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PubMed2001

Intracellular ascorbic acid enhances the DNA single-strand breakage and toxicity induced by peroxynitrite in U937 cells.

A well-established protocol to increase the intracellular content of ascorbic acid was used to investigate the effects of the vitamin on DNA single-strand breakage and toxicity mediated by authentic peroxynitrite (ONOO(-)) in U937 cells. This protocol involved exposure for 60 min to 100 microM dehydroascorbic acid, which was taken up by the cells and converted into ascorbic acid via a GSH-independent mechanism. At the time of exposure to ONOO(-), which was performed in fresh saline immediately after loading with dehydroascorbic acid, the vitamin present in the cells was all in its reduced form. It was found that, in cells that are otherwise ascorbate-deficient, an increase in their ascorbic acid content does not prevent, but rather enhances, the DNA-damaging and lethal responses mediated by exogenous ONOO(-). These results therefore suggest that acute supplementation of ascorbic acid can be detrimental for individuals with pathologies associated with a decrease in ascorbic acid and in which ONOO(-) is known to promote deleterious effects.

Ascorbic Acid↗
PubMed2003

A comparative study between a brain Na+,K(+)-ATPase inhibitor (endobain E) and ascorbic acid.

In the search of Na+,K(+)-ATPase modulators, we have reported the isolation by gel filtration and HPLC of a brain fraction, termed endobain E, which highly inhibits Na+,K(+)-ATPase activity. In the present study we compared some properties of endobain E with those of ascorbic acid. Kinetic experiments assaying synaptosomal membrane K(+)-p-nitrophenylphosphatase (K(+)-p-NPPase) activity in the presence of endobain E or ascorbic acid showed that in neither case did enzyme inhibition prove competitive in nature versus K+ or p-NPP concentration. At pH 5.0, endobain E and ascorbic acid maximal UV absorbance was 266 and 258 nm, respectively; alkalinization to pH 14.0 led to absorption drop and shift for endobain E but to absorbance disappearance for ascorbic acid. After cysteine treatment, endobain E absorbance decreased, whereas that of ascorbic acid remained unaltered; iodine treatment led to absorbance drop and shift for endobain E but to absorbance disappearance for ascorbic acid. HPLC analysis of endobain E disclosed the presence of two components: one eluting with retention time and UV spectrum indistinguishable from those of ascorbic acid and a second, as yet unidentified, both exerting Na+,K(+)-ATPase inhibition.

4-Nitrophenylphosphatase↗
PubMed1987

Mechanism of ascorbic acid regeneration mediated by cytochrome b561.

In summary, ascorbic acid serves as a one-electron donor for dopamine beta-hydroxylase in chromaffin vesicles and probably for peptide amidating monooxygenase in neurohypophyseal secretory vesicles. It appears that the semidehydroascorbate that is produced is reduced by cytochrome b561 to regenerate intravesicular ascorbate. Cytochrome b561, a transmembrane protein, is reduced in turn by an extravesicular electron donor, probably cytosolic ascorbic acid. It will be interesting to see whether other ascorbate-requiring enzymes in other organelles use a similar ascorbate-regenerating system to provide an intravesicular supply of reducing equivalents.

Animals↗
PubMed1993

Clinical trials using ascorbic acid aerosol to aid smoking cessation.

Sensory aspects of cigarette smoke are important for providing smoking satisfaction. In previous studies, we have found that substitution of the sensory cues of smoking with a citric acid aerosol significantly reduces craving for cigarettes and enhances smoking reduction and cessation with people trying to quit smoking cigarettes. In the current study, we conducted two clinical smoking cessation trials using an ascorbic acid aerosol as a sensory substitute. The cigarette substitute consisted of a cigarette-sized tube which delivered a fine aerosol of ascorbic acid (approx. 1 mg/puff, up to a maximum of 300 mg/day). Study 1 examined the overall effectiveness of the ascorbic acid smoking substitute device. One group of subjects which used the device and received clinical counseling was compared with another group which received only clinical counseling. The group using the device showed significantly greater abstinence rates at 3 weeks post-cessation. After the subjects stopped using the device, no difference in abstinence was detected. Study 2 was conducted to focus specifically on the role of tracheobronchial sensations in relieving craving for cigarettes. Two closely matched ascorbic acid delivery systems were compared. One device delivered fine particles of ascorbic acid that were targeted to reach the trachea, while the other delivered coarser particles of ascorbic acid that were not expected to reach the trachea or lower airways. An initial enhancement in smoking reduction was found for subjects using the fine particle device relative to those using the coarse particle device. However, by the end of treatment (5 weeks) both groups showed similar degrees of smoking reduction. For those who were abstinent from smoking at the end of treatment, craving for cigarettes and negative mood were both significantly lower for those using the fine particle device. Also, hunger for food was significantly lower in the fine particle device group. These results suggest that ascorbic acid delivered from a cigarette substitute may be effective in reducing smoking and promoting smoking abstinence.

Adult↗
PubMed1981

Ischaemic heart disease and aged patients: effects of ascorbic acid on lipoproteins.

Aged men and women with ischaemic heart disease had higher total triglyceride levels than controls, and also lower mean percentage cholesterol levels in the high-density lipoprotein fraction. Subnormal levels of leucocyte ascorbic acid were found in 15/25 patients. In men, but not in women, the initial leucocyte ascorbic acid levels were correlated positively with HDL-cholesterol concentrations. After six weeks treatment with ascorbic acid, the mean HDL-cholesterol concentration had increased not only in all men, but also in those women with IHD. Furthermore, total serum cholesterol and LDL-cholesterol concentrations were reduced in men with IHD, but triglyceride levels were not significantly changed; whereas in women with IHD both total serum and VLDL-triglycerides were reduced. Ascorbic acid deficiency appears to contribute to disorders of lipoprotein metabolism in the aged. Latent ascorbic acid deficiency may be one of several preventable 'risk' factors contributing to the present epidemic of IHD in the western world.

Aged↗
PubMed2004

Ascorbic acid suppresses drug-induced apoptosis in human colon cancer cells by scavenging mitochondrial superoxide anions.

Although a high alimentary intake of antioxidant vitamins such as ascorbic acid may play an important role in cancer prevention, a high level of antioxidants may have quite different effects at different stages of the transformation process. In cancer development, the resistance of cells to apoptosis is one of the most crucial steps. We have tested the effects of ascorbic acid on apoptosis in HT-29 human colon carcinoma cells when induced by two potent apoptosis inducers, the classical antitumor drug camptothecin or the flavonoid flavone. Apoptosis was assessed based on caspase-3-like activity, plasma membrane disintegration and finally nuclear fragmentation and chromatin condensation. Ascorbic acid dose-dependently inhibited the apoptotic response of cells to camptothecin and flavone. RT-PCR analysis and western blot analysis revealed that ascorbic acid specifically blocked the decrease of bcl-X(L) by camptothecin or flavone. An increased generation of mitochondrial O(2)(-.) precedes the down-regulation of bcl-X(L) by camptothecin and flavone and ascorbic acid at a concentration of 1 mM prevented the generation of this reactive oxygen species. In conclusion, ascorbic acid functions as a potent antioxidant in mitochondria of human colon cancer cells and thereby blocks drug-mediated apoptosis induction allowing cancer cells to become insensitive to chemotherapeutics.

Antioxidants↗
PubMed1992

Ascorbic acid oxidation: a potential cause of the elevated severity of atherosclerosis in diabetes mellitus?

The exposure of mouse peritoneal macrophages to cholesterol linoleate-containing artificial lipoproteins can lead to intracellular ceroid accumulation. This can be used as a model to study the role of oxidation in macrophage uptake of lipoproteins containing unsaturated fatty acids, considered by many as a primary event in atherosclerotic plaque formation. Our studies show that ascorbic acid can both inhibit and promote the formation of ceroid in such a model system. The transition metal copper (Cu(II)) further elevates ceroid accumulation and EDTA, a metal chelator, inhibits it. When trace levels of transition metals are present, low concentrations of ascorbic acid can elevate ceroid formation. This pro- and antioxidant characteristic of ascorbic acid was confirmed by monitoring the generation of oxidants by various concentrations of ascorbic acid, assessed by benzoic acid hydroxylation or the fragmentation of BSA. We discuss these observations in the context of an apparent increase in ascorbic acid oxidation and elevated severity of atherosclerosis in diabetes mellitus.

Animals↗
PubMed1985

Reduction in hepatic lipid and plasma estradiol in estrogenized chicks injected with ascorbic acid.

Injecting White Leghorn chicks every other day with 20 mg ascorbic acid significantly reduced the increase in liver weight and lipids caused by feeding a diet with 0.1% dienestrol diacetate. In chicks fed two different basal diets containing 0.1% dienestrol diacetate, injecting chicks every other day with 20 mg alpha-tocopherol did not significantly reduce liver weight or lipids while the ascorbic acid injections did. Injecting meat-type chicks implanted with estradiol with 10 mg ascorbic acid daily significantly reduced liver weight, liver lipids, and plasma estradiol, but injecting with 8 mg alpha-tocopherol daily had no significant effect.

Animals↗
PubMed2005

Ascorbic acid improves impaired venous and arterial endothelium-dependent dilation in smokers.

AIM: To compare the acute effects of ascorbic acid on vasodilation of veins and arteries in vivo. METHODS: Twenty-six healthy non-smokers and 23 healthy moderate smokers were recruited in this study. The dorsal hand vein compliance technique and flow-mediated dilation were used. Dose-response curves to bradykinin and sodium nitroprusside were constructed to test the endothelium-dependent and -independent relaxation before and after acute infusion of ascorbic acid. RESULTS: Smokers had an impaired venodilation with bradykinin compared with non-smokers (68.3%+/-13.2% vs 93.7%+/-20.1%, respectively; P<0.05). Ascorbic acid administration in the dorsal hand vein significantly increased the venodilation with bradykinin in smokers (68.3%+/-13.2% vs 89.5%+/-6.3% before and after infusion, respectively; P<0.05) but not in non-smokers (93.7%+/-20.1% vs 86.4%+/-12.4% before and after infusion, respectively). Similarly, the arterial response in smokers had an impaired endothelium-dependent dilation compared with that in non-smokers (8.8%+/-2.7% vs 15.2%+/-2.3%, respectively; P<0.05) and ascorbic acid restored this response in smokers (8.8%+/-2.7% vs 18.7%+/-6.5% before and after infusion, respectively; P<0.05), but no difference was seen in non-smokers (15.2%+/-2.3% vs 14.0%+/-4.4% before and after infusion, respectively). The endothelium-independent dilation did not differ in both the groups studied. No important hemodynamic change was detected using the Portapress device. CONCLUSION: Smokers had impaired endothelium-dependent vasodilation responsiveness in both arterial and venous systems. Ascorbic acid restores this responsiveness in smokers.

Adult↗
PubMed2001

Mechanism of ascorbic acid oxidation by cytochrome b(561).

The 1 equiv reaction between ascorbic acid and cytochrome b(561) is a good model for redox reactions between metalloproteins (electron carriers) and specific organic substrates (hydrogen-atom carriers). Diethyl pyrocarbonate inhibits the reaction of cytochrome b(561) with ascorbate by modifying a histidine residue in the ascorbate-binding site. Ferri/ferrocyanide can mediate reduction of DEPC-treated cytochrome b(561) by ascorbic acid, indicating that DEPC-inhibited cytochrome b(561) cannot accept electrons from a hydrogen-atom donor like ascorbate but can still accept electrons from an electron donor like ferrocyanide. Ascorbic acid reduces cytochrome b(561) with a K(m) of 1.0 +/- 0.2 mM and a V(max) of 4.1 +/- 0.8 s(-1) at pH 7.0. V(max)/K(m) decreases at low pH but is approximately constant at pH >7. The rate constant for oxidation of cytochrome b(561) by semidehydroascorbate decreases at high pH but is approximately constant at pH <7. This suggests that the active site must be unprotonated to react with ascorbate and protonated to react with semidehydroascorbate. Molecular modeling calculations show that hydrogen bonding between the 2-hydroxyl of ascorbate and imidazole stabilizes the ascorbate radical relative to the monoanion. These results are consistent with the following mechanism for ascorbate oxidation. (1) The ascorbate monoanion binds to an unprotonated site (histidine) on cytochrome b(561). (2) This complex donates an electron to reduce the heme. (3) The semidehydroascorbate anion dissociates from the cytochrome, leaving a proton associated with the binding site. (4) The binding site is deprotonated to complete the cycle. In this mechanism, an essential role of the cytochrome is to bind the ascorbate monoanion, which does not react by outer-sphere electron transfer in solution, and complex it in such a way that the complex acts as an electron donor. Thermodynamic considerations show that no steps in this process involve large changes in free energy, so the mechanism is reversible and capable of fulfilling the cytochrome's function of equilibrating ascorbate and semidehydroascorbate.

Animals↗
PubMed2001

Stability of dietary ascorbic acid and the effect of supplementation on reproductive performance of broiler breeder chickens.

1. The purpose of the study was to determine the stability of dietary ascorbic acid and the reproductive responses of broiler breeder chickens to supplemental 75 mg ascorbic acid/kg diet. 2. Six breeder flocks of 13,000 birds each were studied. Egg production, eggshell porosity, fertility, hatchability and plasma ascorbic acid were measured. 3. Storage of the diets under dry heat resulted in a linear decrease in ascorbic acid content and the rate of decline was 5-fold higher in the supplemented diet. 4. Differences were not detected between treatments in egg production, egg weight, eggshell porosity, fertility, hatchability or plasma ascorbic acid. 5. The results did not provide evidence of a beneficial reproductive response to the inclusion of ascorbic acid in commercial broiler breeder diets.

Animals↗
PubMed1985

Elevated levels of dietary ascorbic acid increase immune responses in channel catfish.

Channel catfish fingerlings were fed purified diets containing 0 to 3000 mg/kg of ascorbic acid until external signs of scurvy were seen in the fish fed the ascorbic acid-deficient diet. At this time, resistance to bacterial infection, antibody production, complement activity and phagocytic activity were assessed for fish from the various dietary treatments. Mortality rates of fish experimentally infected with Edwardsiella ictaluri, the bacterium causing enteric septicemia in channel catfish, decreased with increases in dietary ascorbic acid doses, ranging from 100% for fish fed the ascorbic acid-deficient diet to 15% for fish fed 300 mg ascorbic acid per kilogram diet and 0 for fish fed 3000 mg ascorbic acid per kilogram diet. Antibody response to E. ictaluri antigen, hemolysis of sensitized sheep erythrocytes by complement activity and phagocytic engulfment of E. ictaluri by peripheral phagocytes were each impaired in fish fed the diet without supplemental ascorbic acid; intracellular bactericidal activity of the phagocytes was not affected by ascorbic acid deficiency. There were no differences in antibody production, complement activity, or phagocytic activities among fish fed diets containing 30-300 mg ascorbic acid/kg of diet. However, the dose level of 3000 mg ascorbic acid/kg significantly enhanced antibody production and complement activity.

Animal Nutritional Physiological Phenomena↗
PubMed1983

Leucocyte ascorbic acid levels in Nigerian children with protein-energy malnutrition.

Leucocyte ascorbic acid (LAA) levels were estimated in 26 Nigerian infants and preschool children with protein energy malnutrition (PEM) in order to ascertain their ascorbic acid status. The children included eight with kwashiorkor, 12 with marasmus and six with marasmic kwashiorkor. The mean (SD) LAA level of 13.7 (8.2) micrograms/10(8) leucocytes in the malnourished children did not vary significantly from the mean level of 14.4 (8.8) micrograms/10(8) leucocytes found in 26 age-matched controls, and the values were unrelated to the presence or absence of megaloblastic change in the 14 bone marrows examined. It was concluded that ascorbic acid deficiency was not prevalent amongst children with PEM in Lagos, and was therefore not usually contributory to the anaemia, megaloblastic changes or other features of the syndrome seen in Nigerian children in Lagos.

Ascorbic Acid↗
PubMed1975

Transport of ascorbic acid in perfused rat lung.

Rat lungs were perfused by recycling Krebs-bicarbonate solution in an apparatus which allowed negative pressure ventilation of the lungs. After addition of either reduced or oxidized ascorbic acid to the perfusion fluid serial samples were taken over 60 min and assayed for ascorbic acid. At the end of perfusion, lungs were assayed for ascorbic acid. The results show that reduced ascorbic acid was taken up by the lung and concentrated in the tissue. No appreciable transport of oxidized ascorbic acid was measured.

Animals↗
PubMed2004

Coronary endothelial dysfunction is not rapidly reversible with ascorbic acid.

In humans with cardiovascular risk factors, increased vascular production of superoxide anion may contribute to endothelial dysfunction by its reacting with nitric oxide and reducing its biological activity. High concentrations of ascorbic acid scavenge superoxide anion and restore normal endothelium-dependent vasodilation in humans with cardiovascular risk factors. To investigate the contribution of increased superoxide anion to endothelial dysfunction in atherosclerotic coronary arteries, we examined the effect of sequential infusions of ascorbic acid (final concentration 0.1, 1.0, and 10 mmol/L) or placebo on coronary endothelial function in 26 subjects referred for cardiac catheterization to evaluate coronary artery disease. Coronary vasomotor function was evaluated using intracoronary agonist infusion, quantitative angiography, and intracoronary Doppler measurements. At baseline, endothelium-dependent vasodilation of epicardial arteries and coronary microvessels was impaired to an equivalent extent in the ascorbic acid and placebo groups. Sequential ascorbic acid infusions had no effect on the acetylcholine-induced change in coronary artery diameter (-11+/-8, -12+/-10, and -9+/-9%) compared with the effect of placebo (-14+/-13, -16+/-10, and -13+/-9%) infusions (p=0.98). Similarly, the changes in coronary blood flow during acetylcholine infusions were equivalent during ascorbic acid (51+/-44, 67+/-66, and 62+/-52%) and placebo (61+/-104, 55+/-93, and 50+/-69%) infusions (p=0.63). Ascorbic acid also had no effect on the dilator response to intracoronary nitroglycerin (p=0.19). These data argue against an important role for superoxide-mediated "inactivation" of nitric oxide or another rapidly reversible form of oxidative stress as a mechanism of coronary endothelial dysfunction in patients with coronary atherosclerosis.

Acetylcholine↗
PubMed2005

Kinetic spectrofluorimetric determination of trace ascorbic acid based on its inhibition on the oxidation of pyronine Y by nitrite.

A highly sensitive spectrofluorimetric method is proposed for the determination of trace amount of ascorbic acid using a new indication. The method is based on the inhibition of ascorbic acid on the oxidation of pyronine Y (PRY) by nitrite. The detection limit for ascorbic acid is 0.012 microg ml(-1), the linear range of the determination is 0.02-0.36 microg ml(-1). Analytical parameters, such as reagent concentration, pH, reaction temperature and time, were optimized. The relative standard deviations of eleven replication determinations of 0.12 and 0.24 microg ml(-1) ascorbic acid were 1.4 and 0.72%, respectively. This method has been used to determine ascorbic acid in pharmaceuticals, vegetables, fruits and soft drink with satisfactory results.

Ascorbic Acid↗
PubMed1999

Effect of ascorbic acid on iron release from the emulsifier interface and on the oxidative flavor deterioration in fish oil enriched mayonnaise.

This research examines the effect of ascorbic acid (0-800 ppm) on the sensory perception of mayonnaises containing 16% fish oil and on the levels of iron and copper in the aqueous phase. Ascorbic acid increased the formation of fishy off-flavors in fresh mayonnaise. Simultaneously, the iron concentration increased from below the detection limit (1.8 microM) to 34 microM in the aqueous phase of mayonnaises. Model mayonnaises with various concentrations of egg yolk (1-7% w/w) and ascorbic acid (0-8000 ppm) were prepared. Iron concentrations in the aqueous phase increased with increasing ascorbic acid levels, whereas iron concentrations in the assumed interfacial layer decreased. It is proposed that ascorbic acid is able to complex and reduce Fe(3+) to Fe(2+) from phosvitin in the egg yolk, whereby iron is released from the interface. The ascorbic acid-iron complex subsequently reacts with lipid hydroperoxides, resulting in increased lipid oxidation and in the immediate formation of rancid and fishy off-flavors.

Antioxidants↗