Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ASCORBIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 991 records · Page 55Linked to original sources
PubMed2006

An isocratic HPLC method for the simultaneous determination of novel stable lipophilic ascorbic acid derivatives and their metabolites.

2-O-alpha-D-glucopyranosyl-6-O-hexadecanoyl-L-ascorbic acid (6-sPalm-AA-2G), a novel stable lipophilic ascorbic acid derivative, was hydrolyzed to 2-O-alpha-D-glucopyranosyl-L-ascorbic acid (AA-2G), ascorbyl 6-palmitate (6-sPalm-AA) and ascorbic acid (AA) with alpha-glucosidase and lipase. An HPLC method for the simultaneous determination of AA, AA-2G, 6-sPalm-AA and 6-sPalm-AA-2G was developed using a cyanopropyl column with an isocratic solution of methanol-phosphate buffer (pH 2.1) (65:35, v/v) containing 20mg/l of dithiothreitol at a detection wavelength of 240 nm. The calibration curves were found to be linear in the range of 10-200 microM. Linear regression analysis of the data demonstrated the efficacy of the method in terms of precision and accuracy. This method was satisfactorily applied to the determination of 6-sPalm-AA-2G and its three metabolites in a 6-sPalm-AA-2G solution treated with purified enzymes or a small intestine post-mitochondrial supernatant and to the separation of novel stable lipophilic AA derivatives other than 6-sPalm-AA-2G and their metabolites. AA, AA-2G and other well-known stable AA derivatives, ascorbic acid 2-phosphate and ascorbic acid 2-sulfate, were also separated under the same conditions. The results show that the procedure is rapid and simple and that it can be employed for in vitro metabolic analysis of various AA derivatives.

Animals↗
PubMed1988

Ascorbic acid and Mg-ATP co-regulate dopamine beta-monooxygenase activity in intact chromaffin granules.

Ascorbic acid and Mg-ATP were found to regulate norepinephrine biosynthesis in intact secretory vesicles synergistically and specifically, using the model system of isolated bovine chromaffin granules. Dopamine uptake into chromaffin granules was shown to be unrelated to the presence of Mg-ATP and ascorbic acid at external dopamine concentrations of 7.5 and 10 mM. Under these conditions of dopamine uptake, norepinephrine biosynthesis was enhanced 5-6-fold by Mg-ATP and ascorbic acid compared to control experiments with dopamine only. Furthermore, norepinephrine formation was enhanced approximately 3-fold by ascorbic acid and Mg-ATP together compared to norepinephrine formation in granules incubated with either substance alone. The action of Mg-ATP and ascorbic acid together was synergistic and independent of dopamine content of chromaffin granules as well as of dopamine uptake. The apparent Km of norepinephrine formation for external ascorbic acid was 376 microM and for external Mg-ATP was 132 microM, consistent with the larger amounts of cytosolic ascorbic acid and ATP that are available to chromaffin granules. Other physiologic reducing agents were not able to increase norepinephrine biosynthesis in the presence or absence of Mg-ATP. In addition, maximum enhancement of norepinephrine biosynthesis occurred only with the nucleotide ATP and the cation magnesium. The mechanism of the effect of ascorbic acid and Mg-ATP on norepinephrine biosynthesis was investigated and appeared to be independent of a positive membrane potential. The effect was also not mediated by direct action of ADP, ATP, or magnesium on the activity of soluble or particulate dopamine beta-monooxygenase. These data indicate that Mg-ATP and ascorbic acid specifically and synergistically co-regulate dopamine beta-monooxygenase activity in intact chromaffin granules, independent of substrate uptake. Although the mechanism is not known, the data are consistent with the possibility that the chromaffin granule ATPase mediates these effects.

Adenosine Triphosphate↗
PubMed1984

Cerebrospinal fluid ascorbic acid levels in neurological disorders.

The ascorbic acid/dehydroascorbic acid system was analyzed in the cerebrospinal fluid (CSF) of 41 patients with different neurological disorders. The chi-square test of covariance analysis revealed in this sample significant differences in the CSF levels of total ascorbic acid when patients were classified by diagnostic categories. The population analyzed contained a group of 18 patients (back pain/sciatica group) in whom no overt neurological abnormalities were disclosed upon evaluation. Taking the CSF levels of total ascorbic acid and dehydroascorbic acid in these patients as the reference (3.57 +/- 0.87 (SD)/100 ml and 0.53 +/- 0.19 mg/100 ml, respectively), it was found that head-traumatized patients showed a significant reduction in the concentration of total ascorbic acid in the CSF. CSF ascorbic acid levels were also significantly lower in patients with increased intracranial pressure (noninfected hydrocephalus group) and in patients with cerebral tumors. Although the CSF concentration of dehydroascorbic acid did not correspondingly increase over the reference values in these three groups of patients, the tendency existed for dehydroascorbic acid to represent in them a higher percentage of total ascorbic acid. After examining different alternatives, it is concluded that the hypothesis of free radical damage to the central nervous system after certain types of injury (trauma, ischemia, and tumors) may provide a satisfactory explanation of our findings. A rationale for the use of vitamin C in the management of some neurological patients is also derived from this work.

Adolescent↗
PubMed2000

Luteinizing hormone depletes ascorbic acid in preovulatory follicles.

OBJECTIVE: The objective of the present studies was to determine whether luteinizing hormone (LH) depletes ascorbic acid in the preovulatory follicle. DESIGN: Controlled, prospective experimental study. SETTING: University-based research center. ANIMAL(S): Sprague-Dawley female rats. INTERVENTION(S): Follicular growth and ovulation were induced in immature rats by gonadotropin treatment. MAIN OUTCOME MEASURE(S): Analysis of ovary, follicle, and oocyte levels of ascorbic acid by colorimetric analysis and high-pressure liquid chromatography. RESULT(S): Ovarian ascorbic acid was maximally depleted (50%) within 2 h of LH treatment and was sustained for 8 h. Follicle ascorbic acid levels were unchanged 1 h after LH injection but were significantly reduced within 2 h (40%). Incubation of isolated preovulatory follicles for 3 h with hCG or with menadione (a generator of oxygen radicals) reduced ascorbic acid levels. Isolation of cumulus-enclosed or denuded oocytes depleted ascorbic acid to undetectable levels, but follicular ascorbic acid levels were only moderately depleted by isolation and incubation. Accumulation of ascorbic acid by oocytes was significantly enhanced by the presence of intact cumulus cells. CONCLUSION(S): Elevation of LH and the production of oxygen radicals deplete ascorbic acid in the preovulatory follicle.

Animals↗
PubMed2002

Modification of ascorbic acid using transglycosylation activity of Bacillus stearothermophilus maltogenic amylase to enhance its oxidative stability.

Ascorbic acid (1), a natural antioxidant, was modified by employing transglycosylation activity of Bacillus stearothermophilus maltogenic amylase with maltotriose and acarbose as donor molecules to enhance its oxidative stability. The transglycosylation reaction with maltotriose as donor created mono- and di-glycosyl transfer products with an alpha-(1,6)-glycosidic linkage. In addition, two acarviosine-glucosyl transfer products were generated when transglycosylation was performed with acarbose as a donor. All transfer products were observed by TLC and HPLC, and purified by Q-sepharose anion exchange and Biogel P-2 gel permeation chromatographies. LC/MS and (13)C NMR analyses revealed that the structures of the transfer products were 6-O-alpha-D-glucosyl- (2) and 6-O-alpha-D-maltosyl-ascorbic acids (3) in the reaction of maltotriose, and 6-O-alpha-acarviosine-D-glucosyl- (4) and 2-O-alpha-acarviosine-D-glucosyl ascorbic acids (5) in the reaction of acarbose. The stability of the transglycosylated ascorbic acid derivatives was greatly enhanced against oxidation by Cu(2+) ion and ascorbate oxidase. Among them, compound 3 proved to be the most stable against in vitro oxidation. The antioxidant effects of glycosyl-derivatives of ascorbic acid on the lipid oxidation in cooked chicken breast meat patties indicated that they had antioxidant activities similar to that of ascorbic acid. It is suggested that the transglycosylated ascorbic acids can possibly be applied as effective antioxidants with improved stability in food, cosmetic, and other applications.

Acarbose↗
PubMed1987

Electrochemical evaluation of the interaction between ascorbic acid and the cardiotonic drug RS-82856.

The solution phase interaction between ascorbic acid and the cardiotonic drug N-cyclohexyl-N-methyl-4(7-oxy 1,2,3,5-tetrahydroimidazol[2,1-b] quinazolin-2-one butyramide (RS-82856) was evaluated using a differential pulse voltammetric technique. Shifts in the peak potential of ascorbic acid to higher energy as well as decreases in peak current values were monitored as a function of RS-82856 concentration. The electrochemical data were obtained under conditions where both the drug and the ascorbic acid concentrations exhibited linear relationships with peak current values. The methodology was extended to the study of two other structurally related phosphodiesterase inhibitors cilostamide and anagrelide. The complexation of these drugs with ascorbic acid were also characterized by decreases in the diffusion currents of ascorbic acid as well as by anodic shifts in the peak potential. The significance of these observations may be related to the inhibition of cyclic nucleotide phosphodiesterase activity by both the drugs tested and the ascorbic acid.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2002

Role of ascorbic acid in stratum corneum lipid models exposed to UV irradiation.

PURPOSE: The effects of ascorbic acid on Stratum corneum lipid models following ultraviolet irradiation were studied adding iron ions as transition metal catalysts. METHODS: Lipid peroxidation was quantified by the thiobarbituric acid assay. The qualitative changes were studied on a molecular level by mass spectrometry. To elucidate the nature of free radical involvement we carried out electron paramagnetic resonance studies. The influence of ascorbic acid on the concentration of hydroxyl radicals was examined using the spin trapping technique. Moreover, we checked the vitamin's ability to react with stable radicals. RESULTS: Ascorbic acid was found to have prooxidative effects in all lipid systems in a concentration dependent manner. The degradation products of ascorbic acid after its prooxidative action were detected. The concentration of the hydroxyl radicals in the Fenton assay was decreased by ascorbic acid. The quantification assay of 2,2-diphenyl-1-picrylhydrazyl hydrate showed reduced concentration levels of the stable radical caused by ascorbic acid. CONCLUSIONS: Considering human skin and its constant exposure to UV light and oxygen, an increased pool of iron ions in irradiated skin and the depletion of co-antioxidants, the administration of ascorbic acid in cosmetic formulations or in sunscreens could unfold adverse effects among the Stratum corneum lipids.

Ascorbic Acid↗
PubMed1983

Hydrocortisone inhibition of ascorbic acid transport by chromaffin cells.

Adrenal chromaffin cells have been found to accumulate ascorbic acid by a saturable high affinity mechanism that is inhibited by hydrocortisone. The rate of ascorbic acid transport into cells was linear for at least 1 h and had a Km of 103 microM, a value approaching the reported concentration of ascorbic acid in the adrenal vein during stress. The uptake process itself, representing net accumulation rather than exchange, was inhibited by 0 degrees C, lack of sodium, ouabain, and by dinitrophenol and iodoacetate. Hydrocortisone but not the inactive analogue hydrocortisone hemisuccinate was found to inhibit ascorbic acid uptake in a reversible manner, with an ID50 of 62 microM. This value was within the reported steroid concentration in the adrenal portal system during a significant stress. Both ascorbic acid and hydrocortisone are secreted from cortical cells during stress into the adrenal portal system and thus contact medullary chromaffin cells. We suggest that the control of ascorbic acid uptake by hydrocortisone indicates the existence of a heretofore unanticipated biochemical aspect of the adrenal stress response.

Ascorbic Acid↗
PubMed1995

Determination of ascorbic acid and dehydroascorbic acid in plasma by high-performance liquid chromatography with coulometric detection--are they reliable biomarkers of oxidative stress?

The concentrations of the hydrophilic antioxidants ascorbic acid and dehydroascorbic acid in plasma for some time have been considered possible biomarkers of oxidative stress. However, several problems are associated with the accurate measurement of these two compounds. We have developed and validated a selective and reproducible high-performance liquid chromatographic method for the quantification of ascorbic acid and dehydroascorbic acid in plasma. The method meets the requirements of a reliable routine analysis. The plasma samples are stabilized with 5 mM metaphosphoric acid, centrifugated at 4 degrees C before HPLC analysis. For ascorbic acid analysis, the sample pH is adjusted to 2.6, whereas for total ascorbic acid measurement dehydroascorbic acid is reduced to ascorbic acid using dithiothreitol for 5 min at pH 6.2 after which the sample pH is adjusted to 2.6. The samples are analyzed on a reversed-phase system using coulometric detection. Dehydroascorbic acid concentrations ae calculated by subtraction. Within- and between-day coefficients of variation for the complete assay were in the range of 4-8 and 3-6% for ascorbic acid and total ascorbic acid, respectively. The stability of ascorbic acid was monitored under various conditions including storage and the implications as well as the reliability of ascorbic acid as a biomarker are discussed.

Ascorbic Acid↗
PubMed1984

Stress-induced change in tissue levels of ascorbic acid and histamine in rats.

Effects of acute immobilization stress on the metabolism of ascorbic acid and histamine were studied in rats by determining changes in the tissue levels of these substances. Stress provoked a significant rise in the histamine levels of blood, stomach, kidney, lung and skin. The serum ascorbic acid level increased rapidly, whereas the amount of the vitamin in the lung and skin was reduced by stress. The hepatic ascorbic acid levels were modulated biphasically; there was a decrease within 15 minutes after the onset of the stress regimen, followed by an increase occurring during the next 15 minutes. There was a gradual decrease in the amount of ascorbic acid in the adrenal glands with a marked transient accumulation of corticosterone in the tissues. Administration of histamine caused an increase in the serum level of ascorbic acid, while it led to a transitory decrease in the hepatic level of the vitamin. These results suggest that the metabolism of ascorbic acid is modulated in rats suffering from stress. These changes in ascorbic acid metabolism seem to be closely associated with the stress-induced alteration of histamine metabolism.

Animals↗
PubMed1997

Ascorbic acid deficiency decreases the renal level of kidney fatty acid-binding protein by lowering the alpha2u-globulin gene expression in liver in scurvy-prone ODS rats.

The evidence for the role of ascorbic acid in gene expression or protein synthesis in vivo is limited. To investigate this role of ascorbic acid, we surveyed proteins whose tissue levels are changed by ascorbic acid deficiency by using ODS rats with a hereditary defect in ascorbic acid biosynthesis. Male ODS rats (7 wk old, body weight approximately 130 g) were fed a basal diet containing ascorbic acid (300 mg/kg diet) or an ascorbic acid-free diet for 14 d. Ascorbic acid deficiency decreased a renal protein with an apparent molecular mass of 17 kDa. The amino-terminal amino acid sequence of 16 residues of this 17-kDa protein was identical to a kidney fatty acid-binding protein known to be generated by proteolytic degradation of alpha2u-globulin, a major urinary protein of adult male rats. alpha2u-Globulin is synthesized in liver, secreted into blood and excreted into urine, but partially reabsorbed by renal proximal tubules. It exists in kidney in a proteolytically modified form. Ascorbic acid deficiency lowered the renal level of kidney fatty acid-binding protein to 53% (P < 0.05) and lowered the serum level of alpha2u-globulin to 52% (P < 0.05) of the level of the control group, but did not affect the amount of alpha2u-globulin excreted into urine. The hepatic level of alpha2u-globulin mRNA of the ascorbic acid-deficient rats was significantly lower (30%) than that of the control rats. These results suggest that in male ODS rats, ascorbic acid deficiency decreases the renal level of kidney fatty acid-binding protein by lowering alpha2u-globulin gene expression in liver.

Alpha-Globulins↗
PubMed1980

The effect of ascorbic acid on the nature and production of collagen and elastin by rat smooth-muscle cells.

1. The effects of various concentrations of ascorbic acid on the quality and quantity of the insoluble extracellular matrices produced by two strains of cultured rat smooth-muscle cells were studied. 2. Ascorbic acid was necessary for the appearance of insoluble collagen in the extracellular matrix. 3. Secretion of soluble collagen continued in the absence of ascorbic acid, but this soluble collagen was markedly underhydroxylated. 4. The amount of insoluble collagen present in the matrix was directly related to the ascorbic acid concentration. 5. The insoluble collagen that appeared in the matrix under conditions where ascorbic acid was limiting was no more than 7% underhydroxylated. 6. In contrast, the amount of insoluble elastin produced was inversely proportional to the ascorbic acid concentration. 7. The elastin produced in the absence of ascorbic acid had the expected amino acid composition, but hydroxyproline was absent. 8. The hydroxyproline content of elastin was also directly dependent on the ascorbic acid concentration. 9. Ascorbic acid had variable effects on the quantity of glycoprotein(s) present in the matrix. 10. The appearance of insoluble collagen in the extracellular matrices produced by cultured human fibroblasts and calf endothelial cells was also completely dependent on the presence of ascorbic acid.

Amino Acids↗
PubMed1985

Decreased brain levels of ascorbic acid in rats exposed to high pressures.

Ascorbic acid was repeatedly monitored in vivo in the striatum of rats subjected to an increasing pressure (100 bar/h compression rate; 0.5 bar partial pressure of O2 He-O2 mixture, up to 120 bar (121 ATA), to which they were exposed for 1 h. Measurements were performed using differential pulse voltammetry and carbon fiber microelectrodes. High-pressure-exposed animals exhibited a dramatic decrease of striatal ascorbic acid. This decrease was detectable at pressures as low as 50 bar and significant over 70 bar (75% of the control level), and the lower level (25% of the control level) was reached shortly after the end of the compression period. This finding is discussed in relation to the physiological role of ascorbic acid in the brain, e.g., its participation in the defense mechanisms against reactive O2 intermediates and lipid peroxidations and its probable involvement in neurotransmission. Emphasis is placed on a possible increased sensitivity of nerve cell membrane phospholipids to peroxidation under stressful hyperbaric situations.

Animals↗
PubMed1992

Dietary ascorbic acid depresses plasma and low density lipoprotein lipid peroxidation in genetically scorbutic rats.

The effects of dietary ascorbic acid on plasma lipoprotein and liver lipid peroxide concentrations were examined using ODS od/od rats with a genetic defect in the ability to synthesize ascorbic acid. ODS od/od rats were fed purified diets supplemented with 0 to 300 mg ascorbic acid/kg diet for 21 d. An ascorbic acid-free diet induced body weight loss, depleted ascorbic acid in the plasma and increased thiobarbituric acid-reactive substances in the plasma and liver as compared with rats fed ascorbic acid supplemented diets and with normal ODS +/+ rats fed the ascorbic acid-free diet. Increasing ascorbic acid concentration in the diet inhibited the development of these ascorbic acid deficiency symptoms in a dose-dependent manner. The dietary requirement of ascorbic acid to maintain normal body weight gain and plasma lipid peroxide concentrations was approximately 150 mg ascorbic acid/kg diet. On the other hand, even 300 mg ascorbic acid/kg diet was insufficient to maintain a hepatic concentration of ascorbic acid comparable to that in the liver of ODS +/+ rats. The lipid peroxide concentration in plasma LDL and liver was significantly elevated in ODS od/od rats fed the ascorbic acid-free diet. Supplementing the diet with 300 mg ascorbic acid/kg kept those concentrations within the normal ranges seen in the ODS +/+ rats.

Animals↗
PubMed1988

Effect of polychlorinated biphenyls on lipids and ascorbic acid metabolism in streptozotocin-induced diabetic rats.

Metabolic changes in lipids, ascorbic acid, and hepatic microsomal cytochrome P-450 by feeding polychlorinated biphenyls (PCB) were investigated in streptozotocin-induced diabetic rats. Streptozotocin (STZ, 60 mg/kg body weight) was injected in Wistar male rats intraperitoneally. Diabetic and non-diabetic rats were fed ad libitum a 20% casein-based control diet or a PCB-containing diet (200 mg/kg diet) for 9 days. Body weight decreased significantly in STZ-induced diabetic rats with or without PCB (groups PD and D, respectively). In rats of group D, urinary ascorbic acid excretion was 15 times higher than that in non-diabetic rats fed a control diet (group C). Dietary PCB caused 30-fold higher urinary ascorbic acid excretion in non-diabetic rats (group P) than that in group C. In group PD, urinary ascorbic acid was nearly 60 times higher than that in group C. Ascorbic acid in liver and kidney was significantly lower in group D than in group C, and it was significantly lower in group PD than in group P. Liver microsomal cytochrome P-450 and b5 were both increased by dietary PCB in group P. Addition increase in these enzymes was observed in diabetic rats by PCB. Serum total cholesterol was 1.8 times higher in group P than in group C. Further increase in serum total cholesterol was observed in group PD. These data suggest that metabolic changes in lipids and ascorbic acid induced by the dietary xenobiotic were magnified in STZ-induced diabetic rats.

Animals↗
PubMed2002

[Determination of ascorbic acid by suppressed chemiluminescence].

This paper describes a method for determining ascorbic acid by the suppression of DTMC-H2O2 chemiluminescence. Various factors affecting the chemiluminescence determination of ascorbic acid were examined. Under the optimal conditions (1.2 x 10(-4) mol.L-1 of DTMC, 5.0 x 10(-5) mol.L-1 of H2O2, and pH 11.4 Na2HPO4-NaOH), the quenching of the chemiluminescent intensity was proportional to the concentration of ascorbic acid in the range of 1.0 x 10(-7)-8.0 x 10(-6) mol.L-1, and the detection limit was 8.0 x 10(-8) mol.L-1 (S/N = 3). The RSD was 4.6% for 1.0 x 10(-6) mol.L-1 of ascorbic acid (n = 10). The selectivity of this method was high and no making agent required. The proposed method has been applied to the determination of ascorbic acid in real samples. The obtained results were in agreement with those by CuSO4-KI titration.

Ascorbic Acid↗
PubMed1985

Metabolism of L-ascorbic acid in the prostate of normal and scorbutic guinea pigs.

Guinea pig prostate was found to actively participate in the biosynthesis and catabolism of ascorbic acid. The key ascorbic acid biosynthetic enzyme L-gulono-gamma-lactone oxidase and the other two lactonases were found to be present in guinea pig prostate. The activities of dehydroascorbatase and diketogulonate decarboxylase, the enzymes for ascorbic acid degradation, were also detected in guinea pig prostate. Male guinea pigs kept under scorbutic condition for 7, 14, 21 and 28 days, were examined for prostatic metabolism of ascorbic acid. A significant but gradual decrease in the concentration of L-ascorbic acid was observed in prostate, total blood and leukocytes with the progression of scorbutic condition. There was an appreciable decrease in the rate of lipid peroxidation under the scorbutic condition. In the tissue fraction of scorbutic guinea pigs, the activities of biosynthesizing enzymes, measured in vitro, under optimum conditions were found to be higher with no significant alterations in the catabolizing enzymes. The implications of these findings are discussed in this paper.

Animals↗