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 1,315 records · Page 73Linked to original sources
PubMed1989

Transport and metabolism of ascorbic acid in human placenta.

The role of human placenta in cellular transport and metabolism of the potentially toxic oxidized form and the useful reduced form of ascorbic acid was examined in surviving tissue fragments in vitro. At the end of a 60-min incubation with the 14C label nominally present in the reduced form, a tissue-to-medium ratio in excess of unity was reached. The importance of evaluating uptake of the ascorbic acid metabolites is evident from a careful assay of 14C label present in the bathing media. Significant spontaneous oxidation occurs, which is slowed or reversed to a limited extent by the presence of placental tissue. Uptake of the oxidized substrate, dehydro-L-ascorbic acid, proceeds much more rapidly than uptake of ascorbic acid. At the end of a 15-min incubation, most of the substrate taken up was in the reduced form. From an additional evaluation of 14C label in the bath it is calculated that 25% of ascorbic acid formed by the tissue is released within 15 min. The cellular uptake mechanism for dehydro-L-ascorbic acid is not shared by glucose and is not dependent on the presence of Na+ but is dependent on intact cellular metabolism. The finding of avid cellular uptake and reduction of the oxidized form of ascorbic acid supports the concept that the placenta helps to clear the toxic molecule from the maternal circulation, metabolizes it, and delivers the useful reduced form to the fetus.

2,3-Diketogulonic Acid↗
PubMed1988

Brain ascorbic acid levels: mice and rats selected for differences in acute reactions to ethanol.

There are variations of ascorbic acid levels in different brain areas of mice and rats. However, there are no differences in ascorbic acid levels between lines of mice selectively bred for differences in ethanol sensitivity for 25 generations. Thus, it is unlikely that brain ascorbic acid plays a significant role in the acute sedative effects of ethanol in these mice. Studies with inbred strains of mice known to differ in ethanol preference, acute sensitivity and withdrawal sensitivity also failed to reveal any differences in brain ascorbic acid levels. There were differences in ascorbic acid content between selectively bred lines of rats in various brain areas at generation five of selection.

Animals↗
PubMed1979

Effect of dietary supplementation of iron and ascorbic acid on lead toxicity in rats.

In our laboratory, the protective and therapeutic effects of surplus dietary iron and ascorbic acid on cadmium toxicity in rats have been studied and in this experiment, an effect of surplus iron and ascorbic acid on lead toxicity was examined. In young rats ingesting a diet containing 500 ppm of lead, growth retardation and anemia were observed. Suplementation of 400 ppm of iron and 1% of ascorbic acid to the lead containing diet prevented the growth depression and anemia and caused reductions of concentrations of lead in the kidney and tibia. Whereas, addition of 50 ppm of cadmium to the lead containing diet aggravated the growth retardation and anemia, but reduced the concentrations of lead in the kidney and tibia. Dietary supplementation of iron to the lead containing diet prevented the growth depression and anemia and reduced the accumulation of lead in the kidney, however the supplementation of ascorbic acid alone did not show any ameliolative effects. Rats were fed the lead containing diet and then transferred to the basal diet with or without iron and ascorbic acid. Recoveries from the growth retardation and anemia were not observed in rats within a week after the transfer to the non-lead diet with or without iron and ascorbic acid. These results suggest that iron prevents the growth depression and anemia in rats ingesting lead by an inhibition of lead asborption.

Animals↗
PubMed1998

Protection by alpha-tocopherol but not ascorbic acid from hydrogen peroxide induced cell death in normal human breast epithelial cells in culture.

Alpha-tocopherol and ascorbic acid have been suggested to play a role in breast cancer prevention due to their antioxidative capacity. Increased exposure to endogenous and exogenous sex steroids is a known risk factor for breast cancer. We have studied the effects of alpha-tocopherol and ascorbic acid on hydrogen peroxide induced cell death in sex hormone treated normal breast epithelial cells in culture. We found that alpha-tocopherol but not ascorbic acid alone protected the cells. The effect of alpha-tocopherol increased when ascorbic acid was added to the cultures. The hydrogen peroxide degradation rate decreased in cultures treated with alpha-tocopherol alone and in combination with ascorbic acid compared to cells grown in medium or with ascorbic acid only. Oestradiol and progesterone treatment did not influence the results. Possible beneficial effects of combining various antioxidants, endogenous as well as exogenous, on human breast tissue need to be investigated further both in vivo and in vitro.

Ascorbic Acid↗
PubMed2000

Polyhydroxybenzoates inhibit ascorbic acid activation of mitochondrial glycerol-3-phosphate dehydrogenase: implications for glucose metabolism and insulin secretion.

Glycerol-3-phosphate dehydrogenase from pig brain mitochondria was stimulated 2.2-fold by the addition of 50 microm l-ascorbic acid. Enzyme activity, dependent upon the presence of l-ascorbic acid, was inhibited by lauryl gallate, propyl gallate, protocatechuic acid ethyl ester, and salicylhydroxamic acid. Homogeneous pig brain mitochondrial glycerol-3-phosphate dehydrogenase was activated by either 150 microm L-ascorbic acid (56%) or 300 microm iron (Fe(2+) or Fe(3+) (62%)) and 2.6-fold by the addition of both L-ascorbic acid and iron. The addition of L-ascorbic acid and iron resulted in a significant increase of k(cat) from 21.1 to 64.1 s(-1), without significantly increasing the K(m) of L-glycerol-3-phosphate (10.0-14.5 mm). The activation of pure glycerol-3-phosphate dehydrogenase by either L-ascorbic acid or iron or its combination could be totally inhibited by 200 microm propyl gallate. The metabolism of [5-(3)H]glucose and the glucose-stimulated insulin secretion from rat insulinoma cells, INS-1, were effectively inhibited by 500 microm or 1 mm propyl gallate and to a lesser extent by 5 mm aminooxyacetate, a potent malate-aspartate shuttle inhibitor. The combined data support the conclusion that l-ascorbic acid is a physiological activator of mitochondrial glycerol-3-phosphate dehydrogenase, that the enzyme is potently inhibited by agents that specifically inhibit certain classes of di-iron metalloenzymes, and that the enzyme is chiefly responsible for the proximal signal events in INS-1 cell glucose-stimulated insulin release.

Animals↗
PubMed1987

Behavioral effects of salbutamol and/or L-(+)-ascorbic acid in the mouse after single and multiple dosing.

The acute and chronic effects of salbutamol alone and L-(+)-ascorbic acid alone and in combination were evaluated on "open-field" test in mice. Administered singly and acutely (30 min before the test), both salbutamol (0.003 mmol/kg i.p.) and L-(+)-ascorbic acid (0.35-0.71 and 1.42 mmol/kg i.p.) significantly reduced ambulation scores. This decrease was higher in L-(+)-ascorbic acid - than in salbutamol-treated mice. Rearing behavior was significantly increased only in salbutamol-treated animals. In animals treated chronically (once a day for 15 days) the depression of salbutamol-induced ambulation was more marked than in mice treated acutely. This decrease was partially reversed by L-(+)-ascorbic acid treatment. With respect to rearing scores, a significant increase was found after salbutamol and L-(+)-ascorbic acid administered alone or in combination. In conclusion, these experiments show that salbutamol induces a direct effect on behavior, that is to reduce motor activity, being the reduction more marked after chronic treatment. The association of the beta 2-agonist with L-(+)-ascorbic acid can attenuate some of the depressant effects of chronic salbutamol administration on behavior.

Albuterol↗
PubMed1981

Effect of dietary level of ascorbic acid on the growth, hepatic lipid peroxidation, and serum lipids in guinea pigs fed polychlorinated biphenyls.

Rats exposed to polychlorinated biphenyls (PCB) or other xenobiotics exhibit an increase in tissue and urinary ascorbic acid, serum cholesterol and hepatic lipid peroxidation. To clarify the physiological role of ascorbic acid in exposure to PCB, we studied the influence of dietary levels of ascorbic acid (30-2,000 ppm) on the growth, serum lipids and hepatic lipid peroxidation in guinea pigs fed 50 ppm PCB-containing diets. The results showed that the growth depression due to PCB was ameliorated by increasing dietary ascorbic acid. The increases in serum cholesterol and phospholipid and in hepatic lipid peroxidation due to PCB were suppressed by larger amounts of ascorbic acid, which inversely correlated with the changes in growth. PCB intake also increased serum levels of cortisol and triglyceride, but these effects were not influenced by dietary level of ascorbic acid. The optimum requirement of ascorbic acid in the guinea pigs fed PCB was 800-2,000 ppm in the diet for the changes in the growth, serum cholesterol and hepatic lipid peroxidation.

Animals↗
PubMed1986

Scavenging of chlorpromazine cation radical by ascorbic acid or glutathione.

The report presented here demonstrates that scavenging of chlorpromazine cation radical (an absorption maximum = 530 nm) by ascorbic acid or glutathione can be kinetically and stoichiometrically analyzed at pH 1.5 but not at pH 3.0 and 6.0 using a conventional absorption spectrophotometer. The cation radical decays spontaneously about 10 and 200 times faster at pH 3.0 and 6.0, respectively, than at pH 1.5. At pH 1.5, ascorbic acid scavenges the cation radical faster than glutathione does, and the following different scavenging mechanisms are postulated from the above kinetic and stoichiometric analysis. The reaction of the cation radical with ascorbic acid is second order. The ascorbic acid free radical, which decays mainly by dismutation, is generated by the bimolecular reaction. In the case of glutathione, on the other hand, about 70% of the scavenged cation radical disappears through free radical chain reactions that glutathione thiol anion and glutathione free radical probably initiate. The remaining (about 30%) disappears by conjugation with glutathione. It may be due to relative nonreactivity of ascorbic acid free radical that free radical chain reactions, found commonly in radical chemistry, do not occur in the scavenging reaction by ascorbic acid. Based on the above results, the physiological scavenging mechanisms of the cation radical by the two reducing substances are discussed briefly.

Ascorbic Acid↗
PubMedDate not supplied

Ascorbic acid (vitamin C) effects on withdrawal syndrome of heroin abusers.

BACKGROUND: Ascorbic acid (vitamin C), administered orally in high doses has been observed to relieve pain and reduce opioid use in cancer patients. In vitro studies have also shown that antioxidants, such as vitamin C, may, at high concentrations, inhibit the endogenous opioid degrading metalloenzyme and increase endorphin levels. In the present study the effects of oral administration of high doses of vitamin C on withdrawal syndrome of heroin abusers were investigated. MATERIALS AND PATIENTS: Ascorbic acid at doses of 300 mg/kg b.w/day, supplemented with vitamin E (5 mg/kg b.w/day), was orally administered in two groups of heroin addict subjects consisting of in-patients (Group A, 30 males) and one of out-patients(Group B, 10 males), for a minimum of 4 weeks. The group A in-patients were also administered the conventional (diazepam + analgesic) medication. The results on the intensity of withdrawal syndrome (WS), estimated according to DMS-III criteria, were compared to a third group of heroin addict in-patients (group C, 30 males-control group), treated only by conventional medication. RESULTS: The patients of the vitamin C-treated groups (in-patients and out-patients) experienced mild WS (in 46.6% to 50% of the subjects) in contrast to the control group patients, who experienced mild WS in 6.6% of the cases. The vitamin C-treated subjects expressed major WS ranging from 10% to 16.6%, in contrast to the untreated subjects (control group), who expressed a major WS in 56.6% of the cases. CONCLUSIONS: The results indicate that high doses of ascorbic acid administered orally, may ameliorate the withdrawal syndrome of heroin addicts. Further studies are needed in order to estimate the dose- and time-dependent effects of ascorbic acid treatment, and to clarify its mechanisms of action in the withdrawal syndrome.

Adult↗
PubMed1995

Effect of different levels of an ascorbic acid and tea mixture on nonheme iron absorption from a typical Tunisian meal fed to healthy rats.

The aim of our study was to evaluate the bioavailability of iron from a typical Tunisian meal 'couscous' provided to healthy rats with or without appropriate mixtures of tea plus ascorbic acid and to search for the optimal amount of ascorbic acid able to overcome the inhibitory effect of tea prepared under realistic Tunisian circumstances. Our findings show that a tea decoction (100 mg/ml) reduced nonheme iron absorption from couscous by 50% (16.5 vs. 33.1%; p < 0.01). In contrast, administration of 20 mg ascorbic acid increased nonheme iron absorption from couscous by more than 100% (66.8 vs. 33.1%; p < 0.001). Administration of ascorbic acid (20 mg) in a tea decoction (100 mg/ml) completely counteracted the inhibiting effect of tea and significantly improved the nonheme iron absorption from couscous (34 vs. 33% in the control group; NS). The same effect was shown when 10 mg ascorbic acid was added to the tea decoction; however, 5 mg ascorbic acid was not able to overcome the inhibitory effect of tea on nonheme iron absorption from couscous (33.1 vs. 19.4%; p < 0.01). Our findings demonstrate that a molar ratio of ascorbic acid and tea equal or superior to 0.25 or 0.50 is necessary to overcome the inhibitory effect in rats of tea prepared under Tunisian circumstances. In relation to human nutrition, for Tunisians who regularly drink tea, we suggest a much greater amount of ascorbic acid than that normally recommended for normal subjects.

Absorption↗
PubMed1991

The influence of choline ascorbate on the blood levels of ascorbic acid in humans.

Our study has clearly shown that the oral administration of choline ascorbate, which contains approximately 500 mg of ascorbic acid to the volunteers causes an increase in the blood levels of ascorbic acid. This increase is statistically significant (p less than 0.01) compared with the basal level each time. In the control group, vitamin C tablet also causes an increase in the blood level of ascorbic acid. However, this increase is less than that of the test group. Our results indicate that ascorbic acid, as a part of choline ascorbate molecule, reaches the blood circulation without losing its activity.

Administration, Oral↗
PubMed1994

Effect of processing and storage on the ascorbic acid (vitamin C) content of some pineapple varieties grown in the Rivers State of Nigeria.

Ascorbic acid contents of the juice of four different pineapples species grown in the Rivers State of Nigeria were determined before and after storage of whole pineapple and processing and storage of the juice for two months. Ascorbic acid of the fresh juice ranged from 22.5 mg to 33.5 mg/100 g sample. After storage at room temperature (30-32 degrees C) of whole pineapple for two weeks, ascorbic acid was reduced to between 59 and 65 percent of the fresh juice. Processing the juice by pasteurisation reduced the ascorbic acid to between 28 and 46 percent while storage in plastic bottles for two months further reduced the ascorbic acid content to between 10 and 21 percent.

Ascorbic Acid↗
PubMedDate not supplied

In vitro effect of ascorbic acid on neutrophil-endothelial cell interaction.

The effect of different concentrations (0.06, 0.6 and 6.0 mmol/L) of ascorbic acid on neutrophil-endothelial interaction was studied using an in vitro model of human umbilical cord vein endothelial cells and human neutrophils. The aim of the study was to determine changes in chemiluminescence response of neutrophils during adherence to endothelial cells. Because adherence of neutrophils to endothelial cells is an essential component in inflammatory processes leading to endothelial cell injury, the influence of ascorbic acid on adherence and endothelial cell injury have been investigated. Production of oxygen-derived metabolites, measured by chemiluminescence response of neutrophils, decreased significantly in the presence of 6 mmol/L ascorbic acid during coincubation of neutrophils and endothelial cells (p < 0.025). The adherence of neutrophils to endothelial cells was significantly decreased at a concentration of 6 mmol/L (p < 0.0005). The inhibition of neutrophil adherence to endothelial cells was correlated with a diminished neutrophil-mediated endothelial cell injury during incubation with 6 mmol/L ascorbic acid (p < 0.0005). The present results indicate that ascorbic acid might exert a protective effect on neutrophil-mediated endothelial cell injury by decreasing adherence of neutrophils to endothelial cells and by scavenging reactive oxygen metabolites. Moreover, the current investigation points to probable protective effect of ascorbic acid on oxidant-mediated cell damage in diseases (e.g., Adult Respiratory Distress Syndrome).

Ascorbic Acid↗
PubMed2003

Effect of sodium nitrite and ascorbic acid on the growth and acid production of Streptococcus mutans.

UNLABELLED: Nitrite at acid pH has been shown to be antibacterial particularly against the highly cariogenic species Streptococcus mutans. Nitrite might yield nitrosamines in vivo but ascorbic acid (vitamin C) could counteract these potential ill effects. The aim of this study is to determine whether ascorbic acid would interfere with the ability of sodium nitrite to suppress growth and acid production of S. mutans, NCTC 10449(T) and NCTC 10832. Strains were grown in Fastidious Anaerobe Broth before exposure to 200 mM nitrite in the presence of various concentrations of ascorbic acid (0.0, 5.7, 11.4, 17.0, 22.7, 28.4, 56.8, 85.2 mM). End pH was measured after 24 h exposure and cultures were serially diluted for viable counts. Statistical significance of differences in end pH values, each from 10 experiments, was determined using the Mann-Whitney U-Test. At all concentrations of ascorbic acid plus 200 mM nitrite plus S. mutans the pH was higher than with controls lacking ascorbic acid and/or nitrite (p>/=0.001). S. mutans was viable (between 4.5 x 10 (8) and 7.9 x 10 (9) cfuml (-1)) after growth in the presence of ascorbic acid at all concentrations without nitrite, whereas it was not detected when 200 mM nitrite was also present. CONCLUSIONS: ascorbic acid does not prevent the action of nitrite against S. mutans. Therefore ascorbic acid could be used in conjunction with nitrite to help counteract potential ill effects for humans.

Acids↗
PubMed1993

Ascorbic acid and focal cerebral ischaemia in a primate model.

Neuronal cell damage following ischaemia is postulated to be due to free radical induced lipid peroxidation, and ascorbic acid is supposedly an important non-enzymatic scavenger of such free radicals. This study was undertaken to evaluate the protective effect of ascorbic acid on the brain in a primate model after focal cerebral ischemia. Consumption of ascorbic acid in the monkey brain following ischaemia and its effect on macroscopic infarct size as demonstrated by 2, 3, 5, Triphenyl tetrazolium chloride (TTC) staining were used as parameters. The monkeys in the treated group were given 1 gram ascorbic acid parenterally every day for six days. The mean level of total ascorbic acid in right basal ganglia was 35.1 +/- 4.2 micrograms/mg of protein in the treated group as opposed to 22.9 +/- 2.1 micrograms/mg of protein in the nontreated group both before ischaemia. After right middle cerebral artery occlusion to produce focal cerebral ischaemia, the total ascorbic acid in the right basal ganglia 2 hours post ischaemia was 13.3 +/- 3.1 micrograms/mg of protein in the treated group as opposed to 9 +/- 1.6 micrograms/mg of protein in the untreated group. The average consumption of total ascorbic acid was 21.8 micrograms/mg of protein in the treated group and 13.9 micrograms/mg of protein in the nontreated group. Macroscopic infarct size as determined by TTC staining in the right cerebral hemisphere was 11.7 +/- 6.9 in treated group whereas it was 24.4 +/- 4.4 (expressed as percentage of right hemisphere) in the non-treated group. There was significant reduction in the size of the infarct in the treated group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

Megadosage of ascorbic acid in an Antarctic expedition.

1. No difference in health was observed between men on megadosage of ascorbic acid and controls during the year of an Antarctic expedition. 2. All men appeared to have a satisfactory intake of ascorbic acid throughout the year. 3. There was a statistically significant decrease in excretion of ascorbic acid by men on megadosage over the year, and by the controls. 4. The decline in excretion by the control group may be explained by dietary change, but the decline in those on megadosage may be due to altered handling of ascorbic acid by the body. 5. No complications due to megadosage of ascorbic acid were observed.

Antarctic Regions↗
PubMed2002

Ascorbic acid concentration is reduced in the aqueous humor of patients with exfoliation syndrome.

PURPOSE: To investigate whether there is a role for ascorbic acid in the development of exfoliation syndrome (XFS). DESIGN: A case-control study was undertaken that included consecutive patients with and without XFS in whom cataract surgery was indicated. Patients with ophthalmic conditions other than XFS and conditions that may influence ascorbic acid levels were excluded. METHODS: A prospective institutional study was undertaken. A small volume of aqueous humor was aspirated at the beginning of phacoemulsification cataract surgery. Eighty aqueous samples, 40 samples from 40 eyes of 40 cataract patients with XFS and 40 samples from 40 eyes of 40 age matched cataract patients without XFS, were collected and analyzed. Ascorbic acid concentration was evaluated in the aqueous samples with a microplate assay method. RESULTS: The mean +/- SD concentration of ascorbic acid in the aqueous from patients with XFS (0.86 +/- 0.43 mM; range, 0.12 to 1.7 mM) was significantly lower than the concentration of ascorbic acid found in the aqueous of age-matched control patients (1.15 +/- 0.50 mM; range 0.42 to 3.1 mM; P =.0068). Total mean protein concentration was found to be significantly higher in the XFS group (481.1 +/- 196.8 pg/dl versus 336.3 +/- 86.4 pg/dl in the controls; P <.0001). Nevertheless, no correlation could be established between ascorbic level and protein concentration. CONCLUSIONS: A significantly reduced mean level of ascorbic acid was observed in the aqueous humor of patients with XFS. In view of the fact that ascorbic acid is a major protective factor against free radical action, a role for free radical action is possible in the pathobiology of XFS.

Aged↗
PubMedDate not supplied

Uncoupling of incorporation of ascorbic acid and apoptosis induction.

Exposure of human promyelocytic leukemic HL-60 cells to millimolar concentration of sodium ascorbate induced apoptotic cell death. The extent of apoptosis induction was a positive function of temperature at the time of exposure. The incorporation of [1-14C] ascorbic acid into the cytosolic fraction of HL-60 cells was also temperature-dependent, and competitively inhibited by active analogs (L-ascorbic acid, sodium L-ascorbate, D-isoascorbic acid, sodium 6-beta-O-galactosyl-L-ascorbate, sodium 5,6-benzylidene-L-ascorbate), but not by inactive analogs (L-ascorbic acid-2-phosphate magnesium, L-ascorbic acid 2-sulfate). Calcium depletion, which had considerably reduced the apoptosis-inducing activity of sodium ascorbate, did not affect the intracellular incorporation of [14C] ascorbic acid. These data suggests that cell death might not be simply induced by the intracellular incorporation of ascorbate, but rather initiated by the rapid elevation of intracellular Ca2+ concentration, possibly mediated by an as yet unidentified temperature-sensitive mechanism.

Apoptosis↗