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 955 records · Page 53Linked to original sources
PubMed1993

Secreted collagen induced by ascorbic acid in L5 cloned muscle cultures does not affect acetylcholine receptor expression.

Previous studies have shown that ascorbic acid increases both the total surface acetylcholine receptor (AChR) expression and the mRNA for the alpha-subunit of this receptor in myotubes of cloned L5 muscle cultures. Since ascorbic acid increases collagen synthesis in fibroblasts, we studied the effect of ascorbic acid on collagen secretion in L5 muscle cells and investigated the possibility that the effects of ascorbic acid on collagen and AChR are related. We report that L5 muscle cells secrete collagen types I, III, and V, with collagen type I being the most abundant species, and that accumulation of secreted collagens increased in the medium approximately two- to ninefold within 3 h of ascorbic acid treatment. The increase in surface AChRs, on the other hand, developed more slowly, and was detected only about 20-24 h after ascorbic acid treatment. A short (5 h) treatment with ascorbic acid is, however, sufficient to trigger an increase in AChRs 24 h later. Since ascorbic acid caused a rapid increase in collagen secretion, whereas the effect on total surface AChRs occurs more slowly, we tested the possibility that an increase in secreted collagen might be necessary for the increase in AChRs. However, when the L5 cultures were treated with bacterial collagenase, the ascorbic acid-induced increase in secreted collagen was abolished but its inductive effect on AChRs was unchanged. The increase in secreted collagen is therefore not necessary for the increase in AChRs to occur.

Animals↗
PubMed1984

Effects of ascorbic acid deficiency on methyl mercury dicyandiamide toxicosis in guinea pigs.

Methylmercury dicyandiamide (MMD) when given intraperitoneally at a dosage of 4 mg/kg of body weight at weekly intervals for 3 weeks resulted in death of guinea pigs fed an ascorbic acid deficient diet. Controls fed an ascorbic acid deficient diet survived during this period as did guinea pigs given MMD and fed an ascorbic acid adequate diet. In a second experiment, guinea pigs fed an ascorbic acid deficient diet containing 22 ppm of MMD died within 26 days and had severe hemorrhagic and ulcerative gastroenteritis and coagulative necrosis of the liver. Ascorbic acid deficient controls died at 34 days. The MMD-containing ascorbic acid adequate diet killed guinea pigs in 150 days. Guinea pigs fed an ascorbic acid deficient diet with 44 ppm of MMD died within 20 days with acute neurologic signs. Pathologic changes were mostly in the gray matter. Guinea pigs fed MMD and a diet with adequate ascorbic acid survived for 38 days whereas the ascorbic acid deficient controls survived for 47 days. Results indicate that ascorbic acid deficiency can be a factor in the location and severity of clinical signs and lesions of MMD.

Animals↗
PubMed1979

Accelerating effect of ascorbic acid on N-nitrosamine formation and nitrosation by oxyhyponitrite.

The reaction of nitrite ion with ascorbic acid and its effect on the rate of nitrosation of secondary amines have been investigated by differential pulse polarography in aqueous acidic solution. Ascorbic acid shows nonuniform behavior: it accelerates the nitrosation of N-methylaniline between pH 1.00 and 1.95, allows the nitrosation of diphenylamine and iminodiacetonitrile, but inhibits the nitrosation of secondary amines, such as dimethylamine, diethylamine, proline, hydroxyproline, N-methylaminoacetonitrile, N-methylaminopropionitrile, and sarcosine. The nitrosating agent generated by the reaction between ascorbic acid and nitrite ion appears to be oxyhyponitrite ion (N2O3-2).

Ascorbic Acid↗
PubMed2002

Endogenous released ascorbic acid suppresses ethanol-induced hydroxyl radical production in rat striatum.

Previous studies have shown that acute systemic administration of ethanol induced ascorbic acid release in the striatum. However, the pharmacological implications of ethanol-induced striatal ascorbic acid release are unclear. In the present study, ethanol-induced extracellular changes of ascorbic acid and hydroxyl radical levels were detected in rat striatum by using brain microdialysis coupled to high-performance liquid chromatography with electrochemical detection. It was found that both in male and female rats, ethanol (3.0 g/kg, i.p.) increased striatal ascorbic acid release in the first 60 min after ethanol administration. Meanwhile, the extracellular hydroxyl radical levels, detected as 2,3- and 2,5-DHBA, were significantly decreased. However, when the ascorbic acid levels returned to the baseline, hydroxyl radical levels rebounded. Administration of DL-fenfluramine (20 mg/kg, i.p.) had no effect on the basal levels of ascorbic acid and hydroxyl radical, but significantly blocked ethanol-induced ascorbic acid release and increased hydroxyl radical levels significantly. Exogenous administration of ascorbic acid (20 mg/kg, s.c.) increased the extracellular levels of ascorbic acid in the striatum, and inhibited the increase of 2,3- and 2,5-DHBA in DL-fenfluramine plus ethanol group. These results provide first evidence that release of endogenous ascorbic acid in the striatum plays an important role in preventing oxidative stress by trapping hydroxyl radical in the central nervous system.

Alcohol-Induced Disorders, Nervous System↗
PubMed2004

Ascorbic acid and mineral availability in two Nigerian plant foods.

This paper reports the effect of various concentrations of ascorbic acid on the availability of Fe, Zn, Ca and Mg in two popular plant foods--cowpea and amaranthus vegetable--in Nigeria. Ascorbic acid enhancement of iron availability was over 300 % and zinc by 200 % from 0-100 mg concentration. Availability of iron was further increased by 200 mg ascorbic acid in amaranthus but showed a 50 % decrease in the legume. Availability of zinc was decreased by 200 mg ascorbic acid but to different levels in both plant foods. In the legume, maximum enhancement of Ca and Mg availability was exhibited at 100 mg ascorbic acid level but suppressed at higher concentrations. In amaranthus, maximum Ca enhancement was exerted by 200 mg ascorbic acid and 50 mg for Mg. Enhancement of Cu in the legume was marginally affected by ascorbic acid concentrations while inhibition of Cu was observed in amaranthus between 50-300 mg ascorbic acid concentrations. The effect of ascorbic acid on the availability of minerals seems to be concentration dependent and varies with theplant food.

Amaranthus↗
PubMed2002

Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival.

The only proven requirement for ascorbic acid (vitamin C) is in preventing scurvy, presumably because it is a cofactor for hydroxylases required for post-translational modifications that stabilize collagen. We have created mice deficient in the mouse ortholog (solute carrier family 23 member 1 or Slc23a1) of a rat ascorbic-acid transporter, Svct2 (ref. 4). Cultured embryonic fibroblasts from homozygous Slc23a1(-/-) mice had less than 5% of normal ascorbic-acid uptake. Ascorbic-acid levels were undetectable or markedly reduced in the blood and tissues of Slc23a1(-/-) mice. Prenatal supplementation of pregnant females did not elevate blood ascorbic acid in Slc23a1(-/-) fetuses, suggesting Slc23a1 is important in placental ascorbic-acid transport. Slc23a1(-/-) mice died within a few minutes of birth with respiratory failure and intraparenchymal brain hemorrhage. Lungs showed no postnatal expansion but had normal surfactant protein B levels. Brain hemorrhage was unlikely to be simply a form of scurvy since Slc23a1(-/-) mice showed no hemorrhage in any other tissues and their skin had normal skin 4-hydroxyproline levels despite low ascorbic-acid content. We conclude that Slc23a1 is required for transport of ascorbic acid into many tissues and across the placenta. Deficiency of the transporter is lethal in newborn mice, thereby revealing a previously unrecognized requirement for ascorbic acid in the perinatal period.

Animals↗
PubMed1977

Differences in growth response to hydrocortisone and ascorbic acid by human diploid fibroblasts.

The effects of hydrocortisone and ascorbic acid on growth parameters were measured in human diploid skin fibroblasts from fetal and adult donors. In the presence of culture medium containing 10% fetal bovine serum, 0.3 micrometer hydrocortisone produced a 20% increase in the population growth rate and a 50 to 70% increase in the confluent density of fibroblasts from adult donors. Daily addition of 28 micrometer ascorbic acid also stimulated the population growth rate and cell density at confluency. The effects of hydrocortisone and ascorbic acid on the final cell density were additive. The action of hydrocortisone was restricted to cells in log-phase growth, whereas ascorbic acid affected cells in both the log and the post-confluent phases of the growth cycle. In fibroblasts from fetal donors, ascorbic acid was stimulative but hydrocortisone was not. The data suggest that whereas both compounds stimulate cell growth in an additive manner, they do so by different cellular mechanisms.

Adult↗
PubMed1999

Contribution of a high dose of L-ascorbic acid to carnitine synthesis in guinea pigs fed high-fat diets.

Ascorbate is a cofactor of two-enzyme hydroxylation in the pathway of carnitine biosynthesis. The purpose of this study was to investigate the contribution of ascorbate to endogenous carnitine in guinea pigs fed high-fat diets. The contents of carnitine in plasma, urine and tissues of guinea pigs supplemented with L-ascorbic acid were determined and compared with those supplemented with carnitine. Albino-Hartley guinea pigs were fed vitamin C-deficient diets containing lard throughout the experiment. They were administered orally with 5 mg L-ascorbic acid/d/animal for 14 d, and then divided into three groups and administered orally with the following supplements (/d/animal) for 14 d; L (5 mg L-ascorbic acid), LASA (100 mg L-ascorbic acid), and LCAR (10 mg carnitine plus 5 mg L-ascorbic acid). As a control, a normal group was fed vitamin C-deficient diets and administered orally with 5 mg L-ascorbic acid/d/animal for 28 d. The animals fed high-fat diets (L group) had higher free-carnitine contents in the muscle and urine than the normal group. The groups of LCAR and LASA had significantly higher contents of acid-soluble carnitine (p < 0.05) in plasma than the L group. Urinary excretion of carnitine in the LASA group was decreased to the same level as that in the normal group, although no significant difference between the groups of L and LCAR was observed. Moreover, the supplement of ascorbic acid, but not of carnitine, induced a significantly lower content of triacylglycerol in the plasma of the LASA group as compared to the L group (p < 0.05). These data suggest that high doses of ascorbic acid in guinea pigs fed high-fat diets contribute to the enhancement of carnitine synthesis and improvement of the triacylglycerol content in the plasma.

Animals↗
PubMed1984

Inverse association of serum ascorbic acid level and blood pressure or rate of hypertension in male adults aged 30-39 years.

Correlation analyses between serum ascorbic acid and several risk factors of cerebro- and cardio-vascular diseases were performed on apparently healthy adults (194 persons) aged 30-39 in order to estimate possible functions of ascorbic acid in the prevention of the disease. Serum ascorbic acid had an inverse and the strongest association with systolic blood pressure among the risk factors including blood pressure, total cholesterol, triglyceride, gamma-GTP and obesity. The association was independent of the other variables tested. When the subjects were divided into three different serum ascorbic acid level groups, the prevalence of hypertension (140/90 mmHg and above) was decreased with an increase in the ascorbic acid level. The close relationship of serum ascorbic acid and blood pressure observed in the study suggests that ascorbic acid may have a preventive function against hypertension, or a low ascorbic acid status in hypertensives may promote the further development of arteriosclerosis by the lack of favorable effect of ascorbic acid on lipid metabolism and others.

Adult↗
PubMed1992

Protective effect of ascorbic acid on the breakdown of proteins exposed to hydrogen peroxide in chicken skeletal muscle.

Ascorbic acid is believed to protect cells from oxidative damage by reacting with oxygen-derived free radicals. We investigated whether ascorbic acid would affect the rate of breakdown of skeletal muscle proteins in extracts exposed to hydrogen peroxide. Ascorbic acid (20 mmol/L) alone had little or no effect on the rate of ATP-independent or ATP-dependent breakdown of proteins in chicken skeletal muscle. Pretreatment of chicken skeletal muscle extracts with 10 mmol/L H2O2 resulted in a complete loss of ATP-dependent proteolysis and a significant increase (14- to 15-fold) in the rate of ATP-independent protein breakdown. Ascorbic acid (20 mmol/L) did not prevent H2O2 (10 mmol/L) from inactivating the ATP-dependent proteolytic pathway in skeletal muscle. However, ascorbic acid (20 mmol/L) prevented the H2O2-induced increase in the ATP-independent proteolysis of endogenous muscle proteins. Ascorbic acid also slowed the rate of hydrolysis of exogenously added [3H]superoxide dismutase exposed to H2O2 and inhibited the enhanced degradation of [3H]lysozyme and H2O2-treated [3H]superoxide dismutase by the proteolytic systems exposed to H2O2. Thus ascorbic acid seems to inhibit the H2O2-induced increase in ATP-independent proteolysis 1) by preventing damage to proteins by H2O2 resulting in a decreased supply of substrates for the ATP-independent degradative system and 2) by preventing activation of the proteolytic enzymes that participate in the energy-independent degradation of H2O2-treated proteins.

Adenosine Triphosphate↗
PubMed1985

Senile cataract and ascorbic acid loading.

Serum, aqueous humour, and lens ascorbic acid levels were determined by high-performance liquid chromatography in cataract-, closed-angle glaucoma-, and aphakic patients. The total number of 108 patients were subdivided into different groups. In several groups the pre-operative serum and aqueous amounts were tested, whereafter patients in some groups were loaded with ascorbic acid orally. Finally, a second test was performed on samples taken during operation. It turned out that the ascorbic acid concentration mechanism in cataractous eyes needed more than 12 h for maximum reaction on the loading stimulus. The slow reaction is surprising compared to other species, and it may reflect an affection of the secretory process itself in this disease.

Aged↗
PubMed2004

Relation of ascorbic acid to coronary artery calcium: the Coronary Artery Risk Development in Young Adults Study.

Ascorbic acid is an antioxidant nutrient possibly related to the development of atherosclerosis. To examine the relation between ascorbic acid and coronary artery calcium, an indicator of subclinical coronary disease, the authors analyzed data from 2,637 African-American and White men and women aged 18-30 years at baseline who were enrolled in the Coronary Artery Risk Development in Young Adults (CARDIA) Study (1985-2001). Participants completed diet histories at enrollment and year 7, and plasma ascorbic acid levels were obtained at year 10. Coronary artery computed tomography was performed at year 15. The authors calculated odds ratios in four biologically relevant plasma ascorbic acid categories, adjusting for possible confounding variables. When compared with men with high plasma ascorbic acid levels, men with low levels to marginally low levels had an increased prevalence of coronary artery calcium (multivariate odds ratio = 2.68, 95% confidence interval: 1.31, 5.48). Among women, the association was attenuated and nonsignificant (multivariate odds ratio = 1.50, 95% confidence interval: 0.58, 3.85). Ascorbic acid intakes from diet alone and diet plus supplements were not associated with coronary artery calcium. Low to marginally low plasma ascorbic acid levels were associated with a higher prevalence of coronary artery calcium among men but not among women.

Adolescent↗
PubMed1993

Evaluation of tissue ascorbic acid status in different hormonal states of female rat.

The distribution pattern of ascorbic acid in the endocrine organs and/or tissues was investigated during various sexual states of female rats to demonstrate a correlation between ascorbic acid concentration and sex hormone activity. The concentration of ascorbic acid was estimated in the plasma, liver, pancreas, thyroid, ovary, adrenal and pituitary of contraceptive steroid treated, bilaterally ovariectomized, sham-operated and normal control animals at four different phases of estrous cycle to delineate a relationship between the level of ascorbic acid in different organs/tissues at various sex hormonal states. Statistically significant changes were observed in the concentration of ascorbic acid in different endocrine organs/tissues following contraceptive steroid treatment, ovariectomy and during the estrous phases. Our results suggest that the concentration of ascorbic acid in the endocrine organs and/or tissues varies during different sexual states of rat.

Adrenal Glands↗
PubMed1992

Umbilical ascorbic acid levels in fetal distress.

Umbilical arterial and venous blood samples were obtained at birth immediately after clamping the cord in 38 infants. Simultaneously, maternal arterial samples were collected. Arterial blood samples were analyzed for acid-base blood gas content and venous blood samples were analyzed for plasma ascorbic acid levels. The umbilical plasma ascorbic acid level was significantly higher when compared with maternal plasma levels (172.9 +/- 39.2 vs. 57.8 +/- 21.0 mumol/liter, p < 0.0001). Correlations between maternal ascorbic acid levels and umbilical cord levels proved to be insignificant. Umbilical ascorbic acid levels in the 2 groups of infants characterized by the presence or absence of fetal distress showed significantly higher levels in the fetal distressed group (17 infants) when compared to the non-distressed group (21 infants)--191.9 +/- 36.0 vs. 157.4 +/- 34.6 mumol/liter, p < 0.005. The use of an umbilical cord ascorbic acid cut-off point of 95.8 mumol/liter gave a sensitivity of 76% and a specificity of 67% as predictors for the presence or absence of fetal distress (p < 0.025). The results of the present study demonstrate a substantial increase in ascorbic acid levels in infants exposed to intrapartum fetal distress, without any clinical sign of such insult at or after birth.

Adult↗
PubMedDate not supplied

Ascorbic acid enhances hypoxic ventilatory reactivity in elderly subjects.

The reducing properties of ascorbic acid in the carotid body make it a likely modifier of hypoxia-sensing mechanisms. This open-label study aimed to determine the effect of ascorbic acid on the hypoxic ventilatory response (HVR) in a population of elderly women, in whom both hypoxic reactivity and ascorbic acid levels may be deficient. We examined the HVR to progressive eucapnic hypoxia in 18 healthy females aged 60-80 years, before and after 10 days' ascorbic acid supplementation, given as a sustained release preparation of 1 g twice daily. Respiratory variables were recorded breath by breath, and hypoxic sensitivity was assessed from the linear slopes of minute ventilation and mouth occlusion pressure plotted against oxygen saturation. We found that ascorbic acid increased the HVR by a mean of 44%, this effect being driven by a higher occlusion pressure. We conclude that augmentation of hypoxic reactivity by ascorbic acid may have therapeutic potential in pathologies associated with hypoxia, which frequently develop in old age.

Aged↗
PubMed1990

Kinetics of the reaction of prostaglandin H synthase compound II with ascorbic acid.

The reduction of prostaglandin H synthase compound II by ascorbic acid in the presence of diethyldithiocarbamate was studied in 0.1 M phosphate buffer (pH 8.0) at 4.0 +/- 0.5 degrees C, by rapid scan spectrometry and transient state kinetics. A saturation effect and nonzero intercept were observed in the plot of pseudo-first-order rate constant versus ascorbic acid concentration. The saturation behavior suggests formation of a complex between prostaglandin H synthase compound II and ascorbic acid, whereas the nonzero intercept is attributable to the reaction of compound II of prostaglandin H synthase with diethyldithiocarbamate present in the system as a stabilizing agent. A rate equation has been derived which includes all pathways for the conversion of prostaglandin H synthase compound II back to native enzyme. Kinetic parameters for the reduction of compound II by ascorbic acid were obtained. They are the second-order rate constant of (1.4 +/- 0.5) X 10(5) M-1, S-1, for the formation of the compound II-ascorbic acid complex, the first-order rate constant of (14 +/- 4) S-1 for the oxidation-reduction reaction of the complex and its dissociation, and a parameter, Km of 92 +/- 10 microM analogous to the Michaelis-Menten constant. Thus we demonstrate that a quantitative kinetic study on the prostaglandin H synthase reactions can be performed in the presence of diethyldithiocarbamate.

Alkenes↗
PubMed1983

Effects of ascorbic acid deficiency on the in vitro biosynthesis of cyclooxygenase metabolites in guinea pig lungs.

Endogenous levels of ascorbic acid may play a role in regulating the biosynthesis of cyclooxygenase metabolites in lungs of male guinea pigs. The in vitro biosyntheses of prostaglandins, prostacyclin and thromboxane were examined using isolated microsomal membranes from control and ascorbic acid deficient guinea pigs, under conditions in which the substrate concentration ( [3H]-arachidonic acid) was varied from 10-100 microM. Maintenance of guinea pigs for two weeks on an ascorbic acid deficient diet did not alter lung/body weight ratios, nor protein content of the lungs. Lung microsomes from ascorbic acid deficient guinea pigs demonstrated a greater biosynthesis of total cyclooxygenase metabolites at low substrate concentrations. A significant increase in the PGF2 alpha synthesis was observed in the scorbutic microsomes at 20 microM arachidonic acid. At higher substrate concentrations the production of PGF2 alpha was significantly reduced in ascorbic acid deficient animals. By contrast, biosynthesis of thromboxane or prostacyclin in treated animals was not significantly different from control microsomes. At a substrate concentration of 100 microM, there was equivalent synthesis of total cyclooxygenase metabolites in control and vitamin C deficient animals. The changes in prostaglandin biosynthesis were not due to an interaction of ascorbic acid with glutathione levels in the lung. These results support the hypothesis that ascorbic acid may modulate cyclooxygenase activity in the lung in a substrate dependent nature.

Animals↗