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PubMed1998

Four food-frequency categories of fruit intake as a predictor of plasma ascorbic acid level in middle-aged Japanese men.

PURPOSE: Plasma levels of ascorbic acid are assumed to be determined not only by dietary amount of ingested vitamin C, but also by other dietary and nondietary factors. To assess the predictability of plasma ascorbic acid level in Japanese men, we examined its association with dietary sources of vitamin C and other lifestyle factors. METHODS: In a cross-sectional study of 621 healthy men aged 40-49 years who were sampled randomly from five areas in Japan, the weekly intake frequency of foods rich in vitamin C (< 1, 1-2, 3-4, > or = 5 days/week), alcohol consumption per week, use of vitamin C supplements, and smoking were assessed by use of a food-frequency questionnaire (FFQ) (all subjects) and a 3-day weighed dietary record (DR) from 203 volunteers. RESULTS: In univariate analyses of FFQ data, the intake frequency of fruit (R2 = 0.12), pickled vegetables (R2 = 0.03), potatoes (R2 = 0.01), and alcohol consumption (R2 = 0.02) were significant determinants of plasma ascorbic acid in addition to supplement use and study area. In a multivariate analysis, four FFQ categories of fruit intake accounted for 19% of the variation in plasma ascorbic acid among nonsupplement users after adjustment for study area and alcohol intake. The association between plasma ascorbic acid level and quartile of dietary vitamin C intake (mg/day) measured by DR was weaker (R2 = 0.04) than the association between plasma ascorbic acid level and dietary intake of fresh fruit (g/day) (R2 = 0.09). CONCLUSION: The predictability of plasma ascorbic acid by a four-category FFQ assessment of fruit intake was superior to calculated vitamin C or fruit intake assessed by detailed DR.

Adult↗

PubMed1957

Collagen biosynthesis; tissue culture experiments to ascertain the role of ascorbic acid in collagen formation.

Quantitative studies of collagen formation by chick embryonic lung tissue grown in media deficient in, or completely lacking, ascorbic acid have been carried out. Cell growth and collagen formation in such cultures can proceed almost normally in media lacking ascorbic acid. Ascorbic acid in combination with whole embryo extract, dialyzed media, or synthetic mixture number 703 was found to have no appreciable effect on cell growth or total collagen formation. This is in marked contrast to the almost total failure of collagen formation in scorbutic animals and suggests that for slow collagen biosynthesis as distinct from more prolific collagen-producing systems, ascorbic acid plays an indirect role.

Animals↗

PubMed1998

Serum ascorbic acid and cardiovascular disease prevalence in U.S. adults.

To examine the relation between serum ascorbic acid level and the prevalence of cardiovascular disease, we analyzed data from 6,624 U.S. men and women enrolled in the Second National Health and Nutrition Examination Survey. We calculated odds ratios and 95% confidence intervals to estimate the relative prevalence of cardiovascular disease, defined as self-reported coronary heart disease or stroke, or a diagnosis of peripheral vascular disease based on physical examination. Serum ascorbic acid levels were independently associated with prevalence of coronary heart disease and stroke; a 0.5-mg per dl increase in serum ascorbic acid level was associated with an 11% reduction in coronary heart disease and stroke prevalence. We also analyzed the relation of ascorbic acid, grouped into low to marginal, normal, and saturation serum categories, to cardiovascular disease. Compared with participants with low to marginally low serum ascorbic acid levels, we found a 27% decreased prevalence of coronary heart disease (95% confidence interval = 10-41%) and a 26% decreased prevalence of stroke (95% confidence interval = 3-44%) among participants in the highest serum ascorbic acid category. Serum ascorbic acid levels were not consistently associated with prevalence of peripheral vascular disease. These results are consistent with the hypothesis that increased ascorbic acid intake may decrease the risk of coronary heart disease and stroke.

Adult↗

PubMed2004

Ascorbic acid responsive genes during neuronal differentiation of embryonic stem cells.

Ascorbic acid has been reported to enhance differentiation of embryonic stem (ES) cells into neurons, however, the specific functions of ascorbic acid have not been defined yet. To address this issue, gene expression profiling was performed using cDNA microarray. Ascorbic acid increased the expressions of genes involved in neurogenesis, maturation, and neurotransmission. Furthermore, statistical analysis using Fisher's exact test revealed ascorbic acid significantly modulated the genes involved in cell adhesion and development category. These results provide information on the role for ascorbic acid during neuronal differentiation of ES cells and might contribute to large-scale generation of neurons for future clinical treatment.

Animals↗

PubMed1976

The effects of ascorbic acid on diphtheria toxin and intoxicated HeLa cells.

Ascorbic acid (vitamin C) prevented diphtheria toxin from inhibiting the incorporation of [U-14C]-alanine into trichloroacetic acid precipitable material in HeLa cells. Ascorbic acid did not exhibit an effect on the adenosine diphosphate-ribosylation of amino acyl transferase II nor did it separate fragment A from fragment B in "nicked" toxin. A non-specific reducing agent, para-methylaminophenol sulfate, exhibited an effect on HeLa cells very similar to the results of ascorbic acid. Citric acid, a tricarboxylic acid, had no effect on HeLa cells.

Alanine↗

PubMed2003

Ascorbic acid supplementation does not improve efficacy of meso-dimercaptosuccinic acid treatment in lead-exposed suckling rats.

It was suggested that ascorbic acid as a natural chelating agent can influence lead toxicokinetics and improve chelating properties of dimercaptosuccinic acid (DMSA) in adult rats. In this paper potential benefits of ascorbic acid supplementation, alone or combined with DMSA, in decreasing lead retention in suckling rats were evaluated. Such data in young mammals are not available. L-Ascorbic acid (daily dose 650 mg/kg b.wt.) and/or DMSA (daily dose 91 mg/kg b.wt.) were administered orally to suckling Wistar rats either during ongoing 8-day oral lead exposure (as acetate; daily dose 2 mg lead/kg b.wt.) or after 3-day lead exposure (total dose 12 mg lead/kg b.wt.). Lead concentrations were analysed in the carcass (skeleton), liver, kidneys and brain by atomic absorption spectrometry. By ascorbic acid supplementation lead retention was not reduced under either lead exposure condition. Lead concentration was even increased in the carcass. Treatment with DMSA under both exposure conditions significantly reduced lead in all analysed tissues. Combined treatment with ascorbic acid and DMSA during ongoing lead exposure was substantially less effective than DMSA treatment alone, and did not affect DMSA efficacy when administered after lead exposure. It was concluded that ascorbic acid administered either during or after lead exposure in suckling rats has no beneficial effect on either lead retention or DMSA chelation effectiveness.

Administration, Oral↗

PubMed1994

Ascorbic acid and insulin secretion in pancreatic islets.

The effect of ascorbic acid on glucose-induced insulin release from single pancreatic islets was measured using a new, ultra-sensitive enzyme-linked immunosorbent insulin assay. Within 20 s ascorbic acid inhibited insulin secretion; inhibition was dose dependent and completely reversible. There was a 50% inhibition of the secretory response with 200 microM ascorbic acid and 90% inhibition with 400 microM ascorbic acid. The decrease in insulin secretion was recorded as a reduction of the amplitudes of the fast insulin transients, which give rise to the oscillatory nature of insulin secretion. The inhibition of glucose-induced insulin release by ascorbic acid was associated with hyperpolarization of the pancreatic beta-cell. Suppression of glucose-induced membrane depolarization was evident after 20 s, was dose dependent, and was completely reversible. The data here may provide the first explanation of why plasma ascorbate concentrations are tightly controlled.

Animals↗

PubMed2006

Mechanism of ascorbic acid interference in biochemical tests that use peroxide and peroxidase to generate chromophore.

BACKGROUND: Ascorbic acid interferes negatively in peroxidase-based tests (Trinder method). However, the precise mechanism remains unclear for tests that use peroxide, a phenolic compound and 4-aminophenazone (4-AP). We determined the chemical mechanism of this interference, by examining the effects of ascorbic acid in the reaction kinetics of the production and reduction of the oxidized chromophore in urate, cholesterol, triglyceride and glucose tests. Reaction of ascorbic acid with the Trinder method constituents was also verified. RESULTS: Ascorbic acid interfered stoichiometrically with all tests studied. However, it had two distinct effects on the reaction rate. In the urate test, ascorbic acid decreased the chromophore formation with no change in its production kinetics. In contrast, in cholesterol, triglyceride and glucose tests, an increase in the lag phase of color development occurred. Of all the Trinder constituents, only peroxide reverted the interference. In addition, ascorbic acid did not interfere with oxidase activity nor reduce significantly the chromophore formed. CONCLUSIONS: Peroxide depletion was the predominant chemical mechanism of ascorbic acid interference in the Trinder method with phenolics and 4-AP. Distinctive effects of ascorbic acid on the reaction kinetics of urate, cholesterol, glucose and triglyceride might be due to the rate of peroxide production by oxidases.

Ampyrone↗

PubMed1977

Effects of ascorbic acid and its 2-sulfate on rabbit aortic intimal thickening.

Effects of intravenously injected L-ascorbic acid or L=ascorbic acid 2-sulfate on aortic intimal thickening were examined histologically, qualitatively, and quantitatively in the upper, middle and lower thoracic aortic positions of cholesterol-induced atherosclerotic rabbits. A means of evaluating the degree of pathology of the aortic positions was developed employing five descriptive statistics of intimal thickening. Both L-ascorbic acid and L-ascorbic acid 2-sulfate inhibited intimal thickening. The most significant reductions were observed in the upper thoracic aorta.

Adrenal Glands↗

PubMed2004

L-ascorbic acid microencapsulated with polyacylglycerol monostearate for milk fortification.

Efficiency was examined of microencapsulating L-ascorbic acid by polyglycerol monostearate (PGMS), and changes in the chemical and sensorial aspects of L-ascorbic acid and/or iron-fortified milk during storage were evaluated. The selected core materials were ferric ammonium sulfate and L-ascorbic acid. The highest efficiency (94.2%) of microencapsulation was found with the ratio of 5:1 as the coating to core material. The release of ascorbic acid from the microcapsules increased sharply from 1.6 to 6.7% up to 5 d of storage. The TBA value was the lowest in the milk sample with added encapsulated iron and unencapsulated L-ascorbic acid up to 5 d of storage in comparison with the other treated samples. A sensory analysis showed that most aspects were not significantly different between the control and fortified samples encapsulated with ascorbic acid after 5 d of storage. The results indicate that L-ascorbic acid microencapsulated with PGMS can be applied to fortify milk and acceptable milk products can be prepared with microencapsulated L-ascorbic acid and iron.

Animals↗

PubMed1993

Ascorbic acid bioavailability in foods and supplements.

The bioavailability of ascorbic acid from food has been assumed to be high, but little quantitative information has been available to substantiate this assumption because of the limited precision and low statistical power of previous studies. A recent depletion-repletion study with a more effective experimental design has shown clearly that ascorbic acid bioavailability is equivalent in ascorbic acid tablets (with and without iron), orange juice, whole orange sections, and cooked broccoli. The bioavailability of ascorbic acid in raw broccoli was 20% lower, although this difference would probably have little nutritional significance in typical mixed diets.

Adult↗

PubMed2002

Mutagenicity and DNA-damaging activity caused by decomposed products of potassium sorbate reacting with ascorbic acid in the presence of Fe salt.

Although potassium sorbate (PS), ascorbic acid and ferric or ferrous salts (Fe-salts) are used widely in combination as food additives, the strong reactivity of PS and oxidative potency of ascorbic acid in the presence of Fe-salts might form toxic compounds in food during its deposit and distribution. In the present paper, the reaction mixture of PS, ascorbic acid and Fe-salts was evaluated for mutagenicity and DNA-damaging activity by means of the Ames test and rec-assay. Effective lethality was observed in the rec-assay. No mutagenicity was induced in either Salmonella typhimurium strains TA98 (with or without S-9 mix) or TA100 (with S-9 mix). In contrast, a dose-dependent mutagenic effect was obtained when applied to strain TA100 without S-9 mix. The mutagenic activity became stronger increasing with the reaction period. Furthermore, the reaction products obtained in a nitrogen atmosphere did not show any mutagenic and DNA-damaging activity. PS, ascorbic acid and Fe-salts were inactive when they were used separately. Omission of one component from the mixture of PS, ascorbic acid and Fe-salt turned the reaction system inactive. These results demonstrate that ascorbic acid and Fe-salt oxidized PS and the oxidative products caused mutagenicity and DNA-damaging activity.

Ascorbic Acid↗

PubMed1999

Relation of serum ascorbic acid to serum vitamin B12, serum ferritin, and kidney stones in US adults.

BACKGROUND: Concern has been raised that high levels of ascorbic acid consumption may lead to potential adverse effects, such as vitamin B12 deficiency, iron overload, and kidney stones. OBJECTIVE: To examine the relation of serum ascorbic acid level, which reflects intake, to serum vitamin B12 level, serum ferritin level, and kidney stones. METHODS: We analyzed data collected on a random sample of the US population enrolled in the Second National Health and Nutrition Examination Survey, 1976-1980. We analyzed data using linear and logistic regression models. Serum ascorbic acid, serum vitamin B12, hemoglobin, red blood cell mean corpuscular volume (MCV), and serum ferritin levels were measured using standardized protocols. History of kidney stones was determined by self-report. RESULTS: After multivariate adjustment, serum ascorbic acid level was associated with higher serum vitamin B12 levels among women in regression models that assumed a linear relationship; each 57-pmol/L (1.0-mg/dL) increase in serum ascorbic acid level (range, 6-153 micromol/L [0.1 to 2.7 mg/dL]) was independently associated with a serum vitamin B12 level increase of 60 pmol/L (81 pg/ mL) (P<.001). Among men, serum ascorbic acid level was marginally associated with higher serum vitamin B12 levels: each 57-micromol/L (1.0-mg/dL) increase in serum ascorbic acid level was associated with a serum vitamin B12 level increase of 27 pmol/L (36 pg/mL) (P = .10). In addition, serum ascorbic acid level was not associated with correlates of vitamin B12 deficiency, such as higher MCV levels, macrocytosis (MCV >100), or lower hemoglobin concentrations. Serum ascorbic acid level was not independently associated with serum ferritin levels. However, among women only, serum ascorbic acid levels were associated in a nonlinear fashion with prevalence of elevated serum ferritin levels (P = .02). We found no association between serum ascorbic acid level and prevalence of kidney stones in women or men (both P>.05). CONCLUSIONS: Serum ascorbic acid levels were not associated with decreased serum vitamin B12 levels (or indicators of vitamin B12 deficiency), prevalence of kidney stones, serum ferritin levels, or-among men-prevalence of elevated serum ferritin levels. Serum ascorbic acid levels were associated with prevalence of elevated serum ferritin levels among women. Although the clinical relevance of these findings is uncertain, it seems prudent to suggest that women with a genetic susceptibility to iron overload should consider moderating their intake of ascorbic acid.

Adult↗

PubMed1986

Antioxidant protection of phospholipid bilayers by alpha-tocopherol. Control of alpha-tocopherol status and lipid peroxidation by ascorbic acid and glutathione.

Factors affecting the balance between pro- and antioxidant effects of ascorbic acid and glutathione were studied in soybean phosphatidylcholine liposomes challenged with Fe2+/H2O2. Effective antioxidant protection by alpha-tocopherol appeared to be due to efficient reaction with lipid oxy-radicals in the bilayer rather than to interception of initiating oxygen radicals. At concentrations above a threshold level of approximately 0.2 mol % (based on phospholipid content), alpha-tocopherol completely suppressed lipid oxy-radical propagation, which was measured as malondialdehyde production. Both ascorbic acid and glutathione, alone or in combination, enhanced lipid oxy-radical propagation. Alpha-Tocopherol, incorporated into liposomes at concentrations above its threshold protective level, reversed the pro-oxidant effects of 0.1-1.0 mM ascorbic acid but not those of glutathione. Ascorbic acid also prevented alpha-tocopherol depletion. The combination of ascorbic acid and subthreshold levels of alpha-tocopherol only temporarily suppressed lipid oxy-radical propagation and did not maintain the alpha-tocopherol level. Glutathione antagonized the antioxidant action of the alpha-tocopherol/ascorbic acid combination regardless of alpha-tocopherol concentration. These observations indicate that membrane alpha-tocopherol status can control the balance between pro- and antioxidant effects of ascorbic acid. The data also provide the most direct evidence to date that ascorbic acid interacts directly with components of the phospholipid bilayer.

Antioxidants↗

PubMed1983

Loss of ascorbic acid from injured feline spinal cord.

Feline spinal cord contains 0.97 mM ascorbic acid, as measured by the dinitrophenylhydrazine method. Greater than 90% is maintained in the reduced form. When functioning normally, the CNS conserves its ascorbic acid with a turnover rate of 2% per h. Following contusion injury severe enough to produce paraplegia, ascorbic acid is rapidly lost from injured spinal tissue. Thus, ascorbic acid is decreased 30% by 1 h and 50% by 3 h following injury. Oxidized ascorbic acid is increased at 1, but not 3, h following impact. As a consequence of its many functions in CNS, loss of ascorbic acid may contribute to derangements in spinal cord function following injury.

Animals↗

PubMed1987

Relationship between ascorbic acid dose and N-nitrosoproline excretion in humans on controlled diets.

A logarithmic dose-response relationship between ascorbic acid dose and N-nitrosoproline (NPRO) excretion in humans on a controlled diet was established. Seven healthy males were placed on a low-nitrate, low-ascorbic acid diet for 12 consecutive days and given nitrate on days 3-12 and L-proline on days 4-12, after the nitrate dose. Ascorbic acid was given in increasing amounts with the proline on days 5-10. Urine was analysed quantitatively for nitrate, NPRO and ascorbic acid. Ascorbic acid doses as low as 0.05 mmol reduced NPRO excretion by an average of 6 nmol/day; however, as much as 5.68 mmol ascorbic acid did not return NPRO excretion to levels observed before nitrate and proline were administered. Complete inhibition of endogenous NPRO formation from exogenous precursors requires more than the 2:1 molar ratio of ascorbic acid to nitrite that has been demonstrated in vitro. These data may be useful in interpreting epidemiological studies of nitrate exposure and in making dietary recommendations.

Adult↗

PubMed1977

On the absorption of ascorbic acid in man.

The daily intake of ascorbic acid with the diet was strongly restricted in seven healthy non-smoking males and 90 to 180 mg of ascorbic acid were orally supplemented. After an equilibration period of three weeks about 5 muCi of (1-14C) ascorbic acid was orally administered with carrier (30 mg or 60 mg). The daily intake was then increased to 4 X 1000 mg and the cumulative excretion of radioactivity in the urine measured over a period of 10 days. The average absorption was estimated to amount to 80-90% of the dose.

Administration, Oral↗

PubMed1986

Preventive and therapeutic effects of thiamine, ascorbic acid and their combination in lead intoxication.

Thiamine, ascorbic acid and their combination were investigated for their ability to prevent or treat the experimental lead intoxication in rats. The combination of the two vitamins was most effective in reducing the lead induced inhibition in the activity of blood delta-aminolevulinic acid dehydratase, elevation in the level of blood zinc protoporphyrin and the urinary excretion of delta-aminolevulinic acid and the uptake of lead in blood, liver and kidney. The combined treatment post lead exposure was also most effective in restoring the lead induced biochemical alterations and mobilizing lead from the tissues. The order of effectiveness was, thiamine + ascorbic acid less than ascorbic acid less than thiamine. The lead induced changes in brain biogenic amines and the brain concentration of lead remained unaffected by these vitamins.

Animals↗