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PubMed1998

Low levels of serum ascorbic acid in elderly patients with hip fracture.

The serum concentration of ascorbic acid was measured in 40 elderly patients with a recent hip fracture and compared to values measured in 102 home-living elderly. The concentrations were 37 +/- 22 mumol l-1 vs 50 +/- 29 mumol l-1 (p < 0.01). Among the patients admitted from home-living conditions and controls, 20 pairs could be matched with respect to age, sex and season for the test. Serum ascorbic acid concentration was significantly lower in the hip fracture patients (34 +/- 19 mumol l-1 vs 54 +/- 30 mumol l-1, p < 0.01). In the matched pairs, a seasonal variation in serum ascorbic acid concentration was found in the controls, but not in the hip fracture patients. As previous studies have found decreased concentrations of several nutritional factors in hip fracture patients, our findings might indicate that a reduced serum concentration of ascorbic acid could be a part of a general nutritional insufficiency in several patients with hip fracture.

Aged↗
PubMed1993

Analysis of the transformation products of dehydro-L-ascorbic acid by ion-pairing high-performance liquid chromatography.

Dehydro-L-ascorbic acid, the oxidation form of L-ascorbic acid, converts nonenzymatically to a variety of transformation products depending upon the incubating conditions. These products, called the ascorbate cascade, possess different absorption spectra and reducing activities. Ion-pairing high-performance liquid chromatography with multiwavelength uv absorption and amperometric electrochemical detection has proven to be a useful technique for the analysis of these products. Separation and characterization in the present investigations reveal three kinds of transformation products: the polymerized intermediates of browning reaction, the reductant possessing an absorption maximum at 345 nm as the six-carbon compound, and erythro-L-ascorbic acid, 2-furoic acid, 3-hydroxy-2-pyrone, 5-methyl-3,4-dihydroxytetrone, reductic acid, and furfural as the five-carbon compound. These products possess an absorption maximum above 240 nm, and most of them are electrochemically active reducing compounds which are derived from nonreducing dehydro-L-ascorbic acid through the processes of delactonization, decarboxylation, and intramolecular rearrangement.

Chromatography, High Pressure Liquid↗
PubMed2002

Effect of ascorbic acid on the stability of beta-carotene and capsanthin in paprika (Capsicum annuum) powder.

The effect of ascorbic acid, light, and storage on the stability of the pigments beta-carotene and capsanthin in red pepper (Capsicum annuum) powder has been elucidated by determining the amount of pigment in samples treated by various concentrations of ascorbic acid. Determination of pigment concentration has been performed after different storage times using high-performance liquid chromatography. The dependence of the concentration of pigments on the concentration of ascorbic acid, presence of light and the storage time has been assessed by stepwise regression analysis. The concentration of pigments decreased at longer storage time and increased at higher concentration of ascorbic acid, beta-carotene being more sensitive towards storage time and concentration of ascorbic acid than capsanthin. Interaction between the effects of light and storage time, and light and concentration of ascorbic acid has been established.

Antioxidants↗
PubMed2001

Levels of malondialdehyde-deoxyguanosine in the gastric mucosa: relationship with lipid peroxidation, ascorbic acid, and Helicobacter pylori.

Helicobacter pylori infection is associated with elevated gastric mucosal concentrations of the lipid peroxidation product malondialdehyde and reduced gastric juice vitamin C concentrations. Malondialdehyde can react with DNA bases to form the mutagenic adduct malondialdehyde-deoxyguanosine (M(1)-dG). We aimed to determine gastric mucosal levels of M(1)-dG in relation to H. pylori infection and malondialdehyde and vitamin C concentrations. Patients (n = 124) attending for endoscopy were studied. Levels of antral mucosal M(1)-dG were determined using a sensitive immunoslot-blot technique; antral mucosal malondialdehyde was determined by thiobarbituric acid extraction, and gastric juice and antral mucosal ascorbic acid and total vitamin C were determined by high-performance liquid chromatography. Sixty-four H. pylori-positive patients received eradication therapy, and endoscopy was repeated at 6 and 12 months. Levels of M(1)-dG did not differ between subjects with H. pylori gastritis (n = 85) and those with normal mucosa without H. pylori infection (n = 39; 56.6 versus 60.1 adducts/10(8) bases) and were unaffected by age or smoking habits. Malondialdehyde levels were higher (123.7 versus 82.5 pmol/g; P < 0.001), gastric juice ascorbic acid was lower (5.7 versus 15.0 micromol/ml; P < 0.001), and antral mucosal ascorbic acid was unchanged (48.0 versus 42.7 micromol/g) in H. pylori gastritis compared with normal mucosa. Multiple regression analysis revealed that M(1)-dG increased significantly with increasing levels of malondialdehyde, antral ascorbic acid, and total antral vitamin C. M(1)-dG levels were unchanged 6 months (63.3 versus 87.0 adducts/10(8) bases; P = 0.24; n = 38) and 12 months (66.7 versus 77.5 adducts/10(8) bases; P = 0.8; n = 13) after successful eradication of H. pylori. M(1)-dG thus is detectable in gastric mucosa, but is not affected directly by H. pylori.

Adult↗
PubMed2002

Crystalline silica incubated in ascorbic acid acquires a higher cytotoxic potential.

Quartz incubated in an aqueous solution of ascorbic acid is partially dissolved and the potential to generate hydroxyl radicals from hydrogen peroxide is enhanced. In order to investigate whether the surface activation triggered by the treatment with ascorbic acid would also involve an enhancement in cell toxicity, a murine macrophage cell line (RAW 264.7) was exposed to untreated and ascorbic acid-treated quartz. Ascorbic acid pretreated quartz was more toxic than untreated quartz and all cells died within 24 hours after exposure. Tetrandrine (a Chinese drug employed to retard or reverse fibrotic lesions of silicosis in humans) partially reduced cell toxicity generated by ascorbic acid pretreated quartz.

Alkaloids↗
PubMed1996

Plasma ascorbic acid concentrations are related to cardiovascular risk factors in African-Americans.

This study was undertaken to examine relationships among blood pressure, blood lipids, and plasma concentrations of ascorbic acid and malondialdehyde (MDA) equivalents (indicative of lipid peroxidation) in adult African-Americans. Subjects (n = 172, mean age = 48.0 y) were recruited from among the memberships of several Seventh-Day Adventist Churches. Plasma ascorbic acid and MDA equivalents were inversely correlated (r = -0.44, P < 0.0001). There were significant inverse correlations between plasma ascorbic acid levels and both systolic (r = -0.39, P < 0.0001) and diastolic blood pressure (r = -0.25, P < 0.03), and between plasma ascorbic acid and serum total cholesterol (r = -0.25, P < 0.03), LDL-cholesterol (LDL-C) (r = -0.33, P < 0.004), and the ratio of LDL-cholesterol to HDL-cholesterol (LDL-C/HDL-C) (r = -0.32, P < 0.004). Serum HDL-cholesterol was positively related to plasma ascorbic acid (r = 0.22, P < 0.05). The correlations for MDA equivalents and the blood pressure and blood lipid variables were of similar magnitude to those of plasma ascorbic acid, but were in the opposite direction. Multiple regression analysis revealed ascorbic acid to be a significant independent contributor to the prediction of blood pressure and LDL-C concentration. These data suggest that plasma concentrations of ascorbic acid and MDA equivalents are related to several cardiovascular risk indicators in black Americans.

Adult↗
PubMed1981

Collagen biosynthesis by human skin fibroblasts. III. The effects of ascorbic acid on procollagen production and prolyl hydroxylase activity.

Human skin fibroblasts were cultured under conditions optimized for collagen synthesis, and the effects of ascorbic acid on procollagen production, proline hydroxylation and the activity of prolyl hydroxylase were examined in cultures. the results indicated that addition of ascorbic acid to confluent monolayer cultures of adult human skin fibroblasts markedly increased the amount of [3H]hydroxyproline synthesized. Ascorbic acid, however, did not increase the synthesis of 3H-labeled collagenous polypeptides assayed independently of hydroxylation of proline residues, nor did it affect the amount of prolyl hydroxylase detectable by an in vitro enzyme assay. Also long-term cultures of the cells or initiation of fibroblast cultures in the presence of ascorbic acid did not lead to an apparent selection of a cell population which might be abnormally responsive to ascorbic acid. Thus, ascorbic acid appears to have one primary action on the synthesis of procollagen by cultured human skin fibroblasts: it is necessary for synthesis of hydroxyproline, and consequently for proper triple helix formation and secretion of procollagen.

Adult↗
PubMed1986

Effects of dietary vitamin E and high level of ascorbic acid on iron distribution in rat tissues.

The effects of dietary vitamin E and high-level supplementation of ascorbic acid on iron distribution in rat tissues were studied. Weanling male Sprague-Dawley rats, fed ad libitum a vitamin E and ascorbic acid free basal diet, were divided into four groups. They were supplemented with 0 or 45 IU/kg diet of vitamin E, and O or 0.2% ascorbic acid in a 2 X 2 complete factorial design. After 12 weeks, rats were killed; blood, liver, spleen, heart and skeletal muscle were collected for analysis. Vitamin E deficiency resulted in significantly decreased plasma iron levels and total iron binding capacity. The total iron and nonheme iron contents of the liver and spleen were significantly higher in the vitamin E-deficient groups compared with control groups. Vitamin E or ascorbic acid supplementation had no effect on iron content of the heart. Non-heme iron levels on per gram tissue were highest in the skeletal muscle of the group to which no vitamin E or ascorbic acid were supplemented. It appears that vitamin E and ascorbic acid interactively affect the iron distribution in rat tissues.

Animals↗
PubMed2006

Ascorbic acid improves the intrahepatic endothelial dysfunction of patients with cirrhosis and portal hypertension.

Patients with cirrhosis show intrahepatic endothelial dysfunction, characterized by an impaired flow-dependent vasorelaxation. This alteration is responsible for the marked postprandial increase in portal pressure and is attributed to an insufficient release of nitric oxide (NO). Ascorbic acid reverts endothelial dysfunction in other vascular disorders, via the increase of NO bioavailability through the neutralization of superoxide anions, thus preventing the scavenging of NO by superoxide. This study examined whether acute ascorbic acid administration might improve endothelial dysfunction in cirrhosis. Thirty-seven portal hypertensive patients with cirrhosis had measurements of hepatic and systemic hemodynamics, ascorbic acid, and malondialdehyde (MDA). Patients were randomly allocated to receive ascorbic acid (3 g, intravenously, n = 15) or placebo (n = 12) followed by a liquid meal. A third group received ascorbic acid followed by a sham meal (n = 10). Measurements were repeated after 30 minutes (hepatic venous pressure gradient at 15 and 30 minutes). Patients with cirrhosis had significantly lower ascorbic acid levels and higher MDA than healthy controls. Ascorbic acid significantly reduced MDA levels and markedly attenuated the postprandial increase in the hepatic venous pressure gradient (4% +/- 7% vs. 18% +/- 10% in placebo at 30 minutes, P < .001). Ascorbic acid followed by sham meal did not modify hepatic or systemic hemodynamics. In conclusion, patients with cirrhosis exhibited intrahepatic endothelial dysfunction, associated with decreased levels of ascorbic acid and increased levels of MDA. Ascorbic acid improved intrahepatic endothelial dysfunction, blunting the postprandial increase in portal pressure. These results encourage the performance of further studies testing antioxidants as adjunctive therapy in the treatment of portal hypertension.

Aged↗
PubMed1980

[Concentration of ascorbic acid in tissue of ovarian carcinoma (author's transl)].

The levels of ascorbic acid were measured in the tissue of 53 ovarian carcinomas and compared to concentrations in normal human ovarian tissue. The mean ascorbic acid concentrations per gram of tissue was 218 microgram in carcinoma tissue and 382 microgram in intact ovarian tissue. The difference was significant, with p less than 0.001. A relationship was found to exist between ascorbic acid concentrations in tumor tissue, on the one hand, stages of the disease, on the other. The importance of ascorbic acid to tumour growth is discussed.

Adult↗
PubMed1969

L-ascorbic acid synthesis in birds: phylogenetic trend.

The ability of several species of birds to synthesize L-ascorbic acid is correlated with their phylogeny. In the more primitive species, synthesis of L-ascorbic acid occurs in the kidney. Among the highly evolved passeriform species, kidney and liver can synthesize L-ascorbic acid in some, whereas in others synthesis occurs in the liver. In still others, the capacity for the synthesis of L-ascorbic acid is apparently lost. The pattern of evolution of the ascorbic acid pathway among birds is thus similar to that among mammals.

Animals↗
PubMed2000

Opposite effects of sulpiride and SCH 23390 on ethanol-induced striatal ascorbic acid release in intact and 6-hydroxydopamine lesioned rats.

The effects of L-sulpiride and SCH 23390 on ethanol-induced striatal ascorbic acid (AA) release in normal and 6-hydroxydopamine-lesioned rats were studied by using microdialysis coupled to high performance liquid chromatography with electrochemical detection. Ethanol (3.0 g/kg i.p.) significantly stimulated striatal AA release by 200% above the baseline in normal, 6-hydroxydopamine-lesioned, and reserpine-treated rats. L-Sulpiride, a dopamine D(2) antagonist, at the dose of 100 mg/kg i.p., decreased basal ascorbic acid release and showed an inhibitory tendency on ethanol-induced ascorbic acid release. However, at the higher dose of 200 mg/kg i.p., L-sulpiride significantly inhibited ethanol-induced ascorbic acid release in both normal and 6-hydroxydopamine-treated rats. SCH 23390, a dopamine D(1) antagonist, at the doses of 0.5 and 1.0 mg/kg i.p., potentiated ethanol-induced ascorbic acid release in normal rats. However, the potentiation of SCH 23390 on ethanol effect was not significant in 6-hydroxydopamine-treated rats at the dose of 1.0 mg/kg i.p. The present study demonstrates that opposite actions exist in the regulation of ethanol-induced ascorbic acid release in the striatum by dopamine D(1) and D(2) receptor blockade. It also suggests that the postsynaptic dopamine receptors are involved in mediation of ethanol-induced ascorbic acid release in rat striatum.

Animals↗
PubMed1997

Effects of co-supplementation of iron with ascorbic acid on antioxidant--pro-oxidant balance in the guinea pig.

The relationship between intake of iron with ascorbic acid and their uptake into the plasma and liver of guinea pigs was studied. The influence on the antioxidant/pro-oxidant balance of liver microsomes was also determined. Animals were fed a standard pelleted diet low in iron and ascorbic acid for 35 days. The pellet diet was supplemented by oral dosing with a solution containing either maintenance dietary levels of ascorbic acid and iron, or one of three regimens that increased the dosage of these substances ten fold. There were no significant differences in animal growth rate or food intake between these regimens. Liver and plasma total ascorbate levels were significantly increased (p < 0.05) in animals receiving either ascorbic acid alone (liver 126 +/- 36 micrograms/g tissue wet wt. and plasma 51.7 +/- 17.0 microM; n = 9) or ascorbic acid and iron (105 +/- 18 micrograms/g and 40.3 +/- 15.3.0 microM; n = 8) compared to controls (84 +/- 36 micrograms/g and 15.3 +/- 8.5 microM; n = 11). Total iron levels in the liver (76.7 +/- 7.3 micrograms/g; control; n = 6) and plasma (2.4 +/- 0.03 mg/l; control) were not significantly raised in animals under these conditions of iron or ascorbate intake. Liver microsomes isolated from animals receiving iron had a greater susceptibility to oxidative stress in terms of malondialdehyde production during auto-oxidation compared to those from control animals under the same conditions. This effect was eliminated on combining ascorbic acid with the iron supplementation, suggesting that oral administration of vitamin C has a protective rather than a pro-oxidant effect under these circumstances.

Administration, Oral↗
PubMed2004

Ascorbic acid reversibly inhibits proliferation of retinal pigment epithelial cells.

PURPOSE: Proliferation control in adult retinal pigment epithelial (ARPE) cells is an essential factor in the clinical management of proliferative vitreoretinopathy (PVR). Factors which inhibit PVR and which are without toxic potential are therefore of interest in controlling proliferation. The aim of the present study was to gain insight into a possible function of high intraocular ascorbic acid levels as a physiological modulator of proliferation. METHODS: Adult retinal pigment epithelial cells were incubated in vitro with increasing concentrations of ascorbic acid (0.5-4 mmol, pH 7.4). Cell proliferation was assayed by the bromide-deoxy-uridine (BrdU) assay. The culture medium (CM) containing ascorbic acid was replaced with normal CM and the recovery of proliferation was measured after 24 hours. In order to be able to distinguish between proliferation inhibition, apoptosis, necrosis and recovery of proliferation, we performed TUNEL assays and fluorescence analysis cell-counter (FAC) analysis. RESULTS: Ascorbic acid significantly inhibits ARPE cell proliferation if it is present in concentrations above 2 mmol. Proliferation resumed in all ARPE cell cultures after pre-incubation with ascorbic acid, indicating that direct toxicity of ascorbic acid is a negligible factor. The time-point and extent of recovery in proliferation was dependent on the initial ascorbic acid concentration. Fluorescence-labelled cell counts on apoptosis markers (FAC) data showed some induction of apoptosis and necrosis after incubation with 4 mmol ascorbic acid. CONCLUSIONS: Ascorbic acid has a dose-dependent influence on the proliferation of vital ARPE cells. This possibly reflects the role of ascorbic acid at a physiological level within the vitreous cavity in preventing proliferative vitreoretinopathy (PVR). These findings may stimulate the development of new strategies in the clinical treatment of PVR.

Apoptosis↗
PubMed1997

Thiamine oxidative transformations catalyzed by copper ions and ascorbic acid.

In aqueous solutions containing Cu(II) ions and ascorbic acid, thiamine was observed to be oxidized to the fluorescent products thiochrome and oxodihydrothiochrome in neutral and acid media. At high initial concentrations of thiamine, thiochrome was practically the only product of thiamine oxidation. Catalase inhibited the oxidation rate approximately by 30-fold, whereas superoxide dismutase reduced the rate by only 2.5-fold. Aliphatic alcohols, glucose, and high concentrations of ascorbic acid effectively inhibited the production of thiochrome. The yield of thiochrome was also decreased in the presence of aliphatic amino acids, histidine, and particularly human serum albumin (HSA). With complete binding of copper ions by HSA, no formation of fluorescent products was observed. In neutral and acidic media under the action of hydroxyl radicals, thiamine formed a tricyclic semiquinone form which was then oxidized to thiochrome by superoxide anion or H2O2. Ascorbic acid played the main role in the reduction of Cu(II), whereas the contribution of superoxide anions was less significant. Cu(I) interacted with H2O2 to form hydroxyl radicals. The addition of H2O2 both to thiamine and to the mixture of thiamine and Cu(II) ions did not lead to significant production of thiochrome in neutral and acidic media.

Ascorbic Acid↗
PubMed1980

The celluar interaction of ascorbic acid with histamine, cyclic nucleotides and prostaglandins in the immediate hypersensitivity reaction.

The role of ascorbic acid is reviewed in relation to the mechanism of release of chemical mediators in the immediate hypersensitivity reaction. In the initiation, and second, stages of the reaction, the property of ascorbic acid to chelate with calcium appears to play an importnat role in the ultimate release of the mediators. Furthermore, ascorbic acid may also control release of histamine and prostaglandins of the E and F types through its action on cyclic nucleotides and phosphodiesterase. In allergic inflammatory disease, leucocyte and tissue ascorbic acid levels are reduced. This may be due to the increased utilisation by cells involved in the antigen-antibody reaction. The suggestion that the balance between cyclic nucleotides is the main controlling mechanism for the release of chemical mediators during the reaction is inadequate to account for the essential role of other agents including ascorbic acid in the mechanism.

Animals↗
PubMed1992

Effect of ascorbic acid and curcumin on quercetin-induced nuclear DNA damage, lipid peroxidation and protein degradation.

The effects of ascorbic acid and curcumin on quercetin-induced DNA damage, lipid peroxidation protein degradation were investigated in a model system of isolated rat-liver nuclei under aerobic conditions and in the presence of equimolar concentrations of iron or copper. Neither ascorbic acid nor curcumin inhibited quercetin-induced nuclear DNA damage, lipid peroxidation, or protein degradation. In fact, both antioxidants stimulated the oxidative damage to nuclear macromolecules. Ascorbic acid significantly increased the quercetin-induced nuclear DNA damage in the presence of either iron or copper. The increases in quercetin-induced nuclear lipid peroxidation and protein degradation by ascorbic acid were statistically significant only in the presence of iron or copper, respectively. Similarly, stimulation of quercetin-induced DNA damage and lipid peroxidation by curcumin was statistically significant only in the presence of copper or iron, respectively. Curcumin had no significant effect on nuclear protein degradation. These results demonstrate the pro-oxidant properties of ascorbic acid and curcumin, compounds that also demonstrate antioxidant and anticarcinogenic properties. Ascorbic acid and curcumin may therefore each have a dual role in carcinogenesis.

Animals↗