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PubMed1994

Prolonged exposure of human chondrocytes to ascorbic acid modifies cellular behavior in an agarose gel.

Using an agarose gel culture system, the response of adult human chondrocytes to prolonged exposure of ascorbic acid was evaluated using histochemical, immunocytochemical and morphological techniques. The response of these cells to ascorbic acid was different from those previously reported in the literature. Many chondrocytes branched within the agarose gel with continued exposure to ascorbic acid while other chondrocytes maintained a round configuration typical of chondrocytes in vivo. Fibronectin and type I collagen were closely associated with the cell processes of the branching cells. Type II collagen and an alcian blue-staining matrix were associated with the rounded cells but not with the branched cells. These data suggest that the chondrocytes are able to express both dedifferentiated and redifferentiated phenotypes with ascorbic acid under these culture conditions. In addition, human chondrocytes were cultured in a collagen gel and began branching within 1 hour of culture. It is possible that an accumulation of type I collagen in the pericellular matrix of ascorbic acid treated cultures may enhance and explain the branching seen in these cultures. Studies by others have indicated that ascorbic acid may enhance, reduce, and/or modify the cartilage matrices produced by chondrocytes. These controversial reports in the literature are presumably due to variations between species and the culture methods employed.

Ascorbic Acid↗
PubMed2005

Effects of ascorbic acid on cadmium-induced oxidative stress and performance of broilers.

The effects of cadmium on performance, antioxidant defense system, liver and kidney functions, and cadmium accumulation in selected tissues of broiler chickens were studied. Whether the possible adverse effects of cadmium would reverse with the antioxidant ascorbic acid was also investigated. Hence, 4 treatment groups (3 replicates of 10 chicks each) were designed in the study: control, ascorbic acid, cadmium, and cadmium plus ascorbic acid. Cadmium was given via the drinking water at a concentration of 25 mg/L for 6 wk. Ascorbic acid was added to the basal diet at 200 mg/kg either alone or with cadmium. Cadmium decreased the body weight (BW), body weight gain (BWG), and feed efficiency (FE) significantly at the end of the experiment, whereas its effect on feed consumption (FC) was not significant. Cadmium increased the plasma malondialdehyde (MDA) level as an indicator of lipid peroxidation and lowered the activity of blood superoxide dismutase (SOD). Liver function enzymes, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and gamma glutamyl transferase (GGT) activities were not changed by cadmium. Cadmium ingestion did not alter serum creatinine levels. Although the serum cadmium level was not elevated, cadmium mainly accumulated in the kidneys, liver, pancreas, and muscle. Ascorbic acid supplementation resulted in a reduction of MDA level previously increased by cadmium and a restoration in SOD activity. However, ascorbic acid did not ameliorate the growth inhibitory effect of cadmium nor did it prevent accumulation of cadmium in analyzed tissues. These data indicate that oxidative stress, induced by cadmium, plays a role in decreasing the performance of broilers and that dietary supplementation by ascorbic acid might be useful in reversing the lipid peroxidation induced by cadmium and partly alleviating the adverse effect of cadmium on performance of broilers.

Animals↗
PubMed2000

Use of nucleic acids in the mobile phase for the determination of ascorbic acid in foods by high-performance liquid chromatography with electrochemical detection.

The sodium salts of amino acids, nucleic acids and organic acids were examined in a new mobile phase for the determination of ascorbic acid (AA) in foods. It was possible to use disodium guanosine-5'-monophosphate (GMP) (20 mM GMP, pH 2.1) in a new mobile phase after comparison of five mobile phases. The proposed method is simple, rapid (analysis time: ca. 6 min), sensitive (detection limit: ca. 0.1 ng per injection (5 microl) at a signal-to-noise ratio of 3), highly selective and reproducible [relative standard deviation: ca. 2.7% (n=7)]. The calibration graph of AA was linear in the range of 0.1 to 50 ng per injection (5 microl). Recovery of AA was over 90% by the standard addition method.

Ascorbic Acid↗
PubMedDate not supplied

Ascorbic acid feeding of rats reduces copper absorption, causing impaired copper status and depressed biliary copper excretion.

The feeding of diets enriched with ascorbic acid (10 g/kg) to rats has previously been shown to lower plasma and liver copper concentrations. The present studies corroborate this. We hypothesized that ascorbic acid initially reduces copper absorption, this effect being masked later by the stimulatory effect on copper absorption of the impaired copper status. We also hypothesized that the impaired copper status as induced by ascorbic acid feeding is followed by a diminished biliary excretion of copper in an attempt to preserve copper homeostasis. Our hypotheses are supported by the present studies. Ascorbic acid feeding initially reduced apparent copper absorption, and in the course of the experiment this effect tended to turn over into a stimulatory effect. Copper deficiency, as induced by feeding a diet containing 1 mg Cu/kg instead of 5 mg Cu/kg, systematically increased copper absorption. Biliary excretion of copper in rats given ascorbic acid was unaffected initially but became depressed after prolonged ascorbic acid feeding. A similar time course was seen for fecal endogenous copper excretion that was calculated as the difference between true and apparent copper absorption. Copper deficiency systematically reduced biliary copper excretion and fecal endogenous copper loss.

Animals↗
PubMed1981

Collagen synthesis in human fibroblasts: effects of ascorbic acid and regulation by hydrocortisone.

The effects of hydrocortisone and ascorbic acid on collagen and noncollagen protein synthesis, and on growth were examined in fibroblasts derived from normal human dermis. When the medium was supplemented with 0.28 mM ascorbic acid, the apparent rate of collagen production increased 2-3 fold over the culture cycle. Ascorbic acid also caused a small increase in the apparent rate of synthesis of noncollagen protein and an elevation in growth rate and maximum cell density. Growth was not required for the increase in collagen production since addition of ascorbate to confluent cultures induced a similar increase. Hydrocortisone (1.5 microM) blocked the ascorbate-related increase in collagen production during growth and in confluent cultures. The hormone simultaneously increased the apparent rate of noncollagen protein production and maximum cell density, suggesting that the effect on collagen synthesis was specific. Inhibition of collagen production by hydrocortisone was observed only in the presence of ascorbate, while the increase in growth and noncollagen protein production occurred in the presence and absence of the vitamin.

Ascorbic Acid↗
PubMed1989

Ascorbic acid inhibits [3H]SCH-23390 binding to striatal dopamine D1 receptors.

The present study describes the inhibition of [3H]SCH-23390 binding to striatal dopamine D1 receptors in the presence of ascorbic acid. Specific [3H]SCH-23390 binding was maximally inhibited by 0.1 mM ascorbic acid. As determined by Scatchard analysis the binding in the presence of 0.01, 0.1, or 10 mM ascorbic acid was consonant with non-competitive inhibition with a 26%, 38%, or 19% decrease, respectively, in the maximal number of binding sites; the affinity of these binding sites was not affected. Inhibition of [3H]SCH-23390 binding by ascorbic acid was reversible; striatal homogenates incubated with 0.1 mM ascorbic acid and subsequently washed free of ascorbic acid had the same Scatchard parameters as untreated preparations.

Animals↗
PubMed1982

Tissue levels of ascorbic acid during rat gestation.

Maternal rat lung, liver, kidney and portions of small intestine lost up to 40% of their ascorbic acid between early pregnancy and the 15th day of gestation. From then to the end of pregnancy, the ascorbic acid content of the tissues increased by 30 to 60%. Ascorbic acid in fetal lung doubled in concentration on the 18th day of fetal life before a pre and post natal value of 200 micrograms/g tissue was established. Fetal liver had a minor rise in ascorbic acid concentration on the 18th day. Just prior to birth, the ascorbic acid content in fetal lung was 30% and fetal liver 50% higher than maternal.

Animals↗
PubMed2006

Temporal effects of alpha-tocopherol and L-ascorbic acid on in vitro fertilized porcine embryo development.

The susceptibility of embryos to reactive oxygen species (ROS) varies in different stages of embryo development. The present study evaluated temporal effects of alpha-tocopherol and L-ascorbic acid on the porcine embryo development, and investigated whether a single or twice supplements of these two antioxidants at a divided concentrations favors the embryo development. In order to determine temporal effects of alpha-tocopherol and/or L-ascorbic acid, 100 microM alpha-tocopherol or 200 microM L-ascorbic acid were supplemented to the North Carolina State University (NCSU)-23 embryo culture media at 0, 48, 96 and 120 h of culture. In another set of experiments, the concentration was divided into two equal halves, i.e., 50 microM alpha-tocopherol and 100 microM L-ascorbic acid, and supplemented twice at 0 and 48, 0 and 96, or 48 and 96 h of culture. Supplementing culture media with 100 microM alpha-tocopherol for the entire culture period of 168 h or starting from the 48 h of culture yielded higher blastocyst percentage compared with the control or starting from the 96 or 120 h of culture. L-Ascorbic acid (200 microM) alone or together with alpha-tocopherol (100 microM) with a single supplement did not affect the frequency of blastocyst formation or number of cells in blastocyst. L-ascorbic acid with a divided supplements yielded higher blastocyst percentage compared with the control. No synergistic effect was observed on embryo development at a single supplement of these antioxidants. Although, at divided supplements higher blastocyst percentage was observed compared with control group, no further beneficial effect was observed compared with alpha-tocopherol or L-ascorbic acid alone. Our results demonstrated that the embryotrophic effects of alpha-tocopherol and/or L-ascorbic acid, in terms of frequency of blastocyst formation and number of cells in blastocyst, depends on the concentration and supplementation timing.

Animals↗
PubMed1977

The effect of ascorbic acid supplementation on some parameters of the human immunological defence system.

We have investigated the effect of ascorbic acid (vitamin C) supplementation on some parameters of the human immune defence system in a group of 25 healthy, male university students. The subjects ingested 1 g ascorbic acid per day for a period of 75 days. Serum levels of IgA, IgG, IgM, C-3 complement component, cortisol and transcortin were measured before and after the ascorbic acid course. Corresponding measurements were performed on a control group of 20 healthy, male university students receiving no extra-dietary vitamin C. Our results showed that ascorbic acid supplementation caused a statistically significant increase in the serum levels of IgA, IgM and C-3 complement. Our study does not permit of conclusions regarding the mechanisms of action of ascorbic acid.

Adolescent↗
PubMed1997

Ascorbic acid and amino acid values in the aqueous humor of a patient with Lowe's syndrome.

BACKGROUND: Aminoaciduria is found in Lowe's syndrome. No studies of concentrations of ascorbic acid and amino acids in the aqueous humor of the syndrome have been performed. We examined these concentrations in a patient with Lowe's syndrome. METHODS: Ascorbic acid and amino acid levels in the aqueous humor and plasma of a male infant were measured by means of high-performance liquid chromatography. The patient, who had congenital cataract, miotic pupils, opaque corneas, glaucoma, aminoaciduria, normal levels of ascorbic acid and amino acid in the plasma, and renal tubular acidosis, underwent trabeculotomy, lensectomy, and anterior vitrectomy in both eyes. RESULTS: Intraocular pressure in both eyes decreased to within the normal range, but both corneas remained opaque. The amino acid levels in the aqueous humor were similar to those in the plasma, but intracameral ascorbic acid levels were decreased. After topical instillation of ascorbic acid, the corneas became transparent. The proband's mother had good visual acuity but paracentral lens opacities in both eyes. His maternal grandmother had scattered cortical opacities in both lenses. CONCLUSION: In this infant with Lowe's syndrome, we found intracameral levels of amino acids similar to those in the plasma. Levels of ascorbic acid in the aqueous humor were decreased.

Adolescent↗
PubMed1998

Mechanism of ascorbic acid enhancement of the bioavailability and diuretic effect of furosemide.

The following possible explanations for the significant increases in the oral bioavailability and the diuretic and natriuretic effects of orally administered furosemide observed when ascorbic acid was coadministered to dogs were investigated: ascorbic acid might enhance the gastrointestinal (GI) absorption of furosemide, might inhibit GI wall metabolism of furosemide, might enhance the reabsorption of furosemide from the renal tubules, and might increase the unionized fraction of furosemide at the receptor sites. The significant increase in the oral bioavailability with coadministration of ascorbic acid seemed to result from reduced gastric first-pass metabolism of furosemide and not enhanced GI absorption of furosemide. This might be supported by rat studies; the percentages of the oral doses of furosemide recovered from the GI tract at 8 hr after oral administration were similar (p < 0.583) without (39.5%) and with (44.7%) coadministration of ascorbic acid, and the amounts of furosemide remaining per gram of stomach after 30-min incubations of 50 micrograms of furosemide with 9000g supernatant fractions of stomach homogenates were increased significantly (48.5 vs. 42.4 micrograms) by the addition of 100 micrograms of ascorbic acid. The significant increases in the diuretic and natriuretic effects of furosemide with ascorbic acid could be the result of increases in the reabsorption of furosemide from renal tubules and increases in the unionized fraction of furosemide at the renal tubular receptor sites. This was supported by 1.5-4.2-fold increases in urine output and approximately 20% decreases in the time-averaged renal clearance of furosemide when the urine pH was decreased by 1.5-2.5 units by oral administration of ammonium chloride.

Animals↗
PubMed1977

Ascorbic acid flux across mucosal border of guinea pig and human ileum.

The unidirectional influx of L-[14C]ascorbic acid (vitamin C) across the mucosal border of guinea pig and human ileum was determined. Influx follows saturation kinetics, indicating that a carrier mechanism is operative. The maximal influx in guinea pig ileum bathed in Ringer is 140 nmol/cm2-h and the ascorbic acid concentration greater than 6 mM , or when the tissue is bathed in Na-free media, influx is approximately linearly related to the ascorbic acid concentration, and absorption by simple diffusion may predominate. With mucosal ascorbic acid concentration of 0.28 mM, influx is reduced by at least 70% when Na-free media is used; however, influx is not dependent on the intracellular Na concentration. The brush border mechanism appears to be stereospecific and not closely coupled to cellular metabolism. A model of transport is favored that features a carrier-mediated transport mechanism for simultaneous entry of ascorbic acid and Na across the brush border. This model is similar in nature to, but functionally distinct from, the sodium-gradient mechanism postulated to effect sugar and amino acid transport in mammalian ileal mucosa.

Animals↗
PubMed1982

Ascorbic acid in neural tissues.

Large amounts of ascorbic acid were readily removed from neural tissue by washing with warmed saline solutions. In areas where the original level was highest, such as cortex and cerebellum, a higher percentage was removed than from areas of lower concentration, such as pons-medulla. The residual level in both types of tissue was similar. During scurvy, the ascorbic acid retained in the guinea pig brain is more readily removed by washing than is that of the normal brain.

Animals↗
PubMed1987

Ascorbic acid intake and plasma levels in healthy elderly people.

Plasma ascorbic acid concentrations were determined in eight men and nine women over age 65 on controlled intakes of vitamin C. Plasma ascorbic acid levels were significantly lower in elderly men compared with women for vitamin C intakes ranging from 30 to 280 mg/d. A maximum steady-state level of 1.0 mg/dL (56.78 mumol/L) ascorbic acid was observed in male subjects at an intake of approximately 150 mg/d; female subjects approached a plasma ascorbate level of 1.0 mg/dL (56.78 mumol/L) with an intake of approximately 80 mg/d. At a total vitamin C intake of 60 mg/d, plasma ascorbate levels in men were estimated to be 0.4 mg/dL (22.71 mumol/L) or less. The amount of dehydroascorbic acid in plasma did not vary with intake of vitamin C.

Aged↗
PubMed2000

Pharmacological concentrations of ascorbic acid are required for the beneficial effect on endothelial vasomotor function in hypertension.

Increased production of superoxide anion may contribute to impaired bioactivity of endothelium-derived nitric oxide in hypertension. Ascorbic acid is capable of scavenging superoxide anion; however, experimental studies have shown that high physiological concentrations (>1 mmol/L) of ascorbic acid are required to prevent superoxide-mediated vascular dysfunction. To seek kinetic evidence that superoxide anion contributes to endothelial vasomotor dysfunction in human hypertension, we examined the effects of 2.4 or 24 mg/min ascorbic acid intra-arterial infusions on forearm blood flow responses to methacholine or sodium nitroprusside in 30 patients with hypertension and 22 age-matched controls. Endothelium-dependent vasodilation to methacholine was significantly impaired in the hypertensive patients, with a response to the highest dose of methacholine (10 microg/min) of 12.3+/-6.7 compared with 16.1+/-5.8 mL. min(-1). dL tissue(-1) in the controls (P<0.001). The response to sodium nitroprusside was equivalent in the 2 groups. Ascorbic acid at 24 mg/min significantly improved the forearm blood flow response to methacholine in hypertensive patients with a peak response of 16.1+/-7.1 mL. min(-1). dL tissue(-1) (P=0.001). This dose produced a cephalic vein ascorbic acid concentration of 3.2+/-1. 4 mmol/L. In contrast, ascorbic acid at 2.4 mg/min had no effect on the methacholine response. Ascorbic acid at both doses had no effect on the vasodilator response to sodium nitroprusside in hypertensive patients or the methacholine response in the controls. These results agree with the predicted kinetics for superoxide anion-mediated impairment of endothelium-derived nitric oxide action. Thus, superoxide anion may contribute to impaired endothelium-dependent vasodilation in patients with hypertension.

Adult↗
PubMed1992

The crystal structure and physicochemical properties of L-ascorbic acid 2-glucoside.

The stable L-ascorbic acid glucoside produced by the action of the cyclomaltodextrin glucanotransferase (CGTase, EC 2.4.1.19) from Bacillus stearothermophilus was crystallized from an aqueous solution. Determination of the molecular structure by single crystal X-ray analysis showed the compound to be 2-O-alpha-D-glucopyranosyl-L-ascorbic acid (AA-2G). The crystals are orthorhombic, space group P2(1)2(1)2(1), with unit-cell dimensions a = 11.929 A, b = 24.351 A, and c = 4.864 A. The D-glucopyranose residue has the 4C1 conformation. These conclusions are in good agreement with those based on the 13C-NMR spectrum. The general physicochemical properties of crystalline AA-2G are reported.

Ascorbic Acid↗
PubMed1984

The effects of glucose on ascorbic acid uptake in heart endothelial cells: possible pathogenesis of diabetic angiopathies.

Glucose in concentrations of 20 mg% (or greater) significantly inhibited 14C-labelled ascorbic acid (1.25 mg%) uptake in endothelial cells in the presence of insulin (1600 microU/ml). The absence of insulin also significantly reduced ascorbic acid uptake. Furthermore, this reduction could be exacerbated by glucose (40, 160 mg%) but not equimolar concentrations of fructose. Increased ascorbic acid concentrations (two-fold) in the absence of insulin (1) significantly enhanced uptake, and (2) reversed the inhibition of glucose. These findings support earlier reports that ascorbic acid uptake into the cell may be compromised by decreased insulin and/or increased extracellular glucose levels. Since previous animal studies have correlated experimental ascorbic acid deficiencies with atherogenic processes (presumably by altering glycosaminoglycan metabolism), the postulation that the "diabetic condition" (low insulin, hyperglycemia) accelerates the cellular changes leading to atherosclerosis by impairing ascorbic acid uptake into the vascular endothelium, may now be supported.

Animals↗
PubMed2000

Role of ascorbic acid in the osteoclast formation: induction of osteoclast differentiation factor with formation of the extracellular collagen matrix.

Osteoclasts are bone-resorbing multinucleated cells. Tartrate-resistant acid phosphatase-positive (TRAP-positive) mononuclear and multinucleated cells, which are osteoclast-like cells (OCLs), were formed as a result of the coculture of mouse bone marrow cells and clonal stromal ST2 cells in the presence of 1alpha,25-dihydroxy-vitamin D3. Removal of ascorbic acid from the culture medium prevented the formation of TRAP-positive OCLs. Addition of ascorbic acid to the medium formed TRAP-positive OCLs, and the effect of ascorbic acid was dose-dependent. When we examined the level of messenger RNA (mRNA) for osteoclast differentiation factor (RANKL/ODF) in ST2 cells, we found that ascorbic acid caused an approximately 5-fold increase in the level of this mRNA. The half-life of the mRNA was unaffected by ascorbic acid. To characterize the mechanism of action of ascorbic acid, we investigated the relationship between formation of TRAP-positive OCLs and formation of the collagen matrix. Inhibitors of the formation of collagen triple helices blocked both the formation of TRAP-positive OCLs and the expression of the mRNA for RANKL/ODF in response to ascorbic acid. Our findings suggest that ascorbic acid might be essential for osteoclastogenesis and might induce the formation of TRAP-positive OCLs via induction of the synthesis of RANKL/ODF that is somehow mediated by the extracellular matrix.

Animals↗