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PubMedDate not supplied

[Inhibiting effect of domestic, synthetic beta-carotene and ascorbic acid on endogenous carcinogenesis in mice].

Carcinogenesis in mice induced by the tryptophane derivative 3-hydroxyanthranilic acid was studied after administration of synthetic beta-carotene and ascorbic acid. The incidence of induced hemoblastoses and hepatomas was decreased 2-fold, while the latent period of their development was, increased in mice on a lifetime feed containing 15 mg/kg of beta-carotene. The anticarcinogenic effect of ascorbic acid added to drinking water was similar to that of beta-carotene. The additive inhibitory influence of beta-carotene and ascorbic acid on endogenous blastomogenesis was not found in mice.

3-Hydroxyanthranilic Acid↗
PubMedDate not supplied

[Formation of iron complexes with ascorbic acid in physiological conditions in vitro and in tissue in vivo].

Rapid dissociated Fe(III)-ascorbic acid complexes are formed after the mixing of Fe(II) (100 mkM) with ascorbic acid (1 mM) at pH-7,4. As a result of these complexes formation Fe(II) concentration was decreased in solution, but o-phenantrolin addition or pH decreased up to 6.1 lead to the destruction of these complexes and reduction of iron up to Fe(II). Iron-ascorbic acid paramagnetic complexes were not observed in the perfused rat liver homogenate. Probably, these facts were due to the presence of other stronger reductants in the tissue.

Animals↗
PubMed1983

The effect of ascorbic acid on sodium nitrite-induced methemoglobin formation in glucose-6-phosphate dehydrogenase-deficient erythrocytes.

Ascorbic acid significantly reduced the occurrence of sodium nitrite-induced methemoglobin (METHB) formation in a dose-dependent manner in erythrocytes from glucose-6-phosphate dehydrogenase (G-6-PD)-deficient humans in vitro. The ascorbic acid treatment, however, also decreased levels of reduced GSH in a dose-dependent manner, a response indicative of oxidant stress to the erythrocyte membrane. The latter findings are inconsistent with the hypothesis that ascorbic acid supplementation in G-6-PD-deficient humans may help compensate for inherently low levels of erythrocyte GSH. Finally, the ascorbic acid-induced reduction of METHB values, while of statistical significance, does not appear to be of clinical significance.

Ascorbic Acid↗
PubMed1996

The impact of SO2 and SO2 + ascorbic acid treatments on growth and partitioning of dry matter in Trigonella foenum-graecum L.

To study the impact of SO(2) and SO(2) + ascorbic acid on growth and partitioning of dry matter in Trigonella foenum-graecum L., two-week-old plants were exposed to SO(2) for 2 h daily over a 42 day period. One of the exposed sets was treated with ascorbic acid. Plants were grown in a wire house and unexposed plants were used as controls for comparison. The parameters measured, such as dry weights of leaf, stem and root per plant, were found to be lower in the exposed sets than in the controls. The reductions were greater in dry weights of stem and root as compared with weights of leaves, indicating that the partitioning of the dry matter was altered. Greater amounts of soluble sugars and starch in the leaves of exposed plants, compared with the stem, also revealed that translocation was hampered. Reductions were greater in fruiting than in flowering, suggesting that fruit abortion was high. Although ascorbic acid treatment could mitigate the effect of SO(2), the differences were not found to be statistically significant. Significant changes were seen in fruit yield, suggesting that the effect of ascorbic acid is cumulative. The impact of SO(2) and SO(2) + ascorbic acid on partitioning of dry matter to different 'sinks' is discussed.

Journal Article↗
PubMed2000

[Electron spin resonance studies on inhibiting methemoglobin in erythrocyte with exogenous ascorbic acid].

Research on inhibiting the methemoglobin (MetHb) in erythrocyte by means of exogenous ascorbic acid is helpful to elucidating whether exogenous antioxidant inhibits the oxidative denaturation of hemoglobin when the erythrocyte does not inhibit such denaturation with its own antioxidation system. Using electron spin resonance (ESR) technique, we have studied the oxidative denaturation of hemoglobin and the inhibition of MetHb in erythrocyte with the exogenous ascorbic acid. The results indicate that there is the ESR absorption of high spin MetHb (g = 6) at the 5th, 35th and 90th min after the blood was mixed with NaNO2. The ESR absorption of high spin MetHb increases with time. Yet, in the case where the blood was mixed with exogenous ascorbic acid in advance, the ESR absortpion of high spin MetHb (g = 6) only appears at the 35th min among the ESR measures at the 5th, 35th, and 90th min after the blood was mixed with NaNO2. These findings suggest that exogenous antioxidant can inhibit the oxidative denaturation of hemoglobin when the erythrocyte does not inhibit such dematuration with its own antioxidation system.

Adult↗
PubMed2000

Cisternal irrigation therapy with urokinase and ascorbic acid for prevention of vasospasm after aneurysmal subarachnoid hemorrhage. Outcome in 217 patients.

BACKGROUND: Cisternal irrigation therapy with urokinase and ascorbic acid was introduced to prevent symptomatic vasospasm after aneurysmal subarachnoid hemorrhage (SAH). To dissolve and wash out the subarachnoid clot, cisternal irrigation with urokinase is used. Ascorbic acid is added to degenerate oxy-hemoglobin, one of the strongest spasmogenic substances, into verdohemelike products, which are nonspasmogenic. The efficacy and safety of this therapy were evaluated. METHODS: This therapy was performed consecutively in 217 patients. The degree of SAH of the patients was classified as Fisher CT Group 3, and the highest CT number (Hounsfield number) exceeded 60 in the SAH, which suggested a significant risk for symptomatic vasospasm. All patients underwent surgery within 72 hours from the onset of SAH. After clipping the aneurysm, irrigation tubes were placed in the Sylvian fissure (inlet) unilaterally or bilaterally and in the prepontine or chiasmal cistern (outlet). Lactated Ringer's solution with urokinase (120 IU/mL) and ascorbic acid (4 mg/mL) was infused at a rate of 30 mL/hour/side for approximately 10 days. RESULTS: Of the 217 patients studied, symptomatic vasospasm was observed in 6 cases (2.8%), and two of these six cases (0.9%) demonstrated sequelae. The average total blood volume calculated from the drainage fluid was approximately 114 mL. Analysis of the absorption spectrum of the drainage fluid revealed disappearance of the oxy-hemoglobin-specific 576-nm peak. Complications occurred in eight patients during irrigation therapy; two patients experienced seizures, two patients developed meningitis, and four patients had an intracranial hemorrhage. However, all of these patients recovered without neurological deficits. CONCLUSIONS: These results suggest that cisternal irrigation therapy with urokinase and ascorbic acid is effective in preventing symptomatic vasospasm after aneurysmal SAH.

Adult↗
PubMed2005

Antigenotoxic effects of ascorbic acid against megestrol acetate-induced genotoxicity in mice.

The genotoxicity of megestrol acetate was studied in mouse bone marrow cells using sister chromatid exchanges (SCEs) and chromosomal aberrations (CAs) as parameters. Megestrol acetate (8.12, 16.25 and 32.50 mg/ kg of body weight) was injected intraperitoneally separately in different groups of animals. Both CAs and SCEs were statistically increased at 16.25 and 32.50 mg/kg of body weight. Our earlier in vitro studies show the generation of free oxygen radicals, by synthetic progestins responsible for the genotoxic damage. As the genotoxic effects of steroids can be reduced by natural products having antioxidant properties, and ascorbic acid possesses antioxidant activity, ascorbic acid (20, 40 or 60 mg/kg of body weight) administered together with megestrol acetate (32.50 mg/kg of body weight) significantly decreased CAs and SCEs, suggesting an antigenotoxic role of ascorbic acid against megestrol acetate-induced genotoxic damage in mice bone marrow cells. The antigenotoxic effect was clearly dose dependent. The highest protective effect was observed at 60 mg/kg body weight of ascorbic acid treated with 32.50 mg/kg body weight of megestrol acetate.

Animals↗
PubMed2003

Iron and ascorbic Acid: proposed fortification levels and recommended iron compounds.

An adequate supply of dietary iron during the 1st 24 mo of life is essential for preventing iron deficiency with its attendant negative effects on mental, motor and emotional development as well as later cognitive performance. Iron reserves and the small amount of highly bioavailable iron in human milk are adequate to satisfy the iron requirements of breast-fed infants of adequate birth weight for the 1st 6 mo of life. Thereafter, complementary foods, iron supplements or both are needed to meet this requirement. Complementary foods should not displace the consumption of human milk. The quantities eaten, particularly by younger infants, may therefore be quite small. As a consequence it is essential that the iron be supplied in a highly bioavailable form. This can be achieved by fortifying complementary foods with ferrous sulfate and ascorbic acid provided that the ascorbic acid is not lost during storage or meal preparation. Suggested fortification levels for ferrous sulfate and ascorbic acid for some types of complementary foods are given. The use of ferrous fumarate or an elemental iron powder instead of ferrous sulfate has not been evaluated adequately. There is a need to develop alternative strategies for improving iron bioavailability in complementary foods because it may not be possible to preserve ascorbic acid activity in many of them.

Ascorbic Acid↗
PubMed1996

Iron (II) ions induced oxidation of ascorbic acid and glucose.

Lipid peroxidation (LPO) of polyunsaturated fatty acids (PUFAs) is suspected to be involved in the generation of chronic diseases. A model reaction for LPO is the air oxidation of PUFAs initiated by Fe2+ and ascorbic acid. In the course of such model reactions glycolaldehyde (GLA) was detected as main aldehydic product. Since it is difficult to explain the generat on of GLA by oxidation of PUFAs, it was suspected that GLA might be derived by oxidation of ascorbic acid. This assumption was verified by treatment of ascorbic acid with Fe2+. Produced aldehydic compounds were trapped by addition of pentafluorobenzylhydroxylamine hydrochloride (PFBHA-HCl), trimethylsilylated and finally identified by gas chromatography/mass spectronetry (GC/MS). Oxidation of ascorbic acid with O2 in presence of iron ions produced not only glycolaldehyde (GLA), but also glyceraldehyde (GA), dihydroxyacetone (DA) and formaldehyde. Glyoxal (GO) and malondialdehyde (MDA) were detected as trace compounds. The yield of the aldehydic compounds was increased by addition of lipid hydroperoxides (LOOH) or H2O2. The buffer influenced the reaction considerably: Iron ions react with Tris buffer by producing dihydroxyacetone (DA). Since ascorbic acid is present in biological systems and Fe2+ ions are obviously generated by cell damaging processes, the production of GLA and other aldehydic components might add to the damaging effects of LPO. Glucose suffers also oxidation to short-chain aldehydic compounds in aqueous solution, but this reaction requires addition of equimolar amounts of Fe2+ together with equimolar amounts of H2O2 or 13-hydroperoxy -9-cis-11-trans-octadecadienoic acid (13-HPODE). Therefore this reaction, also influenced by the buffer system, seems to be not of biological relevance.

Aldehydes↗
PubMed1992

Ascorbic acid overdosing: a risk factor for calcium oxalate nephrolithiasis.

A total of 15 patients with unilateral nephrostomy tubes after extracorporeal shock wave lithotripsy received either 0 (placebo), 100, 500, 1,000 or 2,000 mg. ascorbic acid on days 2 and 3 postoperatively. Before and after administration, successive 6-hour urine specimens were collected from the nephrostomy tube and from the contralateral kidney directly into a preservative to stabilize ascorbic acid and oxalate. In 1 patient in each group preservative was omitted from the collection pouch. Urinary oxalate was then measured enzymatically after removal of ascorbic acid with sodium nitrite. Preservatives proved necessary for full recovery of analyte. At doses of 500 mg. or more of ascorbic acid there was a statistically significant increase in urinary oxalate equivalent to 1.2 to 1.8% of the millimoles of ascorbate administered. This represented an increase in urinary oxalate excretion of 6 to 13 mg. per day per 1,000 mg. ascorbic acid supplement. This amount would increase the risk of calcium oxalate urolithiasis.

Adult↗
PubMed2004

Ascorbic acid deficiency, iron overload and alcohol abuse underlie the severe osteoporosis in black African patients with hip fractures--a bone histomorphometric study.

Osteoporosis and femoral neck fractures (FNF) are uncommon in black Africans although osteoporosis accompanying iron overload (from traditional beer brewed in iron containers) associated with ascorbic acid deficiency (oxidative catabolism by iron) has been described from sub-Saharan Africa. This study describes histomorphometric findings of iliac crest bone biopsies and serum biochemical markers of iron overload and of alcohol abuse and ascorbic acid levels in 50 black patients with FNFs (29 M, 21 F), age 62 years (40-95) years (median [min-max]), and in age- and gender-matched black controls. We found evidence of iron overload in 88% of patients and elevated markers of alcohol abuse in 72%. Significant correlations between markers of iron overload and of alcohol abuse reflect a close association between the two toxins. Patients had higher levels of iron markers, i.e., siderin deposits in bone marrow (P < 0.0001), chemical non-heme bone iron (P = 0.012), and serum ferritin (P = 0.017) than controls did. Leukocyte ascorbic acid levels were lower (P = 0.0008) than in controls. The alcohol marker mean red blood cell volume was elevated (P = 0.002) but not liver enzymes or uric acid. Bone volume, trabecular thickness, and trabecular number were lower, and trabecular separation was greater in patients than in controls, all at P < 0.0005; volume, surface, and thickness of osteoid were lower and eroded surface was greater, all at P < 0.0001. There was no osteomalacia. Ascorbic acid deficiency accounted significantly for decrease in bone volume and trabecular number, and increase in trabecular separation, osteoid surface, and eroded surface; iron overload accounted for a reduction in mineral apposition rate. Alcohol markers correlated negatively with osteoblast surface and positively with eroded surface. Relative to reported data in white FNF patients, the osteoporosis was more severe, showed lower osteoid variables and greater eroded surface; FNFs occurred 12 years earlier and were more common among men. We conclude that the osteoporosis underlying FNFs in black Africans is severe, with marked uncoupling of resorption and formation in favor of resorption. All three factors--ascorbic acid deficiency, iron overload, and alcohol abuse--contributed to the osteoporosis, in that order.

Adult↗
PubMed2001

Effects of nitrogen dioxide exposure and ascorbic acid supplementation on exhaled nitric oxide in healthy human subjects.

BACKGROUND: Nitric oxide (NO) is detectable in the exhaled breath, is involved in airway defence and inflammation, and probably modulates bronchial smooth muscle tone. Given the sensitivity of nitrogen oxides to local redox conditions, we postulated that exposure to oxidant or antioxidant compounds could alter concentrations of NO in the exhaled breath (eNO). We assessed the effect of nitrogen dioxide (NO(2)) and ascorbic acid exposure on eNO in healthy human subjects. METHODS: Ten healthy subjects were randomised to undergo a 20 minute single blind exposure to NO(2) (1.5 parts per million) or medical air in a crossover fashion. Exhaled NO and pulmonary function were measured before and for 3 hours after exposure. In a separate double blind crossover study 20 healthy subjects received ascorbic acid 500 mg twice daily or placebo for 2 weeks with a 6 week interim washout. Serum ascorbic acid levels and eNO were measured before and after each supplementation phase. RESULTS: NO(2) induced a decrease of 0.62 (95% CI 0.32 to 0.92) ppb in the mean post-exposure eNO (p<0.01) with no change in forced expiratory volume in 1 second (FEV(1)). Oral supplementation with ascorbic acid increased the mean serum ascorbic acid concentration by 7.4 (95% CI 5.1 to 9.7) microg/ml (63%) but did not alter eNO. CONCLUSIONS: NO(2) exposure causes a decrease in eNO, an effect which may be mediated through changes in epithelial lining fluid redox state or through a direct effect on epithelial cells. In contrast, ascorbic acid does not appear to play a significant role in the metabolism of NO in the epithelial lining fluid.

Adult↗
PubMed1985

Protection against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity by the antioxidant ascorbic acid.

Administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 2 X 8 mg/kg retro-orbital) to BALB/cBy mice reduced [3H]mazindol binding to striatal membranes by 50%. Reactive oxygen derivatives have been suggested to be involved in MPTP neurotoxicity; therefore we examined the effects of ascorbic acid (an antioxidant). Ascorbic acid (100 mg/kg) given 20 min prior to MPTP administration appreciably prevented the reduction of [3H]mazindol binding. The involvement of oxidative processes in the mechanism of MPTP neurotoxicity may suggest a relationship to the etiology of Parkinson's disease, and the possible benefit of treatment with ascorbic acid.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1980

Correlations between adenohypophyseal weight, serum polyphenol oxidase activity (ceruloplasmin) and hypothalamic ascorbic acid after estrogen treatment in rats.

Serum polyphenol oxidase activity (ceruloplasmin) and the hypothalamic ascorbic acid concentration were determined in control rats and rats given estradiol for 2-6 months. A significant positive correlation (r = 0.5948, p less than 0.001) was found between adenohypophyseal weight and the ceruloplasmin level and a negative correlation between adenohypophyseal weight and the ascorbic acid concentration in the hypothalamus (r = -0.5728, p less than 0.01) and between the hypothalamus ascorbic acid concentration and the ceruloplasmin level (r = -0.7059, p less than 0.01). The ways in which an increase in serum polyphenol oxidase activity might modulate the adenohypophyseal reaction to estradiol are discussed.

Animals↗
PubMed1992

Radiation effect on ascorbic acid and riboflavin biosynthesis in germinating soybean.

The influence of irradiation on biosynthesis of ascorbic acid and riboflavin in germinating soybean seeds in tap and distilled water at ambient (25-35 degrees C) conditions was investigated. Ascorbic acid was not detectable in the original seeds and the initial level of riboflavin was 3.3 micrograms/g. The rate of synthesis of these vitamins increased with increasing germination time up to 72-96 hr followed by a decreasing pattern depending upon the treatment. The effect of irradiation and germination on the synthesis of these vitamins was statistically significant (P less than 0.01). Maximum amounts of ascorbic acid 16.2 and 15.0 mg/100g (fresh weight basis) were found in the 0.10 kGy sample after 72 hr of germination in tap and distilled water, respectively. However, a radiation dose of 0.20 kGy resulted in the development of maximum values of riboflavin, 30.0 and 27.0 micrograms/g (dry weight basis) on germination in tap and distilled water respectively.

Ascorbic Acid↗
PubMed1994

Importance of supplemental vitamin C in determining serum ascorbic acid in controls from a cervical cancer case-control study: implications for epidemiological studies.

Classification of individuals by their vitamin C intake was investigated in 493 control subjects from a cervical cancer case-control study. The influence of dietary and supplemental sources of vitamin C, as well as demographic and life-style factors, on serum ascorbic acid were examined. Usual dietary intakes of vitamin C were determined from a food frequency questionnaire and recent intakes from a 24-hour recall taken at the time of blood collection. Vitamin supplement information was obtained at both times. In a regression analysis, the factors found to predict serum ascorbic acid were total recent vitamin C intake, an indicator variable for supplement use, body mass index, number of cigarettes smoked per day, race, education, and age. Higher levels of serum ascorbic acid were found among older nonsmoking highly educated leaner white women. Consideration of supplements, in addition to dietary sources of vitamin C, improved correlation coefficients between serum ascorbic acid and usual vitamin C intake from 0.19 to 0.32 and between serum ascorbic acid and recent intake from 0.36 to 0.56. Furthermore, whereas only a twofold difference between the first and fourth quartiles of serum ascorbic acid was observed using recent dietary vitamin C without supplements, this range increased to sixfold with addition of supplement data. Epidemiological studies should consider use of total vitamin C intakes from supplement and food sources to permit accurate classification of individuals.

Adult↗