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 721 records · Page 40Linked to original sources
PubMed2001

Effect of dietary vitamin C on concentrations of ascorbic acid in plasma and milk.

The addition of exogenous ascorbic acid to milk reduces the development of oxidized flavor. This experiment was conducted to determine whether feeding ascorbic acid to cows influenced vitamin C concentrations in milk. Thirty-two midlactation Holstein cows were fed a basal diet of 56% forage, 36.6% concentrate, and 7.4% roasted whole soybeans (dry basis) that was top-dressed with a premix that provided 0, 3, 16.5, or 30 g/d of L-ascorbic acid (provided by ascorbyl-2-polyphosphate) for 28 d. Supplementation had no effect on milk yield or composition or dry matter intake. Treatment linearly increased plasma concentrations of ascorbic acid (19.8, 22.3, 21.9, and 25.7 mumol/L, respectively) but had no effect on plasma dehydro-L-ascorbic acid (DHAA). Concentrations of ascorbic acid (103.7 mumol/L) and DHAA (9.5 mumol/L) in milk were not affected by treatment. Secretion of ascorbic acid into milk appeared to follow Michaelis-Menton kinetics, with a Vmax of 3.92 mmol/d and a Km of 3.59 mumol/L. Milk flavor as evaluated by a panel was normal for all samples after 1 d of storage. After 7 d of storage, the average flavor score was 2.5 (moderate oxidized flavor), but no differences among treatments were observed. Supplemental dietary vitamin C did not increase vitamin C concentration in milk, probably because the maximum potential secretion of the vitamin was occurring in unsupplemented cows.

Animals↗
PubMed1997

Mechanisms by which ascorbic acid increases ferritin levels in cultured lens epithelial cells.

A previous study demonstrated that ascorbic acid increased the concentration of the iron storage protein, ferritin. In cultured lens epithelial cells. The current study was designed to determine the mechanism by which ascorbic acid exerts this effect. Ascorbic acid increased both ferritin mRNA levels (by about 30%) and translation of ferritin (de novo synthesis was increased up to 15-fold) within 6 hr. Cycloheximide completely abolished the ability of ascorbic acid to increase ferritin levels, whereas actinomycin D only decreased it by about 30%. Therefore, the ascorbic-acid induced increase in ferritin concentration is due mainly to an increase in ferritin synthesis at the translational levels. This is a novel role for ascorbic acid. Addition of iron with ascorbic acid further increased de novo synthesis of ferritin, but this additive effect was only noted at a later time point (20 hr). Factors which decrease ferritin mRNA translation, such as the reducing agent dithiothreitol or the iron chelator desferrioxamine, reduced the ascorbic acid effect on de novo ferritin synthesis. The effects of ascorbic acid on ferritin mRNA levels may be mediated by its oxidation product, H2O2, since, like ascorbic acid, H2O2 increased ferritin mRNA levels by 30%. However, in contrast to the ascorbic acid-induced increase in translation of ferritin, H2O2 substantially decreased de novo ferritin synthesis. This effect of H2O2 could have physiological significance in eyes where concentrations of H2O2 in the aqueous humor are elevated. High levels of H2O2 could decrease the concentration of ferritin within the lens. Since ferritin sequesters iron and has been shown to decrease oxidative damage by limiting the availability of iron to catalyse free radical reactions, H2O2-induced reduction in ferritin concentration in the lens could have deleterious effects. The ability of ascorbic acid to increase ferritin concentration in lens epithelial cells could provide an additional protective mechanism for this antioxidant vitamin. The importance of ferritin to normal lens functioning is underscored by the recent finding that humans with a dominantly inherited abnormality in ferritin synthesis exhibit early bilateral cataracts.

Animals↗
PubMed2001

Oral intake and serum levels of ascorbic acid in continuous ambulatory peritoneal dialysis patients.

Oral intake of ascorbic acid is essential for optimum health in human beings. Continuous ambulatory peritoneal dialysis (CAPD) patients have an increased need for ascorbic acid, because of increased loss through dialysate, reduced intake owing to nausea and loss of appetite, and increased oxidative stress. However, optimum intake is still controversial. We studied 50 clinically stable patients to determine the relationship between oral ascorbic acid intake and serum ascorbic acid (SAA) level. Total oral intake ranged from 28 mg daily to 412 mg daily. Only one patient had an oral intake of ascorbic acid below 60 mg per day. The SAA levels ranged from 1 mg/L to 36.17 mg/L. Although a strong correlation existed between intake and SAA (p < 0.001, R2 = 0.47), the variation in SAA at any given intake level was wide. Of the studied patients, 62% had an SAA < 8.7 mg/L, 40% had an SAA < 5.1 mg/L (below the level in a healthy population), and 12% had a level below 2 mg/L (scorbutic). None of the patients demonstrated clinical manifestations of scurvy. Our results show that, in CAPD patients, ascorbic acid deficiency can be reliably detected only with SAA measurements, and oral intake may influence SAA level. To maintain ascorbic acid in the normal range for healthy adults, daily oral intake needs to be increased above the U.S. recommended dietary allowance to 80-140 mg.

Aged↗
PubMed1982

Inhibitory effects of ascorbic acid on the binding of [3H]dopamine antagonists to neostriatal membrane preparations: relationship to lipid peroxidation.

Ascorbic acid, sodium ascorbate, and isoascorbic acid (the stereoisomer of ascorbic acid) inhibited the stereospecific binding of [3H]spiroperidol to neostriatal membrane preparations. Greater inhibitory effects were obtained at intermediate concentrations of the three ascorbic acid analogs (i.e., 0.06 and 0.6 mM) than at higher (6 mM) or lower (0.006 mM) concentrations. In parallel experiments, the three ascorbic acid analogs induced lipid peroxidation, which was also greater at the two intermediate than at higher or lower concentrations. Several known inhibitors of lipid peroxidation, including propyl gallate, butylated hydroxyanisole, butylated hydroxytoluene, alpha-naphthol, and cobalt chloride, as well as the iron chelating agents EDTA and DETAPAC (diethylenetriaminepentaacetic acid) were able to counteract the effects of the ascorbic acid analogs on both lipid peroxidation and on [3H]spiroperidol binding. These data strongly suggest that an iron-catalyzed lipid peroxidation is responsible for the observed inhibitory effects on binding. In other experiments, neostriatal membrane preparations that were preincubated with ascorbic acid (0.6 mM) and subsequently washed still had greatly diminished capacity to bind [3H]spiroperidol, indicating that ascorbic acid need not be physically present during the binding assay in order to affect binding. This experimental procedure also appears to be a way in which [3H]spiroperidol binding sites can be inactivated and washed free of the inactivating agent.

Animals↗
PubMed1994

Ascorbic acid and plasma lipids.

We examined the association between plasma lipids and total ascorbic acid in 256 men and 221 women age 20-65 years. Among men, we observed that high-density lipoprotein (HDL) cholesterol was 2.1 mg per dl higher, total:HDL cholesterol was 5.4% lower, total cholesterol was 4.8 mg per dl lower, low-density lipoprotein (LDL) cholesterol was 5.6 mg per dl lower, and triglyceride was 5.2% lower for each 0.5 mg per dl increment in ascorbic acid. The association between ascorbic acid and total:HDL cholesterol ratio in men was modified by glucose concentration. Among women, we observed that HDL cholesterol was 14.9 mg per dl higher for women with ascorbic acid levels < or = 1.05 mg per dl and 0.9 mg per dl lower for women with ascorbic acid levels > 1.05 mg per dl for each 0.5 mg per dl increment in ascorbic acid. Total:HDL cholesterol ratio was 10.9% lower for women with ascorbic acid concentrations < or = 1.45 mg per dl and 0.6% higher for women with ascorbic acid concentrations > 1.45 mg per dl for each 0.5 mg per dl increment. The associations among ascorbic acid concentration, total and LDL cholesterol, and triglyceride concentrations were weak or absent among women. These results are consistent with earlier observations relating ascorbic acid and HDL cholesterol and indicate that ascorbic acid might also be related to total and LDL cholesterol concentrations in men.

Adult↗
PubMed1991

Ascorbic acid regeneration in chromaffin granules. In situ kinetics.

We have investigated in intact chromaffin secretory vesicles the kinetics, specificity, and mechanism of intragranular ascorbic acid regeneration by extragranular ascorbic acid. The apparent Km of internal ascorbic acid regeneration for external ascorbic acid was 280 microM by Lineweaver-Burk analysis and 287 microM by Eadie-Hofstee analysis. Intragranular ascorbic acid regeneration was specifically mediated by extragranular ascorbic acid or its isomer isoascorbic acid; the reducing agents glutathione, thiourea, homocysteine, NADH, and NADPH did not support regeneration. The structural analog D-glucose did not inhibit regeneration by external ascorbic acid, suggesting specificity at the membrane site of electron transfer. The driving force for regeneration of intragranular ascorbic acid was independent of membrane potential, absolute intragranular and extragranular pH, and ATPase activity, but might be coupled to the pH difference across the chromaffin granule membrane. Since the apparent Km of regeneration was approximately 10-fold below the cytosolic concentration of ascorbic acid, the reaction may proceed at Vmax in situ.

Adenosine Triphosphatases↗
PubMed1993

Control of enzymatic browning in apple slices by using ascorbic acid under different conditions.

Control of phenol oxidase activity in apple slices by the use of ascorbic acid at different pH values, temperature and time of incubation was investigated. The enzyme was almost inactivated at 1% and 1.5% ascorbic acid. Ascorbic acid solution (1%) caused a remarkable inhibition with the increasing acidity up to pH = 1. Heating treatments for apple slices dipped in 1% ascorbic acid caused a reduction of enzymatic browning, optimum temperature for inactivation of the enzyme was between 60-70 degrees C for 15 minutes. Increasing the time of dipping apple slices in 1% ascorbic acid solutions and at different pH values reduce phenolase activity.

Ascorbic Acid↗
PubMed1987

Effect of ascorbic acid on the synaptosomal uptake of [3H]MPP+, [3H]dopamine, and [14C]GABA.

The effects of ascorbic acid on the synaptosomal uptake of [3H]MPP+, [3H]dopamine, and [14C]GABA were examined in attempts to understand the mechanism of ascorbic acid attenuation of MPTP neurotoxicity. [3H]Dopamine uptake was increased at lower levels (0.01 and 0.1 mM) and decreased at higher levels (10 mM) of ascorbic acid. Ascorbic acid inhibited [3H]MPP+ uptake (IC50 = 0.1 mM) and [14C]GABA uptake (IC50 = 10 mM). Washout of ascorbic acid restored uptake of [3H]dopamine and [3H]MPP+, suggesting that ascorbic-acid-induced lipid peroxidation was not involved in the effect on uptake. In addition to the possible involvement of antioxidant mechanisms in the in vivo attenuation of the neurotoxicity of MPTP by ascorbic acid, the present results indicate a direct effect of ascorbic acid in inhibiting the uptake of MPP+ into dopaminergic nerve terminals.

1-Methyl-4-phenylpyridinium↗
PubMed1992

[Ascorbic acid. Cytotoxic effect on cultivated bovine lens epithelium cells].

Ascorbic acid is one of the main components (1.16 mM/l) of the aqueous humor. The molarity of this molecule is 25 times higher than in the plasma of the cow, man or horse. Now the question arises as to which function ascorbic acid has in this extremely high concentration referring to the proliferation of the lens epithelial cells. Thus, the effect of ascorbic acid was investigated upon bovine lens epithelial cells (BLEC) in the range of 0-3 mM/l. These cells were cultivated under various culture conditions (serum-free, serum-containing, aqueous-humor-containing medium) and also incubated with such mitogens as retinal extract (RE), crude endothelial cell growth factor (cECGF), basic fibroblast growth factor (bFGF) or with calcium. In each culture condition 1 mM/l ascorbic acid caused remarkable inhibition of the proliferation of BLEC. Higher concentrations (> 1.5 mM/l) revealed cytotoxic effects. These effects were independent of small variations in the pH value caused by ascorbic acid. In addition, the effect of 2 mM/l ascorbic acid in combination with catalase in a concentration of 500 Um/ml and 1000 Um/ml, respectively, was investigated. It could be shown that catalase is capable of preventing the cytotoxic effect of ascorbic acid. These results show the inhibitory effect of ascorbic acid in its physiological concentration in the proliferation of BLEC.

Animals↗
PubMed1976

Effect of organic phosphates on methemoglobin reduction by ascorbic acid.

The rate of methemoglobin reduction by ascorbic acid was accelerated in the presence of ATP,2,3-diphosphoglycerate (2,3-DPG), and inositol hexaphosphate (IHP). The acceleration was as much as three times, four times, and ten times in the presence of ATP, 2.3-DPG, and IHP at pH 7.0, respectively. The changes of the concentrations of methemoglobin and ascorbic acid during the methemoglobin reduction were determined, and the reaction was found to proceed stoichiometrically in the presence of IHP. The reduction rate of methemoglobin by ascorbic acid was compared at different concentrations of organic phosphates (ATP,2,3-DPG, and IHP) at various pH values (6.3, 7.0, 7.7). From the changes in the reduction rate under different concentrations of organic phosphates, the dissociation constants of ATP, 2,3-DPG, and IHP to methemoglobin could be determined and were estimated to be 3.3 X 10(-4) M, 2 X 10(-3) M, and 8 X 10(-6) M at pH 7.0, respectively. On the basis of these results, the acceleration mechanism of methemoglobin reduction by ascorbic acid due to the presence of organic phosphates was described. The physiological role of 2,3-DPG in human red cells was discussed in relation to the reduction of methemoglobin by ascorbic acid.

Adenosine Triphosphate↗
PubMed1993

Regulation of collagen synthesis in human dermal fibroblasts in contracted collagen gels by ascorbic acid, growth factors, and inhibitors of lipid peroxidation.

Ascorbic acid has been shown to stimulate collagen synthesis in monolayer cultures of human dermal fibroblasts. In the present studies, we examined whether the presence of a collagen matrix influences this response of dermal fibroblasts to ascorbic acid. Fibroblasts and collagen were mixed and allowed to gel and contract for 6 days to form a matrix prior to determining the concentration and time dependence for ascorbic acid to affect collagen synthesis by fibroblasts within the matrix. Collagen synthesis was stimulated at levels at or above 10 microM ascorbic acid and was maximal after 2 days of treatment. This concentration and time dependence is similar to that of cells grown in monolayer cultures. The effects of transforming growth factor-beta (TGF-beta) and fibroblast growth factor (FGF) were also examined in this model. TGF-beta increased and FGF inhibited collagen synthesis in the gels, as has been shown for cells in monolayer cultures. The effects of potential inhibitors of lipid peroxidation induced by ascorbic acid were also examined in these matrices and compared to previous results obtained in monolayer cultures. Propyl gallate, cobalt chloride, alpha,alpha-dipyridyl, and alpha-tocopherol inhibited the ascorbic acid-mediated stimulation of collagen synthesis while mannitol had no effect. Natural retinoids inhibited total protein synthesis without the specific effect on collagen synthesis that was seen in monolayer cultures. These results indicate that ascorbic acid stimulates collagen synthesis in fibroblasts grown in a collagen matrix in a manner similar to that found in monolayer cultures. In contracting collagen gels, however, the magnitude of the effect is less and retinoids do not specifically inhibit collagen synthesis.

2,2'-Dipyridyl↗
PubMed1989

Stimulation of collagen gene expression by ascorbic acid in cultured human fibroblasts. A role for lipid peroxidation?

Ascorbic acid stimulates collagen gene expression in cultural fibroblasts (Lyons, B. L., and Schwartz, R. L. (1984) Nucleic Acids Res. 12, 2569-2579), but the mechanisms responsible for this effect are poorly understood. In the presence of the transitional metal iron, ascorbic acid could induce lipid peroxidation with the formation of reactive aldehydes. Since another aldehyde, acetaldehyde, the first metabolite of ethanol, also stimulates collagen transcription in cultured fibroblasts (Brenner, D. A., and Chojkier, M. (1987) J. Biol. Chem 262, 17690-17696), we investigated whether ascorbic acid induces lipid peroxidation in cultured cells and if this is the mechanism by which ascorbic acid stimulates collagen gene expression. Ascorbic acid (0.2 mM) induced lipid peroxidation in cultured human fibroblasts judging by the production of thiobarbituric acid-reactive substances and carbonyl groups, and by the presence of malondialdehyde- and 4-hydroxynonenal-protein adducts. Ascorbic acid stimulated (2-3-fold) the net production of collagen relative to total proteins, the levels of procollagen alpha 1 (I) mRNA and the transcription of this gene. Inhibition of the ascorbic acid-induced lipid peroxidation in cultured human fibroblasts with alpha-tocopherol (50 microM) or methylene blue (10 microM) prevented the stimulation of collagen gene expression. The addition of malondialdehyde (200 microM), a product of lipid peroxidation, to cultured human fibroblasts also increased 2-3-fold collagen production and procollagen alpha 1 (I) mRNA levels. Thus, ascorbic acid induces lipid peroxidation and reactive aldehydes and this step may be necessary for the stimulation of collagen gene expression by ascorbic acid in cultured human fibroblasts.

Ascorbic Acid↗
PubMed1993

Suppression of gamma- and neutron-induced neoplastic transformation by ascorbic acid in Balb/c 3T3 cells.

The effects of ascorbic acid on the neoplastic transformation induced by 60Co gamma-rays or 252Cf fission neutrons were studied. The transformation induced by each of the radiations was markedly suppressed when ascorbic acid was added daily to the culture medium during the first 8 days of the post-irradiation period. If ascorbic acid was added for a total of 8 days as mentioned above, but with 1 day interruption in the middle, the suppression of transformation was decreased. Ascorbic acid also suppressed the promotion of radiation transformation by 12-O-tetradecanoylphorbol-13-acetate (TPA) when both chemicals were added to the medium together. However, promotion of radiation transformation by TPA was observed if both the chemicals were added sequentially during the post-irradiation period, i.e. ascorbic acid for the first 7 days followed by TPA. These results suggest that continuous administration of ascorbic acid for a certain number of days is needed to suppress the radiation transformation, and also suggest that it acts on the promotion stage of transformation.

3T3 Cells↗
PubMed1983

The effect of ascorbic acid on the human lymphocyte.

Human lymphocytes obtained from normal, healthy subjects were studied for their in vitro responses to ascorbic acid. Ascorbic acid inhibited the incorporation of 3H-uridine as well as the phytohaemagglutin-associated enhancement of 3H-thymidine incorporation.

Ascorbic Acid↗
PubMed2003

Evaluation of the population of NADPH-diaphorase-stained and myosin-V myenteric neurons in the ileum of chronically streptozotocin-diabetic rats treated with ascorbic acid.

We investigated the effect of the ascorbic acid on the nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d)-stained and myosin-V myenteric neurons in the ileum of chronically diabetic rats. The study was performed 4 months after inducing experimental diabetes with streptozotocin. Diabetic rats showed increased (p<0.05) glycaemia and glycated haemoglobin. Three groups were compared, i.e., nondiabetic rats, diabetic rats and diabetic rats treated with ascorbic acid. Myosin-V immunohistochemistry and NADPH-d histochemistry were employed. We investigated the areas of 500 cell bodies of myosin-V neurons and of 500 NADPH-d-stained neurons from all groups. The quantitative analysis was performed by using an area of 8.96 mm(2) from each ileum. The two groups of diabetic rats and diabetic rats treated with ascorbic acid showed reduction in the number and an increased area of the myosin-V-immunostained myenteric neurons. In addition, we observed increased relative proportion of NADPH-d-stained neurons in diabetic rats and diabetic rats treated with ascorbic acid. However, the area of these neurons in the diabetic rats group was larger than those evidenced in the nondiabetic rats and diabetic rats treated with ascorbic acid.

Animals↗
PubMed1983

Evaluation of ascorbic acid in protecting labile folic acid derivatives.

The use of ascorbic acid as a reducing agent to protect labile, reduced derivatives of folic acid has been evaluated by high-performance liquid chromatographic separations and Lactobacillus casei microbiological assay of eluate fractions. Upon heating for 10 min at 100 degrees C, solutions of tetrahydropteroylglutamic acid (H4PteGlu) in 2% sodium ascorbate gave rise to 5,10-methylene-H4PteGlu and 5-methyl-H4PteGlu. H2PteGlu acid gave rise to 5-methyl-H4PteGlu and PteGlu. 10-Formyl-H4PteGlu gave rise to 5-formyl-H4PteGlu and 10-formyl-PteGlu. 5-Formyl-H4-PteGlu gave rise to a small amount of 10-formyl-PteGlu. 5-Methyl-H4PteGlu and PteGlu appeared stable to these conditions. These interconversions were not seen when solutions of these folate derivatives were kept at 0 degrees C in 1% ascorbate. These observations indicate that elevated temperatures are necessary for the interconversions of folates in ascorbate solutions. Assays of ascorbic acid solutions indicated the presence of formaldehyde (approximately equal to 6 mM). This was confirmed by the identification of 3,5-diacetyl-1,4-dihydrolutidine by UV, visible, and fluorescence spectroscopy and by thin-layer chromatography of chloroform extracts of the reaction mixture of ascorbic acid solutions, acetylacetone, and ammonium acetate. These results indicate that solutions of sodium ascorbate used at elevated temperatures are not suitable for extracting tissue for the subsequent assay of the individual folic acid derivatives.

Ascorbic Acid↗
PubMed1990

Abnormalities of ascorbic acid metabolism and diabetic control: differences between diabetic patients and diabetic rats.

Ascorbic acid is required in the synthesis of collagen and is also an important anti-oxidant. In a previous study, plasma ascorbic acid concentration was found to be decreased in diabetic patients but there was no relationship with blood glucose level. In the current study of diabetic patients, both plasma ascorbic acid and its urinary excretion correlated inversely with glycosylated hemoglobin level. Plasma ascorbic acid was also lower in diabetic rats but urinary ascorbic acid was elevated. The divergent trend in urinary ascorbic acid excretion observed in diabetic patients and diabetic rats may be due to difference in the ability of these two species to synthesize ascorbic acid. Difference in renal reabsorption of ascorbic acid may also be a relevant factor. The lower plasma and urinary ascorbic acid levels in diabetic patients with more severe hyperglycaemia indicates that this group of patients is particularly at risk of developing deficiency of this vitamin. As ascorbic acid has many important functions in the body, it may be necessary to supplement this vitamin in patients with chronically poorly controlled diabetes.

Adult↗