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PubMed1991

Comparison of absorption of erythorbic acid and ascorbic acid in guinea pig small intestine.

Both the ascorbic acid (AsA) and erythorbic acid (ErA) absorption in the small intestine of guinea pigs were determined by the perfusion of the small intestine using isotonic phosphate buffer recycled in situ. The absorption rate of AsA in the small intestine of guinea pigs was higher than that of ErA; however, Km of AsA absorption was lower than that of ErA in normal guinea pigs. In AsA-deficient guinea pigs, the absorption rates of both AsA and ErA were higher than those in normal ones. The absorption of AsA and ErA in the small intestine of guinea pigs was inhibited by ouabain. Furthermore, AsA and ErA inhibited each other's absorption. Based on the results, the net amount of the absorbed ErA in the small intestine may be lower than that of AsA, and ErA absorption mechanism seemed to be similar to that of AsA. The absorption rate of both AsA and ErA in the small intestine of guinea pig might be dependent on the AsA level in the tissues.

Animals↗
PubMed2004

Lipoic acid and ascorbic acid affect plasma free amino acids selectively in the teleost fish pacu (Piaractus mesopotamicus).

Most studies on the antioxidants, lipoic acid (LA) and ascorbic acid (AA), focused on species that, unlike teleost fish, are not scurvy-prone, and are able to synthesize AA. The antioxidant properties of LA may make it useful in aquaculture nutrition, but several effects must first be investigated, and we address here plasma free amino acids (FAA). In mammals, LA and AA in high doses were claimed to alter plasma FAA profile; to our knowledge, however, no data are available in fish. We therefore studied the effects of dietary LA and AA on plasma FAA in the South American teleost fish pacu, which is being used increasingly in aquaculture. LA treatment decreased concentrations of 18 of 23 individual FAA; specifically, dispensable and total FAA were significantly affected. Ornithine was elevated (+26%) in LA-treated fish and significantly decreased ratios of plasma [Arg]/[Orn] and other individual [FAA]/[Orn] were observed. LA and AA both affected sulfur FAA concentrations. Plasma cystine levels were significantly increased in the LA-supplemented groups. AA had little effect on most amino acids, and no interaction with LA was detected. AA supplementation did, however, significantly lower taurine (-42%) and cystathionine (-31%) levels in plasma. No effect on the branched chain:aromatic amino acid ratios was observed. The data indicate that at the dietary level studied, LA and AA independently affect selected plasma FAA in pacu, and suggest that any use of LA in particular as a dietary supplement should take into account an altered plasma FAA profile.

Amino Acids↗
PubMed2006

Ferulic acid with ascorbic acid synergistically extenuates the mitochondrial dysfunction during beta-adrenergic catecholamine induced cardiotoxicity in rats.

Disruption of mitochondria and free radical mediated tissue injury have been reported during cardiotoxicity induced by isoproterenol (ISO), a beta-adrenergic catecholamine. The present study was designed to investigate the effect of the combination of ferulic acid (FA) and ascorbic acid (AA) on the mitochondrial damage in ISO induced cardiotoxicity. Induction of rats with ISO (150 mg/kg b.wt., i.p.) for 2 days resulted in a significant decrease in the activities of respiratory chain enzymes (NADH dehydrogenase and cytochrome c-oxidase), tricarboxylic acid cycle enzymes (isocitrate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, alpha-ketoglutarate dehydrogenase), mitochondrial antioxidants (GPx, GST, SOD, CAT, GSH), cytochromes (b, c, c1, aa3) and in the level of mitochondrial phospholipids. A marked elevation in mitochondrial lipid peroxidation, mitochondrial levels of cholesterol, triglycerides and free fatty acids were also observed in ISO intoxicated rats. Pre-co-treatment with the combination of FA (20 mg/kg b.wt.) and AA (80 mg/kg b.wt.) orally for 6 days significantly enhanced the attenuation of these functional abnormalities and restored normal mitochondrial function when compared to individual drug treated groups. Mitigation of ISO induced biochemical and morphological changes in mitochondria were more pronounced with a combination of FA and AA rather than the individual drug treated groups. Transmission electron microscopic observations also correlated with these biochemical parameters. Hence, these findings demonstrate the synergistic ameliorative potential of FA and AA on mitochondrial function during beta-adrenergic catecholamine induced cardiotoxicity and associated oxidative stress in rats.

Adrenergic beta-Agonists↗
PubMed2002

Interfering with nitric oxide measurements. 4,5-diaminofluorescein reacts with dehydroascorbic acid and ascorbic acid.

4,5-Diaminofluorescein (DAF-2) is widely used for detection and imaging of NO based on its sensitivity, noncytotoxicity, and specificity. In the presence of oxygen, NO and NO-related reactive nitrogen species nitrosate 4,5-diaminofluorescein to yield the highly fluorescent DAF-2 triazole (DAF-2T). However, as reported here, the DAF-2 reaction to form a fluorescent product is not specific to NO because it reacts with dehydroascorbic acid (DHA) and ascorbic acid (AA) to generate new compounds that have fluorescence emission profiles similar to that of DAF-2T. When DHA is present, the formation of DAF-2T is attenuated because the DHA competes for DAF-2, whereas AA decreases the nitrosation of DAF-2 to a larger extent, possibly because of additional reducing activity that affects the amount of available N(2)O(3) from the NO. The reaction products of DAF-2 with DHA and AA have been characterized using capillary electrophoresis with laser-induced fluorescence detection and electrospray mass spectrometry. The reactions of DAF-2 with DHA and AA are particularly significant because DHA and AA often colocalize with nitric-oxide synthase in the central nervous, cardiovascular, and immune systems, indicating the importance of understanding this chemistry.

Animals↗
PubMedDate not supplied

Stabilization of (90)y-labeled DOTA-biomolecule conjugates using gentisic acid and ascorbic acid.

Radiolytic degradation of radiolabeled compounds is a major challenge for the development of new therapeutic radiopharmaceuticals. The goal of this study is to explore the factors influencing the solution stability of a (90)Y-labeled DOTA-peptide conjugate (RP697), including the amount of total activity, the activity concentration, the stabilizer concentration, and the storage temperature. In general, the rate of radiolytic decomposition of RP697 is much slower at the lower activity concentration (<4 mCi/mL) than that at the higher concentration (>10 mCi/mL). RP697 remains relatively stable at the 20 mCi level and room temperature while it decomposes rapidly at the 100 mCi level under the same storage conditions. Radical scavengers, such as gentisic acid (GA) and ascorbic acid (AA), were used in combination with the low temperature (-78 degrees C) to prevent the radiolytic decomposition of RP697. It was found that RP697 remains stable for at least 2 half-lives of (90)Y when GA or AA (10 mg for 20 mCi of (90)Y) is used as a stabilizer when the radiopharmaceutical composition is stored at -78 degrees C. The stabilizer (GA and AA) can be added into the formulation either before or after radiolabeling. The post-labeling approach is particularly useful when the use of a large amount of the stabilizer interferes with the radiolabeling. The radiopharmaceutical composition developed in this study can also apply to other (90)Y-labeled DOTA-biomolecule conjugates. The amount of the stabilizer used in the radiopharmaceutical composition and storage temperature should be adjusted according to the sensitivity of the radiolabeled DOTA-biomolecule conjugate toward radiolytic decomposition.

Ascorbic Acid↗
PubMed2001

Covalent modification of glassy carbon electrode with glutamic acid for simultaneous determination of uric acid and ascorbic acid.

A novel covalently modified glassy carbon electrode with glutamic acid has been fabricated via an electrochemical oxidation procedure and was applied to the catalytic oxidation of uric acid (UA) and ascorbic acid (AA), reducing the overpotentials by about 0.2 V and 0.3 V, respectively. Based on its strong catalytic function toward the oxidation of UA and AA, the modified electrode resolved the overlapping voltammetric response of UA and AA into two well-defined voltammetric peaks with both cyclic voltammetry (CV) and differential pulse voltammetry (DPV), which can be used for the simultaneous determination of these species in a mixture. The catalytic peak current obtained from DPV was linearly dependent on the UA and AA concentration in the range 2 x 10(-6)-4 x 10(-4) mol L-1 and 1.0 x 10(-6)-4 x 10(-4) mol L-1 with correlation coefficients of 0.996 and 0.997, respectively. The detection limits (3 delta) for UA and AA were 1.1 x 10(-6) mol L-1 and 9.2 x 10(-7) mol L-1, respectively. The modified electrode shows good sensitivity, selectivity and stability, and has been applied to the determination of UA and AA simultaneously in human urine samples with satisfactory results.

Ascorbic Acid↗
PubMed2006

Synergistic salubrious effect of ferulic acid and ascorbic acid on membrane-bound phosphatases and lysosomal hydrolases during experimental myocardial infarction in rats.

Altered membrane integrity has been suggested as a major factor in the development of cellular injury during myocardial necrosis. The present study was designed to investigate the effect of the combination of ferulic acid (FA) and ascorbic acid (AA) on lysosomal hydrolases and membrane-bound phosphatases during isoproterenol (ISO) induced myocardial necrosis in rats. Induction of rats with 1SO (150 mg/kg b.wt, i.p.) for 2 days resulted in a significant increase in the activities of lysosomal hydrolases (beta-D-glucuronidase, beta-D-galactosidase, beta-D-N-acetylglucosaminidase, acid phosphatase and cathepsin-D) in the heart and serum. A significant increase in plasma lactate level, cardiac levels of sodium, calcium and a decrease in cardiac level of potassium was also observed, which was paralleled by abnormal activities of membrane-bound phosphatases (Na(+)-K(+) ATPase, Ca(2+) ATPase and Mg(2+) ATPase) in the heart of ISO-administered rats. Pre-co-treatment with the combination of FA (20 mg/kg b.wt) and AA (80 mg/kg b.wt) orally for 6 days significantly attenuated these abnormalities and restored the levels to near normalcy when compared to individual drug treated groups. The combination of FA and AA preserved the membrane integrity by mitigating the oxidative stress and associated cellular damage more effectively when compared to individual treatment groups. In our study, the protection conferred by FA and AA might be through the nitric oxide pathway and by their ability of quenching free radicals. In conclusion, these findings indicate the synergistic modulation of lysosomal hydrolases and membrane phosphatases by the combination of FA and AA.

Animals↗
PubMed1986

The tissue distribution of L-ascorbic acid and dehydro-L-ascorbic acid in the guinea pigs injected intravenously with dehydro-L-ascorbic acid.

The tissue distribution of L-ascorbic acid (AsA) and dehydro-L-ascorbic acid (DAsA) in guinea pigs injected with DAsA intravenously was examined using high-performance liquid chromatography. DAsA injected into guinea pigs fed normal diets containing AsA (control group) was readily taken into erythrocytes, and AsA contents of plasma and other tissues rapidly increased after DAsA injection. In animals fed vitamin C-deficient diets, DAsA was also detected in erythrocytes; however, the increase of AsA in their tissues was considerably less than that of control group. From these results, it was suggested that utilization of DAsA as AsA in vitamin C-deficient guinea pigs was less than that of control animals, and the reduction mechanism of DAsA to AsA in vitamin C-deficient guinea pigs may have differed from that of control groups.

Administration, Oral↗
PubMed1984

Plasma ascorbic acid concentration following ascorbic acid loading in chicks.

Three trials were conducted to determine the changes in plasma ascorbic acid (AA) associated with varying levels and duration of supplemental AA. In Trial 1, supplemental AA was provided in the drinking water at 0, 5, 25, 50, 100, 250, 500, 1000, and 2000 micrograms/ml (ppm). Plasma AA concentrations were significantly elevated in chicks receiving 250 ppm AA or greater. In Trial 2, plasma AA concentrations increased significantly within 4 hr of supplementation in chicks receiving 1000 ppm AA. Statistically, maximum AA values occurred some 8 hr following the initiation of supplementation. Removal of the supplemented water resulted in rapid declines in plasma AA in Trial 3. Plasma AA values significantly higher than controls were maintained 16 hr after the removal of the supplemental water. Values returned to those of controls within 20 hr.

Animals↗
PubMed1986

Response of lingual ascorbic acid test and salivary ascorbate levels to changes in ascorbic acid intake.

This study sought to determine whether the lingual ascorbic acid test (LAAT) and measurement of salivary ascorbate reflect plasma and leukocyte ascorbate levels during controlled periods of ascorbic acid depletion and supplementation. Eleven healthy non-smoking men, aged 19-28 years, ate a diet that was repeated every seven days and was adequate in all nutrients except ascorbic acid (AA). This basal diet, which provided less than 5 mg of AA per day, was supplemented with 60 mg of AA per day for two weeks, 0 mg (placebo) per day for four weeks, 600 mg per day for three weeks, and 0 mg per day for four weeks. Oral examinations, the lingual ascorbic acid test, and measurement of salivary, plasma, and leukocyte ascorbate concentrations were conducted throughout the study. Ascorbic acid concentrations in plasma and leukocytes responded rapidly to changes in vitamin C intake. LAAT-derived ascorbate values were unrelated to ascorbic acid intake and plasma and leukocyte ascorbate concentrations. Salivary ascorbate levels approached the lower limits of detection of the assay and remained constant throughout the investigation. Oral hygiene was consistently excellent, and no severe mucosal or periodontal changes were observed. It was concluded that lingual ascorbic acid test values and salivary ascorbate levels are not related to changes in ascorbic acid intake and are not consistent with plasma or leukocyte ascorbate concentrations.

2,6-Dichloroindophenol↗
PubMedDate not supplied

Leucocyte ascorbic acid concentration and plasma ascorbic acid levels in children with various infections.

In this study leucocyte ascorbic acid concentrations and plasma ascorbic acid levels were measured simultaneously and correlation between these two variables was sought in various bacterial and viral infections. A total of 258 patients were studied. The control group consisted of 21 healthy children in the same age group. Except for scarlet fever no significant differences were observed between the patients' leucocyte ascorbic acid levels during and after the infections and also no differences were observed in leucocyte ascorbic acid levels between control's and patient's. However plasma ascorbic acid values were significantly decreased during infection in all patients. During infection ascorbic acid is utilized rapidly, and our findings seem to indicate that there is transfer of ascorbic acid from plasma to leucocytes in order to keep the leucocyte ascorbic acid levels within normal limits.

Ascorbic Acid↗
PubMed2004

6-Bromo-6-deoxy-L-ascorbic acid: an ascorbate analog specific for Na+-dependent vitamin C transporter but not glucose transporter pathways.

Vitamin C intracellular accumulation is mediated by Na(+)-dependent vitamin C transporters SVCT1 and -2 and dehydroascorbic acid transporters GLUT1 and -3. It is unclear which pathways dominate in vivo. As a new step to resolve this issue, we identified and tested 6-bromo-6-deoxy-L-ascorbic acid as a specific candidate for SVCTs. In high performance liquid chromatography and electron paramagnetic resonance analyses, the reduced compounds ascorbic acid and 6-bromo-6-deoxy-L-ascorbic acid were similar. The oxidized products 6-bromo-6-deoxy dehydroascorbic acid (BrDHA) and dehydroascorbic acid (DHA) had comparable stabilities, based on reduction recoveries. Upon expression of GLUT1 or GLUT3 in Xenopus oocytes, BrDHA was neither transported nor bound, in contrast to robust transport of DHA. The findings were not explained by differences in the oocyte reduction of DHA and BrDHA because lysed oocytes reduced both compounds equally. Further, there was no transport of the reduced compound, 6-bromo-6-deoxy-L-ascorbic acid, by GLUT1 or GLUT3. As a prerequisite for investigating 6-bromo-6-deoxy-L-ascorbic acid transported by SVCTs, SVCT2 transport activity in oocytes was enhanced 14-fold by construction and use of a vector that added a fixed poly(A) tail to the 3' end of cRNA. For SVCT1 and SVCT2 expressed in oocytes, similar K(m) and V(max) values were observed for ascorbic acid and 6-bromo-6-deoxy-L-ascorbic acid. In human fibroblasts, predicted to have SVCT-mediated ascorbate accumulation, K(m) and V(max) values were again comparable for ascorbic acid and 6-bromo-6-deoxy-L-ascorbic acid. Using activated human neutrophils, predicted to have ascorbate accumulation mediated predominantly by DHA and GLUT transporters, 6-bromo-6-deoxy-L-ascorbic acid accumulation was <1% of accumulation when compared with ascorbic acid. We conclude that 6-bromo-6-deoxy-L-ascorbic acid is the first transport substrate identified as completely specific for SVCTs, but not GLUTs, and provide a new strategy to determine the contribution of each pathway to ascorbate accumulation.

Animals↗
PubMed2002

Enhanced secretion of tissue plasminogen activator by simultaneous use of retinoic acid and ascorbic acid from tissue cultured gastroepiploic artery.

Tissue-type plasminogen activator (tPA) is a key enzyme in the fibrinolysis system and the regulation of its expression has been extensively studied in cultured vascular endothelial cells. Many kinds of supplements including growth factors are needed, however, to keep endothelial cells viable, which leads the culture condition far from the physiological milieu. Using a new device of amorphous calcium phosphate coated culture plate, we succeeded in culturing ring-cut gastroepiploic artery in a basic medium of RPMI 1640 containing 10% fetal calf serum. The overall normal vessel architecture and the antigenicity of von Willebrand factor, tPA and plasminogen activator inhibitor type 1 (PAI-1) were retained for at least 9 days. tPA was constantly secreted into the conditioned medium at least up to day 12. Employing this organ culture technique, we analyzed the effects of two well-known profibrinolytic vitamins of retinoic acid (Vit. A) and ascorbic acid (Vit. C) on the release of tPA and PAI-1. The cultured artery responded well and the tPA secretion was enhanced by factors of 1.5 fold by Vit. A, 1.7 fold by Vit C and 3.2 fold by their combination, whereas none of these stimuli increased PAI-1 secretion. These results suggested that the cultured ring-cut artery retained functional endothelial cells for at least 9 days and was suitable in analyzing the regulatory mechanism of protein synthesis and secretion from the vascular wall. Using this method, vitamins A and C were shown to lead the intravascular condition to a profibrinolytic state.

Ascorbic Acid↗
PubMed1975

Automated single-column analysis of amino acids using ascorbic acid as reductant for air-stable ninhydrin.

The procedure for operation of a constant-temperature, single-column automated amino acid analyser in the sub-nanomole range is described. The cycle time for a complete analysis is 90 min including equilibration for next cycle. Eluting buffers can be made in the laboratory or commercially available concentrates (Pico-Buffers) can be used. A novel reducing agent, ascorbic acid, incorporated into the column buffers was used to reduce air-stable ninhydrin.

Amino Acids↗
PubMed1989

Renal metabolism of the oxidized form of ascorbic acid (dehydro-L-ascorbic acid).

We evaluated whether specific transport and metabolic properties exist in rat and guinea pig kidney for handling the immediate oxidative product of ascorbic acid, dehydro-L-ascorbic acid. Isolated tubules were used to measure uptake of 10 microM [14C]-dehydro-L-ascorbic acid over an 8-min incubation period. Uptake did not show dependence on the bathing media electrolyte composition but was inhibited to some extent by glucose. In tubules of both animal species the majority of 14C label present in the tissue extract was in the reduced form. No degredative enzymatic effect on dehydro-L-ascorbic acid is evident. Thirty-six percent of the [14C]dehydro-L-ascorbic acid reduced by the tubules was released during an 8-min incubation. Recently formed ascorbic acid is not substantially bound to cellular components. A factor necessary for dehydro-L-ascorbic acid reduction in renal cortex was found primarily in the 55-70% ammonium sulfate fraction. It is retained by mol wt 12,000 dialysis tubing, is heat labile, pH sensitive, inhibited by thiol reagents, and is most active in the presence of NADPH and glutathione. It has a molecular weight between that of blue dextran and cytochrome c as indicated by gel chromatography. We suggest that a cytosolic enzyme functions in reduction of dehydro-L-ascorbic acid and thereby is important in maintaining the redox state of ascorbic acid derived from the glomerular filtrate or from peritubular fluid.

Animals↗