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At least 631 records · Page 35Linked to original sources
PubMed1980

Stimulation of prostaglandin synthesis by ascorbic acid via hydrogen peroxide formation.

Ascorbic acid causes an increase in prostaglandin (PG) synthesis in human lung fibroblasts in culture. This is accompanied by an increase in fatty acid release from cellular lipid stores. The effects of ascorbic acid on prostaglandin synthesis and fatty acid release are erased if the cultures are treated simultaneously with catalase, but not if treated with superoxide dismutase. The action of catalase points to a role of hydroperoxides in the synthesis of prostaglandins. The addition of hydrogen peroxide itself increases prostaglandin synthesis by these cells.

Arachidonic Acids↗
PubMed1997

Ascorbic acid and dehydroascorbic acid as biomarkers of oxidative stress caused by smoking.

Using a reliable, newly developed assay for ascorbic acid (reduced form) and dehydroascorbic acid (DHAA; the oxidized form) in plasma, we studied the influence of age, sex, and smoking on 219 healthy, age-stratified, and randomly selected subjects representing the Danish population. The mean (+/-SD) plasma total ascorbic acid (ascorbic acid + DHAA) concentration was lower in smokers (62.8 +/- 24.9 mumol/L) than in nonsmokers (74.9 +/- 23.6 mumol/L) (P < 0.001) and the DHAA content was 1.8 +/- 4.0% of the total ascorbic acid in smokers compared with 0.1 +/- 3.1% in nonsmokers (P < 0.001). A significant inverse correlation between the DHAA fraction and the total ascorbic acid concentration was found in smokers (P < 0.002) but not in smokers; the slopes of the linear regressions were significantly different in the two groups (P < 0.005). The mean plasma concentration of total ascorbic acid was higher in females than in males (P < 0.005); this difference persisted in multivariate analysis when smoking was adjusted for. No age dependence could be identified. The data show that smoking results in severe oxidative stress, depletion of the ascorbic acid pool, and insufficient reduction capacity to maintain ascorbic acid in the reduced form in plasma. We suggest that the additional analysis of DHAA allows further differentiation in the assessment of oxidative stress and may provide an objective way of determining vitamin C requirements in smokers. Preliminary findings suggest that a vitamin C dose that results in a plasma concentration of approximately 70 mumol/L or higher is required in smokers.

Adult↗
PubMed1989

Ehlers-Danlos syndrome type VI with normal lysyl hydroxylase activity cannot be explained by a defect in cellular uptake of ascorbic acid.

The uptake of ascorbic acid by cultured skin fibroblasts from two siblings with Ehlers-Danlos syndrome type VI, in extracts of which there is no deficit in lysyl hydroxylase activity, was found to be normal. Decreased availability of ascorbic acid to lysyl hydroxylase in cellula cannot, therefore, provide an explanation for the disorder in these patients, the cause of which remains obscure.

Adolescent↗
PubMed1990

Effect of cytochalasin B on the uptake of ascorbic acid and glucose by 3T3 fibroblasts: mechanism of impaired ascorbate transport in diabetes.

Hyperglycemia and/or hypoinsulinemia have been found to inhibit L-ascorbic acid cellular transport. The resultant decrease in intracellular ascorbic acid may de-inhibit aryl sulfatase B and increase degradation of sulfated glycosaminoglycans (sGAG). This could lead to a degeneration of the extracellular matrix and result in increased intimal permeability, the initiating event in atherosclerosis. The present studies show that the glucose transport inhibitor cytochalasin B blocked the uptake of 3H-2-deoxy-D-glucose (2.5 mg%) by mouse 3T3 fibroblasts. Cytochalasin B also blocked the uptake of 14C-L-ascorbic acid (1.25 mg%). The results of these studies further support the hypothesis that glucose and ascorbate share a common transport system. This may have important implications concerning the vascular pathology associated with diabetes mellitus.

Animals↗
PubMed1981

[Modification of urinary pH through ascorbic acid].

The influence of orally administered ascorbic acid on the urinary pH of 10 healthy volunteers and 10 patients with infected urine was investigated. During a four-day period of investigation urinary pH and the concentration of ascorbic acid in the respective urines were measured five times a day. On the second and third day three times a dose of 2 g ascorbic acid was given, while the diet was under control all four days. A correlation between pH decrease and ascorbic acid concentration is only observed if the concentration of the latter is higher than 200 mg%. The mean decrease in urinary pH between days with ascorbic acid supply and days without is -0,16 pH units for the volunteers respectively -0,18 pH units for the patients. Therefore, vitamin C can not be recommended to lower the pH of alkaline urines.

Administration, Oral↗
PubMed2001

Regulation of cigarette smoke-induced cytochrome P4501A1 gene expression in osteogenic disorder Shionogi rat liver and in lung by large ascorbic acid dose.

The effects of a large ascorbic acid dose on cytochrome P4501A1 gene expression induced by cigarette smoke exposure was studied in Osteogenic Disorder Shionogi rats, which lack ascorbic acid biosynthesis. The rats were divided into four groups and were administered either a minimal amount (4 mg/day, 4S and 4C) or a large amount (40 mg/day, 40S and 40C) of ascorbic acid. The 4S group and 40S group were daily exposed to cigarette smoke for 2 hours, while the 4C group and 40C group were not. At the end of the 25-day experiment, the rats were killed. The cytochrome P4501A1 mRNA level both in the liver and lung was measured by a competitive reverse transcription-polymerase chain reaction method. When a minimal amount of ascorbic acid was administered, the cytochrome P4501A1 mRNA increased in the liver of the cigarette smoke-exposed group (4S) compared with the control group (4C). On the other hand, when a large amount of ascorbic acid was administered, this increase was not observed in the cigarette smoke-induced group (40S) in liver. On the other hand, in lung, an increased mRNA level in 4S group was not decreased by large ascorbic acid administration (40S). This is the first direct mRNA-level evidence of the effects of a large ascorbic acid dose on the gene expression stimulated by cigarette smoke.

Animals↗
PubMed1996

Endocrine regulation of ascorbic acid transport and secretion in luteal cells.

Luteal ascorbic acid depletion by LH and prostaglandin (PG) F2 alpha is well known, but how such depletion occurs is not. We therefore investigated the nature and regulation of ascorbic acid uptake and depletion in the rat CL and luteal cells. In vivo studies showed that blockade of steroidogenesis by aminoglutethimide prevented ascorbate depletion by LH, but not PGF2 alpha. Also, the time course for half-maximal depletion of ascorbic acid in vivo in response to PGF2 alpha was extremely rapid (2-3 min) compared to that known for LH (60 min). Thus, ascorbate depletion by LH and PGF2 alpha appears to occur by different mechanisms. In luteal cells, ascorbate uptake was energy-, sodium-, and microfilament-dependent with a Michaelis constant (Km) of 33 microM, similar to that reported for other cells. In contrast to findings for other cells, PGF2 alpha was found to be a potent and rapid inhibitor of ascorbate uptake with a half-maximal inhibition (IC50) of about 5 nM in luteal cells. Ascorbate uptake was unaffected by LH, PGE2, glucose, bromo-cAMP, progesterone, phorbol ester, ionomycin, hydrogen peroxide (H2O2), or aminoglutethimide. Also novel was the finding that luteal cell secretion of ascorbic acid was rapidly and potently stimulated by PGF2 alpha (IC50 about 5 nM), an effect mimicked by LH, H2O2, generators of reactive oxygen, calcium ionophore, and cytochalasin B. Basal release of ascorbic acid was energy-dependent, as secretion was blocked by a mitochondrial uncoupler and lowered temperature. Phorbol ester, bromo-cAMP, progesterone, aminoglutethimide, and ouabain had no effect on ascorbic acid secretion in luteal cells. These findings indicate that the secretion of ascorbic acid induced by PGF2 alpha, and possibly LH, may be mediated by calcium, reactive oxygen, and cytoskeletal changes. The ability of PGF2 alpha to inhibit ascorbate transport and to stimulate secretion implicates these processes as the basis for the rapid depletion of ascorbic acid in the CL. Ascorbate depletion by LH is associated with stimulation of steroidogenesis and an increase in ascorbic acid secretion.

Aminoglutethimide↗
PubMed1995

The in vivo cytoprotection of ascorbic acid against ischemia/reoxygenation injury of rat liver.

The in vivo effects of ascorbic acid on the reoxygenated liver tissue were examined, with regard to the following effects: (i) the effects of scavenging radicals and/or reducing peroxidative reactions, and (ii) the effects of the chelation with low-molecular-weight iron and increasing its reactivity (radical production). Ascorbic acid is one of the water-soluble vitamins known to have various physiological effects involving both chelating and reducing properties at once. Lipid peroxidation of the reoxygenated liver tissue estimated by the production of TBARS (thiobarbituric acid-reactive substance) and LPO (lipid hydroperoxides) was suppressed effectively by the preischemic intraperitoneal administration of ascorbic acid. Ascorbic acid also showed this anti-oxidant effect in a dose-dependent manner. The analysis of the levels of ascorbic acid and glutathione of the liver tissue revealed that ascorbic acid works as an anti-oxidant probably by being oxydized finally to dehydroascorbic acid just after the reoxygenation. The latter was reduced to ascorbic acid again, coupled with the conversion of GSH to GSSG in the postischemic time course. The predominant effect of ascorbic acid on the reoxygenated liver tissue seems to be caused by the scavenging radicals and/or reducing peroxidative reactions, rather than by chelating iron and increasing its reactivity (radical production). Cellular integrity (estimated by the release of GOT, GPT, and LDH) and the energy state of the postischemic liver tissue (estimated by the tissue ATP level) were also well preserved by the administration of ascorbic acid.

Adenosine Triphosphate↗
PubMed1999

L-Ascorbic acid potentiates nitric oxide synthesis in endothelial cells.

Ascorbic acid has been shown to enhance impaired endothelium-dependent vasodilation in patients with atherosclerosis by a mechanism that is thought to involve protection of nitric oxide (NO) from inactivation by free oxygen radicals. The present study in human endothelial cells from umbilical veins and coronary arteries investigates whether L-ascorbic acid additionally affects cellular NO synthesis. Endothelial cells were incubated for 24 h with 0.1-100 microM ascorbic acid and were subsequently stimulated for 15 min with ionomycin (2 microM) or thrombin (1 unit/ml) in the absence of extracellular ascorbate. Ascorbate pretreatment led to a 3-fold increase of the cellular production of NO measured as the formation of its co-product citrulline and as the accumulation of its effector molecule cGMP. The effect was saturated at 100 microM and followed a similar kinetics as seen for the uptake of ascorbate into the cells. The investigation of the precursor molecule L-gulonolactone and of different ascorbic acid derivatives suggests that the enediol structure of ascorbate is essential for its effect on NO synthesis. Ascorbic acid did not induce the expression of the NO synthase (NOS) protein nor enhance the uptake of the NOS substrate L-arginine into endothelial cells. The ascorbic acid effect was minimal when the citrulline formation was measured in cell lysates from ascorbate-pretreated cells in the presence of known cofactors for NOS activity. However, when the cofactor tetrahydrobiopterin was omitted from the assay, a similar potentiating effect of ascorbate pretreatment as seen in intact cells was demonstrated, suggesting that ascorbic acid may either enhance the availability of tetrahydrobiopterin or increase its affinity for the endothelial NOS. Our data suggest that intracellular ascorbic acid enhances NO synthesis in endothelial cells and that this may explain, in part, the beneficial vascular effects of ascorbic acid.

Antioxidants↗
PubMed1976

Hypercholesterolemia due to ascorbic acid.

Rats fed a purified diet containing ascorbic acid developed hypercholesterolemia. Because rats do not require exogenous ascorbic acid, they may be comparable to humans who supplement their diets with ascorbic acid in capsular form. The amount of ascorbic acid in this experiment was equivalent to 82 to 630 mg of capsular ascorbic acid ingested by an average man and was well below the amount ingested by those in search of respiratory benefit. The data are consonant with those on humans consuming controlled diets.

Animals↗
PubMed1995

Partial characterization of a unique 84-kDa polypeptide stimulated by ascorbic acid in skin fibroblasts.

Ascorbic acid stimulated the synthesis of a noncollagenous 84 kDa polypeptide by up to 3.5-fold in primary cultures of chick skin fibroblasts. Stimulation was observed with concentrations ranging 0.4 to 50 micrograms/ml and was dose-dependent within the concentrations up to 10 micrograms/ml during 24 h treatment under conditions in which procollagen synthesis was increased. This protein was found to be translated with a molecular size of 84 kDa in an in vitro cell-free translation experiment, indicating that the 84 kDa polypeptide was a primary translate. The stimulation was accompanied by a 1.7-fold increase in translational activity of the mRNA for this polypeptide. Its synthesis rapidly reduced when the cells were serially passaged until the third subcultivation, whereas procollagen synthesis remained essentially constant. These results indicate that the stimulation of this unique 84 kDa polypeptide by ascorbic acid was modulated at least in part at a translational level and its synthesis appears to be related to in vitro cellular aging.

Animals↗
PubMed1996

Comparison of the response of serum ceruloplasmin and cholesterol, and of tissue ascorbic acid, metallothionein, and nonprotein sulfhydryl in rats to the dietary level of cystine and cysteine.

The effects were compared of the addition of graded levels of L-cystine and of L-cysteine (0.3, 3, or 5%) to a 10% casein diet on several metabolic parameters in rats. The growth-promoting effect of cystine was equivalent to that of cysteine. Supplementation of these two amino acids elevated serum cholesterol, liver ascorbic acid, liver nonprotein sulfhydryl (SH) and kidney metallothionein, and reduced the activity of serum ceruloplasmin. The responses of serum cholesterol, liver nonprotein SH, and serum ceruloplasmin to cystine were greater than of those to cysteine. When the basal diet was supplemented with 0.3% of these amino acids, the elevation of liver ascorbic acid by cystine supplementation was less than that by cysteine supplementation. However, when supplemented with 5% of these amino acids, the elevation of liver ascorbic acid by cystine was greater than that by cysteine. There was no difference in the influence of cystine and cysteine on kidney metallothionein. This study demonstrates that dietary cystine and cysteine had the same influence on growth, but had a differential influence on such metabolic parameters as liver nonprotein SH, serum ceruloplasmin, serum cholesterol, and tissue ascorbic acid.

Animals↗
PubMed2004

Glassy carbon electrode modified with gold nanoparticles and DNA for the simultaneous determination of uric acid and norepinephrine under coexistence of ascorbic acid.

A novel biochemical sensor was assembled on a glass carbon electrode by a electrodeposition process. Gold nanoparticles were deposited by potential +1.5 V on the glass carbon electrode. CT-DNA was deposited by potential +1.5 V on the gold nanoparticles array electrode. The properties of the modified electrode were characterized by electrochemical impedance spectroscopy (EIS), X-ray photoelectron spectroscopy (XPS) and atomic force microscopy (AFM). Our results showed that gold nanoparticles increase the DNA membrane capacitance and reduce the membrane resistance. This modified electrode can selectively determine uric acid and norepinephrine in the presence of a larger amount of ascorbic acid. The fabricated electrode showed good sensitivity, reproducibility, and stability.

Ascorbic Acid↗