, greater current responses for both species were recorded at higher temperatures. The cause for such an increase in peak current is unraveled using ac impedance measurements. Presented are preliminary results for determining dopamine and uric acid at temperatures higher than ambient. Much improved voltammetric peak separation and sensitivity is obtained at these higher temperatures compared to ambient.

Ascorbic Acid↗
PubMed1975

Ascorbic acid in cholesterol and bile acid metabolism.

Latent chronic ascorbic acid deficiency provokes in guinea pigs a metabolic disorder in the liver, causing an impaired cholesterol transformation to its principal catabolic product, bile acids. This metabolic disorder induces hypercholesterolemia and accumulation of cholesterol in the liver and slows the release of cholesterol from the circulation. Ascorbic acid probably intervenes into the biosynthesis of bile acids at the stage of 7 alpha-hydroxylation of the cholesterol nucleus. High doses of ascorbic acid significantly stimulate cholesterol transformation to bile acids in guinea pigs and decrease plasma cholesterol concentration in humans.

Aged↗
PubMed1989

Ascorbic acid in the human stomach.

Ascorbic acid, the reduced form of vitamin C, may protect against gastric cancer. Accordingly, this study assessed the variability of ascorbic acid and vitamin C in the gastric juice of 77 patients with dyspepsia. There was a vitamin C concentration gradient from gastric juice down to plasma in subjects with normal gastric mucosa, but not in those with chronic gastritis. Patients with chronic gastritis had significantly lower gastric concentrations of vitamin C and ascorbic acid, and ascorbic acid concentrations were especially low in subjects with hypochlorhydria. The presence of the concentration gradient suggests that a mechanism for the secretion of vitamin C into the stomach exists. This is compromised by chronic gastritis. The very low ascorbic acid concentrations in hypochlorhydria may be a consequence of oxidation by bacterial nitrite. Those patients who by the Correa model are at greatest risk for gastric cancer have the lowest gastric levels of ascorbic acid.

Adult↗