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PubMed1977

Effect of large-dose ascorbic acid on the two-drop clinitest determination.

A study was conducted to determine if high doses of ascorbic acid would affect the two-drop Clinitest determination for glucosuria in normal individuals. Numerous secondary literature sources indicate that large doses of ascorbic acid may cause a false positive Clinitest result. Three-gram and nine-gram doses of ascorbic acid following two dosing schedules (once daily and three times daily) were taken by nine normal individuals to determine if the renal excretion of large enough quantities of ascorbic acid or its metabolites would produce false positive results with the two-drop Clinitest procedure. Each dose was given for seven days in each schedule. There were only two (0.27%) trace positive Clinitest determinations reported out of 748 Clinitest determinations. High doses of ascorbic acid in normal individuals do not appear to affect the two-drop Clinitest determination for urinary glucose. The study indicates a need to be cautious about secondary literature references on drug-laboratory test interferences.

Ascorbic Acid↗
PubMedDate not supplied

Ultrastructural reorganizations in the rat cerebral cortex after injection of ascorbic acid into the ventricular fluid.

A brief increase in the ascorbic acid concentration in the rat cerebral cortex after intraventricular bilateral injection of 20 microliters of a 0.1% or 1% ascorbic acid solution and also intracisternal injection of 20 microliters of a 0.5% solution results in a prolonged (not less than 21 days) ultrastructural reorganization in the nucleus and cytoplasm of the cortical neurons: the amount of lysosomes, polysomes, vesicles of the Golgi complex, and subsurface cisterns increases, this demonstrating an increasing RNA and protein synthesis, catabolic processes, and neuronal-glial interaction. Changes in the ultrastructure of the synaptic terminals, such as disintegrating mitochondria, formation of myelin-like bodies, and, in addition, after interstitial injection, protrusions into the adjacent dendrite, demonstrate that synapses are one of the sites where excess ascorbic acid affects the CNS. Over a long period, 3 and 6 months after injection, the changes mentioned are not observed but in the glial processes one can observe vacuoles containing degenerating elements.

Animals↗
PubMed1976

Drug biotransformation interactions in man VI: acetaminophen and ascorbic acid.

Oral administration of 3 g of ascorbic acid 1.5 hr after an oral dose of 1 g of acetaminophen caused a rapid and pronounced decrease in the excretion rate of acetaminophen sulfate in five healthy adult volunteers. There was a statistically significant increase in the fractions of the dose of acetaminophen excreted as such as as acetaminophen glucuronide but a decrease in the fraction excreted as acetaminophen sulfate. The apparent biological half-life of acetaminophen increased from 2.3 +/- 0.2 (mean +/- SD) to 3.1 +/- 0.5 hr. Concomitant administration of sodium sulfate prevented these effects. Ascorbic acid, which itself is metabolized in part to the sulfate, inhibits the conjugation of acetaminophen with sulfate by competing for available sulfate in the body.

Acetaminophen↗
PubMed1990

Effect of dietary ascorbic acid on heat-induced eye lens protein damage in guinea pigs.

The effect of large intake of dietary ascorbic acid on heat-induced eye lens protein damage has been studied. Male guinea pigs of the Hartley strain were used. Ascorbic acid was administered to the experimental animals in the drinking water. The mean daily ascorbic acid intakes for the control and experimental animals were 10 and 366 mg/kg body weight, respectively. The ascorbic acid level in the lens of the experimental animals was significantly higher than in the controls, but no differences in the content of water-soluble lens proteins were observed. When a solution of water-soluble protein was incubated at 60 degrees C, insoluble aggregates were formed. The loss of water-soluble proteins from the lens of the experimental animals was significantly less than that of the controls. The results indicated that large quantities of dietary ascorbic acid were able to protect lens constituents against heat-induced damage.

Animals↗
PubMed2002

Kinetic-spectrophotometric determination of ascorbic acid by inhibition of the hydrochloric acid-bromate reaction.

A new analytical method was developed for the determination of ascorbic acid in fruit juice and pharmaceuticals. The method is based on its inhibition effect on the reaction between hydrochloric acid and bromate. The decolourisation of Methyl Orange by the reaction products was used to monitor the reaction spectrophotometrically at 510 nm. The linearity range of the calibration graph depends on bromate concentration. The variable affecting the rate of the reaction was investigated. The method is simple, rapid, relatively sensitive and precise. The limit of detection is 7.6 x 10(-6) M and calibration rang is 8 x 10(-6)-1.2 x 10(-3) M ascorbic acid. The relative standard deviation of seven replication determinations of 8 x 10(-6) and 2 x 10(-5) M ascorbic acid was 2.8 and 1.7%, respectively. The influence of potential interfering substance was studied. The method was successfully applied for the determination of ascorbic acid in pharmaceuticals.

Ascorbic Acid↗
PubMed1993

Effect of ascorbic acid administration on B and E apoproteins in rats fed a cholesterol enriched diet.

The effect of ascorbic acid on cholesterol metabolism is very well documented; it is ascribed to the activation of this vitamin on cholesterol 7 alpha-hydroxylase (EC 1.14) that activates the catabolism of cholesterol. In this paper we have studied the effect of the administration of ascorbic acid on B and E apoproteins of rats fed a diet enriched with 1.5% of cholesterol. The results obtained show that ascorbic acid is able to affect cholesterol metabolism by modifying the serum levels of apo B in total serum and in lipoprotein classes of density less than 1.050 g/ml. Moreover the ascorbic acid treatment reduced the amount of cholesterol and triglycerides in all lipoprotein classes examined. No significant change of total serum apo E was observed following ascorbic acid administration.

Animals↗
PubMed1998

Osteoclast differentiation requires ascorbic acid.

Osteoclast differentiation assays are usually conducted in alpha minimal essential medium (alpha-MEM). We reasoned that determining which components of this media are critical for osteoclast differentiation might provide insight into the mechanisms that regulate osteoclast differentiation. This study demonstrates that ascorbic acid is the crucial component of alpha-MEM that stimulates differentiation of murine osteoclasts in cocultures with murine mesenchymal support cells. Thus, supplementation with ascorbic acid allows osteoclast differentiation to occur in basal MEM media as well as in RPMI-1640 and basal media Eagle (BME) media. The conclusion that osteoclast differentiation is stimulated by ascorbic acid was obtained whether osteoclast differentiation was induced by 1,25-dihydroxyvitamin D3 or parathyroid hormone, whether ST2 or CIMC-2 cells were used as mesenchymal support cells, and whether osteoclast precursors were obtained from spleen or bone marrow. Time course studies revealed that although ascorbic acid only modestly increases the rate at which osteoclast precursors begin to express tartrate-resistant acid phosphatase, it strongly increases the rate at which precursors fuse into mature, multinucleated cells. Moreover, ascorbic acid strongly increases the life span of both osteoclasts and their precursors. The increases in precursor formation, fusion, and life span induced by ascorbic acid are together responsible for the stimulation of osteoclast differentiation by ascorbic acid. Given the known effects of ascorbic acid on differentiation of mesenchymal cells, it may stimulate osteoclast differentiation indirectly by regulating the differentiation state of the mesenchymal cells that support osteoclast differentiation.

Animals↗
PubMed1986

The influx of ascorbic acid into the rat's brain.

The influx of [14C]ascorbic acid into the rat's brain through the cerebral capillaries was measured by the steady-state initial-rate technique. Ascorbic acid was found to pass through the capillaries by a carrier-mediated process and by simple diffusion. The carrier system was found to have an apparent Vmax of 1.2 nmol . min-1 . g-1 of cerebral tissue and a Kt of 125 microM. The apparent constant of transfer, Kd, of the diffusional component was 0.98 microliter. min-1 . g-1. The contribution of the cerebral capillaries to the movement of ascorbic acid into the brain is discussed and was found to be the major route of entry into the brain for this vitamin.

Animals↗
PubMedDate not supplied

[Bound form of ascorbic acid combined with the blood serum proteins].

The fractional distribution of combined forms of ascorbic acid in the blood serum of man and animals was studied by the method of gel-filtration with sephadex. The investigations revealed the presence of a free ascorbic acid and the one combined with high-molecular proteins and peptides. A difference in binding ascorbic acid with high molecular proteins and peptides was noted. Saturation of the organism with ascorbic acid leads to its increased binding within the peptides zone alone.

Animals↗
PubMed1996

Ascorbic acid preferentially enhances type I and III collagen gene transcription in human skin fibroblasts.

Ascorbic acid is a potent stimulator for type I and III collagen expression in human skin fibroblasts; stimulation of type I and III collagen synthesis and their mRNA levels by ascorbic acid has been reported previously. Nuclear run-on experiments demonstrated that ascorbic acid enhanced the transcription of type I and III collagen genes 4- and 3.4-fold respectively, whereas transcription of type IV collagen was slightly stimulated (1.7-fold). The results suggest that ascorbic acid preferentially enhanced type I and III collagen transcription.

Ascorbic Acid↗
PubMed2004

Effect of ascorbic acid on forearm reactive hyperaemia in patients with hypercholesterolaemia.

BACKGROUND: This study was designed to research the effect of hypercholesterolaemia and ascorbic acid on forearm blood flow (FBF) reactive hyperaemia (RH). Reactive hyperaemia seems to be at least partly endothelium-dependent. Endothelial dysfunction has been described in patients with hypercholesterolaemia, and has been reversed with ascorbic acid administration. METHOD: Forearm blood flow was studied with venous occlusion plethsmography in 26 healthy volunteers and 46 hypercholesterolaemic patients. Hypercholesterolaemic patients were divided into two groups. Group A comprised 25 patients, who received ascorbic acid and group B comprised 21 patients, who received placebo. All subjects underwent measurement of FBF at baseline and during RH (phase A). Forearm blood flow during RH was measured every 15 seconds for three minutes. Subsequently patients in group A received 2 g of ascorbic acid orally in the form of effervescent tablets, and patients in group B received placebo orally in the same form. Forearm blood flow measurements at baseline and during RH were repeated two hours later (phase B). RESULTS: Maximal percent increase of FBF was significantly higher in healthy subjects than in hypercholesterolaemic patients (139.1+/-12.1% versus 73.1+/-11.0% respectively, P<0.05). Duration of RH was smaller in hypercholesterolaemic patients compared to normal subjects (60.9+/-17.1 seconds versus 105.6+/-10.2 seconds, P<0.05). Administration of ascorbic acid but not of placebo increased the duration of RH (69.1+/-11.1 seconds versus 104.1+/-12.2 seconds, P<0.05) but not of peak RH FBF. CONCLUSION: Hypercholesterolaemia seems to impair both the early and late phase of RH. Ascorbic acid improves only the duration of RH, possibly due to its antioxidant effect on endothelium.

Adult↗
PubMed1982

Lack of effect of subclinical ascorbic acid deficiency upon antipyrine metabolism in man.

The influence of experimentally induced subclinical ascorbic acid deficiency upon antipyrine metabolism was assessed in five healthy male volunteers maintained in a hospital metabolic ward and fed a controlled diet deficient in ascorbic acid. Antipyrine pharmacokinetic parameters were determined four times during the study: at the end of an initial control period, after 28 and 63 days of depletion, and at the end of a second control period. No differences in antipyrine metabolism were observed despite the fact that the subjects had plasma ascorbate levels indicative of vitamin C deficiency (i.e., plasma levels less than 0.3 mg/dl) for 5 days (28 day-depletion) or 40 days (63 day-depletion). This experiment demonstrates that pronounced ascorbic acid deficiency of relatively short duration does not alter antipyrine metabolism in man.

Adult↗
PubMed1998

Glucocorticoid stimulation of Na+-dependent ascorbic acid transport in osteoblast-like cells.

Ascorbic acid (AA) is an essential cofactor for osteoblast differentiation both in vivo and in vitro. Before it can function, this vitamin must be transported into cells via a specific Na+-dependent AA transporter. In this study, we examine the regulation of this transport activity by glucocorticoids, a class of steroid hormones known to stimulate in vitro osteoblast differentiation. Dexamethasone stimulated Na+-dependent AA transport activity approximately twofold in primary rat calvarial osteoblasts. Effects of hormone on ascorbic acid transport were rapid (detected within 24 h) and were maximally stimulated by 25-50 nM dexamethasone. Similar effects of dexamethasone on transport activity were also observed in murine MC3T3-E1 cells. This preosteoblast cell line was used for a more detailed characterization of the glucocorticoid response. Transport activity was stimulated selectively by glucocorticoids (dexamethasone > corticosterone) relative to other steroid hormones (progesterone and 17-beta-estradiol) and was blocked when cells were cultured in the presence of cycloheximide, a protein synthesis inhibitor. Kinetic analysis of AA transporter activity in control and dexamethasone-treated cells indicated a Km of approximately 17 microM for both groups. In contrast, dexamethasone increased Vmax by approximately 2.5-fold. Cells also contained an Na+-independent glucose transport activity that has been reported in other systems to transport vitamin C as oxidized dehydroascorbic acid. In marked contrast to Na+-dependent AA transport, this activity was inhibited by dexamethasone. Thus, glucocorticoids increase Na+-dependent AA transport in osteoblasts, possibly via up-regulation of transporter synthesis, and this response can be resolved from actions of glucocorticoids on glucose transport.

Animals↗
PubMed2006

Ascorbic acid enhances the inhibitory effect of aspirin on neuronal cyclooxygenase-2-mediated prostaglandin E2 production.

Inhibition of neuronal cyclooxygenase-2 (COX-2) and hence prostaglandin E2 (PGE2) synthesis by non-steroidal anti-inflammatory drugs has been suggested to protect neuronal cells in a variety of pathophysiological situations including Alzheimer's disease and ischemic stroke. Ascorbic acid (vitamin C) has also been shown to protect cerebral tissue in a variety of experimental conditions, which has been attributed to its antioxidant capacity. In the present study, we show that ascorbic acid dose-dependently inhibited interleukin-1beta (IL-1beta)-mediated PGE2 synthesis in the human neuronal cell line, SK-N-SH. Furthermore, in combination with aspirin, ascorbic acid augmented the inhibitory effect of aspirin on PGE2 synthesis. However, ascorbic acid had no synergistic effect along with other COX inhibitors (SC-58125 and indomethacin). The inhibition of IL-1beta-mediated PGE2 synthesis by ascorbic acid was not due to the inhibition of the expression of COX-2 or microsomal prostaglandin E synthase (mPGES-1). Rather, ascorbic acid dose-dependently (0.1-100 microM) produced a significant reduction in IL-1beta-mediated production of 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha), a reliable indicator of free radical formation, suggesting that the effects of ascorbic acid on COX-2-mediated PGE2 biosynthesis may be the result of the maintenance of the neuronal redox status since COX activity is known to be enhanced by oxidative stress. Our results provide in vitro evidence that the neuroprotective effects of ascorbic acid may depend, at least in part, on its ability to reduce neuronal COX-2 activity and PGE2 synthesis, owing to its antioxidant properties. Further, these experiments suggest that a combination of aspirin with ascorbic acid constitutes a novel approach to render COX-2 more sensitive to inhibition by aspirin, allowing an anti-inflammatory therapy with lower doses of aspirin, thereby avoiding the side effects of the usually high dose aspirin treatment.

Antioxidants↗
PubMedDate not supplied

Ascorbic acid supplementation restores defective leukocyte-endothelial interaction in alloxan-diabetic rats.

BACKGROUND: Defective leukocyte-endothelial interactions are observed in experimental diabetes and may reduce the capacity to mount an adequate inflammatory response. The present study investigated the effect of ascorbic acid, an inhibitor of free radical and glycated protein formation as well as an aldose reductase inhibitor, on leukocyte-endothelial interaction in alloxan-diabetic rats. METHODS: Rats were rendered diabetic by alloxan injection (40 mg/kg; iv). After 30 days, diabetic and nondiabetic controls were supplemented for 12 days with ascorbic acid (50 or 200 mg/kg/day) or received saline by gavage. The number of rollers, stickers after zymosan-activated plasma (10%) or leukotriene B(4) (1 microM) applied topically, and migrated cells after local injection of carrageenan (100 microg) were determined in the venules of the internal spermatic fascia by intravital microscopy. Erythrocyte velocity and wall shear rate were determined as well. Reactive oxygen species formation by endothelial cells was measured in vivo by the same technique. Immunocytochemistry for ICAM-1 detection on the endothelium of the venules of the internal spermatic fascia was carried out in cross sections of the whole testis of the animals. RESULTS: The reduced number of rollers, stickers and migrated cells, as well as the higher production of reactive oxygen species by endothelial cells in diabetic rats was corrected by ascorbic acid supplementation. The low immunoreactivity for ICAM-1 in the venules of diabetic rats was improved by ascorbic acid supplementation. Ascorbic acid supplementation did not interfere with erythrocyte velocity or wall shear stress. Ascorbic acid administered to control rats did not alter the parameters studied above. CONCLUSION: We conclude that ascorbic acid improves leukocyte-endothelial interaction in diabetic rats at least in part by restoring the expression of ICAM-1 in the venules of diabetic rats.

Animals↗
PubMed1980

An improved method for determination of L-ascorbic acid and L-dehydroascorbic acid in blood plasma.

Various conditions for reducing L-dehydroascorbic acid were studied, using dithiothreitol. This led to an improved method for the separate determination of L-ascorbic acid and L-dehydroascorbic acid in blood plasma. The content of ascorbic acid was determined by an alpha,alpha'-dipyridyl method (A). Dehydroascorbic acid was reduced to ascorbic acid by incubation with dithiothreitol at room temperature for 10 min at pH 6.5 to 8.0. After removing the excess dithiothreitol with N-ethylmaleimide, total ascorbic acids, i.e. reduced plus original, were determined by the alpha,alpha'-dipyridyl method (B). The amount of dehydroascorbic acid could then be calculated from these results (B minus A).

2,2'-Dipyridyl↗
PubMed2004

Effect of ascorbic acid and particle size on iron absorption from ferric pyrophosphate in adult women.

The effects of added ascorbic acid and particle size on iron absorption from ferric pyrophosphate were evaluated in adult women (9-10 women/study) based on erythrocyte incorporation of iron stable isotopes (57Fe or 58Fe) 14 days after administration. Three separate studies were made with test meals of iron-fortified infant cereal (5 mg iron/meal) and the results are presented as geometric means and relative bioavailability values (RBV, FeSO4 = 100%). The results of study 1 showed that iron absorption was significantly lower from ferric pyrophosphate (mean particle size 8.5 microm) than from FeSO4 in meals without ascorbic acid (0.9 vs. 2.6%, p < 0.0001, RBV 36%) and in the same meals with ascorbic acid added at a 4:1 molar ratio relative to fortification iron (2.3 vs. 9.7%, p < 0.0001, RBV 23%). Ascorbic acid increased iron absorption from ferric pyrophosphate slightly less (2.6-fold) than from FeSO4 (3.7-fold) (p < 0.05). In studies 2 and 3, RBV of ferric pyrophosphate with an average particle size of 6.7 microm and 12.5 pm was not significantly different at 52 and 42% (p > 0.05), respectively. In conclusion, the addition of ascorbic acid increased fractional iron absorption from ferric pyrophosphate significantly, but to a lesser extent than from FeSO4. Decreasing the mean particle size to 6.7 microm did not significantly increase iron absorption from ferric pyrophosphate.

Adult↗
PubMedDate not supplied

[Effect of ascorbic acid on glucocorticoid metabolism in guinea pigs].

Ascorbic acid administered for 18-20 days (daily by 100 mg per 1 kg of weight per os) causes redistribution of certain fractions of 17-OCS excreted with urine (a decrease in the content of free F and F/E ratio, an increase in the content of THF, THE and THS, a more frequent appearance of substances). In the blood plasm and adrenals concentration of 11-OCS rises. When determining the available functional reserves of the adrenal cortex under these conditions, an increase in the content of F, E and S unchanged forms is observed in response to ACTH administration as distinct from the initial state. The rise in concentration of 11-OCS in the adrenals and blood plasm is less pronounced than in the control. A conclusion is drawn that ascorbic acid affects metabolism of glucocorticoids and changes the reaction of the adrenaocortical system on the action of ACTH.

11-Hydroxycorticosteroids↗