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PubMed1975

False-negative stool occult blood tests caused by ingestion of ascorbic acid (vitamin C).

In a female patient with unexplained anemia, ascorbic acid ingestion and apparent false-negative occult blood tests were related. When she stopped ascorbic acid, her stools became strongly reactive ("4+") by three tests for occult stool blood; this association was observed repeatedly. A test developed to measure stool occult blood in the presence of ascorbic acid remained reactive throughout this observation, and the observation was confirmed by in-vitro studies. Current tests for occult blood depend on the pseudoperoxidase activity of heme and are inhibited by low levels of ascorbic acid. Reducing substances chemically similar to ascorbic acid also inhibits occult blood tests; oxidized ascorbic acid and sulfhydryl reducing agents do not inhibit them at physiologic levels.

Ascorbic Acid↗
PubMed2003

The role of ascorbic acid on the redox status and the concentration of malondialdehyde in streptozotocin-induced diabetic rats.

We investigated the role of ascorbic acid on the redox status in streptozotocin-induced diabetic rats. In the plasma of diabetic rats, the ratio of reduced/total ascorbic acid was significantly decreased as compared with normal control. Ascorbic acid supplementation increased the reduced and total ascorbic acid contents as compared with diabetic control. In the rutin-treatment group, reduced and total contents of ascorbic acid were significantly decreased, however, the ratio of reduced/total contents of ascorbic acid had no difference as compared with diabetic rats. In the insulin-treatment group, this ratio is not significantly different as compared with diabetic control. However, in the insulin plus ascorbic acid treatment group, reduced form and the ratio of reduced/total ascorbic acid were significantly increased as compared with diabetic control. In addition, we measured the contents of malondialdehyde (MDA) in the plasma of diabetic rats. The contents of MDA was increased as compared with normal control, however, in insulin-treatment group, the contents of MDA was decreased as compared with diabetic rats. Ascorbic acid had no effects on the increases of MDA in diabetic rats. In conclusion, plasma ascorbic acid level and its reduced/total ratio reflects the status of the oxidative stress in the diabetic rats. Supplement of ascorbic acid did not correct the ratio of the reduced/ total ascorbic acid. However, supplement of insulin and ascorbic acid corrected the ratio of reduced/total ascorbic acid.

Animals↗
PubMedDate not supplied

Ascorbic acid in cerebrospinal fluid - a possible protection against free radicals in the brain.

The function of ascorbic acid in living organisms is complex. Previous studies emphasize its protective role against harmful effect of free radicals, and its presence is necessary for the function of numerous enzymes. Ascorbic acid is a powerful reducing agent due to its dienol molecular structure, which is not present in the oxidized form, dehydroascorbic acid. The ratio of ascorbic acid and dehydroascorbic acid might be a marker of oxidative-reductive processes. We measured and compared the level of ascorbic acid and dehydroascorbic acid in the plasma of healthy persons and those of senile dementia patients, who represent pathological aging of the brain. In senile dementia patients, ascorbic acid and dehydroascorbic acid levels were also measured in the cerebrospinal fluid. Concentrations were determined by high performance liquid chromatography with electrochemical detection. In the plasma of senile dementia patients, very low ascorbic acid levels were found (ca. 30% of the healthy control). In lumbar cerebrospinal fluid, the concentration of ascorbic acid is 2.7 times higher compared to that of the plasma level. After intravenous infusion of ascorbic acid, a slow but marked increase of the concentration in the cerebrospinal fluid was measured. Our results support an active transport process for ascorbic acid through the blood-CSF barrier. Ascorbic acid level might be an important factor representing the protection of the central nervous system against free radicals.

Journal Article↗
PubMedDate not supplied

Flow injection system with chemiluminometric detection for enzymatic determination of ascorbic acid.

A simple, selective and rapid method for determination of ascorbic acid from fruit juices was developed by combining a flow injection analysis (FIA) system with a chemiluminometric detector and a reactor with L-ascorbate oxidase immobilized on controlled pore glass. It was found that some reducing agents (eg ascorbic acid and mercaptoacetic acid) give chemiluminescence with luminol in the presence of hexacyanoferrate (III) in an alkaline solution. We used this new type of chemiluminescent reaction for the enzymatic determination of ascorbic acid. The background substraction method was used in order to avoid interference during ascorbic acid determination. Accordingly, two chemiluminometric signals were registered for each determination, one signal corresponding to the sample that passed through the enzymatic reactor that decomposed the ascorbic acid completely, and the second signal corresponding to the sample that does not pass through the reactor. The difference between the two signals corresponds to ascorbic acid from the sample. The linear range of the method was 10-1000 micromol/L of ascorbic acid and the detection limit was 5 micromol/L The throughput was four samples/h and RSD 3.13% (n = 10). This method was applied for determination of ascorbic in fruit juices. The results were compared with those found by the reference method, based on titrimetric determination with 2,6-dichlorophenolindophenol, and the concordance was excellent.

Ascorbate Oxidase↗
PubMed1992

Changes with aging and physical exercise in ascorbic acid content and proliferative response of murine lymphocytes.

Ascorbic acid content and lymphoproliferative response to phytohemagglutinin were measured in lymphocytes from axillary nodes, spleen and thymus of young (15 +/- 2 weeks) and old (60 +/- 5 weeks) BALB/c mice. Ascorbic acid content in lymphocytes from spleen and thymus was found to be significantly higher and the lymphoproliferative response in the three immunocompetent organs significantly lower in old mice as compared to young mice. Moreover, young and old BALB/c mice were required to maintain a swimming activity until exhaustion (exhaustive exercise) or 90 min of swimming each day for a total of 20 days (continuous exercise). In both young and old mice the stress produced by exhaustive exercise and confirmed by the existence in serum of significantly increased levels of corticosterone compared to controls, caused a significant decrease in ascorbic acid content as well as in lymphoproliferative response. Continuous exercise, characterized by the presence in serum of significantly decreased levels of corticosterone compared to controls, produced the most significant decrease in ascorbic acid content from young and old murine lymphocytes. Moreover, this exercise resulted in a significant increase in lymphoproliferative response. Our results suggest that aging results in an increase in the ascorbic acid content of lymphocytes accompanied by a decline in the lymphoproliferative response in old BALB/c mice.

Aging↗
PubMed2006

Hemin-mediated hemolysis in erythrocytes: effects of ascorbic acid and glutathione.

In the present work, we investigated the effect of ascorbic acid and glutathione on hemolysis induced by hemin in erythrocytes. Ascorbic acid not only enhanced hemolysis, but also induced formation of thiobarbituric acid-reactive substances in the presence of hemin. It has been shown that glutathione inhibits hemin-induced hemolysis by mediating hemin degradation. Erythrocytes depleted of glutathione became very sensitive to oxidative stress induced by hemin and ascorbic acid. H(2)O(2) was involved in hemin-mediated hemolysis in the presence of ascorbic acid. However, a combination of glutathione and ascorbic acid was more effective in inhibiting hemolysis induced by hemin than glutathione alone. Extracellular and intracellular ascorbic acid exhibited a similar effect on hemin-induced hemolysis or inhibition of hemin-induced hemolysis by glutathione. The current study indicates that ascorbic acid might function as an antioxidant or prooxidant in hemin-mediated hemolysis, depending on whether glutathione is available.

Ascorbic Acid↗
PubMed1976

The effect of leucocytosis on leucocyte ascorbic acid levels.

White-blood counts, polymorph counts, leucocyte ascorbic-acid and plasma ascorbic-acid levels were measured in 91 samples of blood obtained from patients admitted to a geriatric assessment unit. There was a correlation between both white-blood counts and polymorph counts and leucocyte ascorbic-acid levels. There was no correlation between white-blood counts and polymorph counts and plasma ascorbic-acid concentrations. It is suggested that this phenomenon represents migration of ascorbate-rich polymorphs to areas of infection and infarction.

Aged↗
PubMedDate not supplied

Routine analysis of ascorbic acid in citrus juice using capillary electrophoresis.

A procedure to monitor citrus juice samples was established to quantitate vitamin C by capillary electrophoresis using a previously developed method. Dilution and filtration were the only preparation requirements and separation was achieved with an uncoated capillary using a 35mM sodium borate buffer (pH 9.3) containing 5% (v/v) acetonitrile at 21 kV and 23 degrees C. Detection was performed by high speed scanning between 200 and 360 nm. From the multiwave length scan, the electropherogram at 270 nm was extracted and used to quantitate ascorbic acid. The ascorbic acid concentration was calculated with an internal standard method, with ferulic acid as internal standard. The level of ascorbic acid during analysis was stabilized with ethylenediaminetetraacetic acid and dithiothreitol was used to reduce dehydroascorbic acid to ascorbic acid to estimate the total vitamin C level. Results were similar to those obtained by liquid chromatography and the method is now used to determine routinely the level of ascorbic acid in citrus juices.

Acetonitriles↗
PubMed1981

Acute effects of alcohol on plasma ascorbic acid in healthy subjects.

The acute effects of ethanol on plasma ascorbic acid were assessed in healthy subjects. After the ingestion of 2.0 g ascorbic acid and breakfast, plasma ascorbic acid rose from a fasting concentration of 7.5 +/- 0.8 ng/ml at 0900 h. to a peak of 26.9 +/- m 2.0 ng/ml at 1500 h. When 35 g ethanol was ingested with ascorbic acid and breakfast, plasma ascorbic acid concentrations were significantly lower for at least 24 h.

Adult↗
PubMed1992

Effect of oxygen on ascorbic acid uptake and concentration in embryonic chick brain.

The effects of oxygen on ascorbic acid concentration and transport were studied in chick embryo (Gallus gallus domesticus). During normoxic incubations, plasma ascorbic acid concentration peaked on fetal day 12 and then fell, before increasing again on day 20 when pulmonary respiration began. In contrast, cerebral ascorbic acid concentration rose after day 6, was maintained at a relatively high level during days 8-18, and then fell significantly by day 20. Exposure of day 16 embryos for 48 h to 42% ambient O2 concentration decreased ascorbic acid concentration by four-fifths in plasma and by one-half in brain, compared to values in normoxic (21% O2) or hypoxic (15% O2) controls. Hyperoxic preincubation of embryos also inhibited ascorbic acid transport, as evidenced by decreased initial rates of saturable and Na(+)-dependent [14C]ascorbic acid uptake into isolated brain cells. It may be concluded that changes in ascorbic acid concentration occur in response to oxidative stress, consistent with a role for the vitamin in the detoxification of oxygen radicals in fetal tissues. However, changing O2 levels have less effect on ascorbic acid concentration in brain than in plasma, indicating regulation of the vitamin by brain cells. Furthermore, the effect of hyperoxia on cerebral vitamin C may result, in part, from inhibition of cellular ascorbic acid transport.

Animals↗
PubMed1976

Leucocyte ascorbic acid in abnormal leucocyte states.

Leucocyte ascorbic acid was estimated in patients with abnormal leucocyte states and other haematological disorders. Levels below the normal range were found in most cases of chronic myeloid leukaemia and chronic lymphatic leukaemia. Subnormal levels were found in more than a third of patients with acute leukaemias, lymphomas, glandular fever, myelofibrosis, and polycythaemia, and in the same proportion of patients receiving cytotoxic drugs, and also in those with a polymorph leucocytosis and those with purpura. Most patients with anaemia but a normal leucocyte count, and those with myelomatosis had normal levels. The majority of pregnant women tested had subnormal levels. In a wide variety of leucocyte disorders the leucocyte ascorbic acid may not be an accurate index of the body's Vitamin C status. The results also support the supposition that leucocyte ascorbic acid is mostly carried by normal mature polymorphs.

Ascorbic Acid↗
PubMed2003

Effect of ascorbic acid administration in hemodialysis patients on in vitro oxidative stress parameters: influence of serum ferritin levels.

BACKGROUND: Ascorbic acid supplementation has been recommended to circumvent resistance to erythropoietin, which sometimes occurs in iron-overloaded uremic patients. In considering the pro-oxidant effect of ascorbic acid, the authors hypothesize that adjuvant therapy with larger doses of ascorbic acid in hemodialysis patients with iron overload may raise the risk of increasing free radical generation. The oxidative stress of intravenous ascorbic acid supplementation in hemodialysis patients was evaluated in this study. METHODS: Six healthy subjects and 29 hemodialysis patients were enrolled. Chemical scavenging activity of various compounds was measured by in vitro 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay. Free radical generation was determined in vitro by lucigenin-enhanced chemiluminescence (LucCL) assay on blood samples. Blood biochemistries were also measured simultaneously in hemodialysis patients 1 minute before and 5 minutes later in the presence or absence of intravenous injection of 300 mg ascorbic acid. RESULTS: Ascorbic acid presented a strong antioxidant effect in DPPH chemical reaction. On the contrary, it exerted pro-oxidant effect when mixed with plasma or whole blood of healthy subjects and hemodialysis patients. The pro-oxidant effect of ascorbic acid detected by LucCL was attenuated by various iron chelators and superoxide dismutase. In hemodialysis patients, the changes of LucCL intensity were significantly higher in the ascorbic acid-treated group than those in the control group (1261.0 +/- 401.9 v 77.4 +/- 62.5 relative light unit [RLU]; P < 0.05). Adjuvant ascorbic acid therapy resulted in significantly higher LucCL intensity in hemodialysis patients with ferritin > or =600 ng/mL (1,348.2 pmol/L) than those with ferritin less than 600 ng/mL (2,296.0 +/- 763.8 v 414.3 +/- 88.0 RLU; P<0.05). The changes of LucCL intensity were positively correlated with serum ferritin level (R2=0.8673; P<0.05). However, there was no significant correlation between the responses of LucCL intensity to ascorbic acid administration and transferrin saturation (R2=0.195; P=0.0665). CONCLUSION: Persons with excess ascorbic acid supplement in the blood or plasma generate iron-chelator-suppressible chemiluminescents suggestive of free radical formation. Whether the findings occur in vivo or that the free radicals generated in vitro lead to toxicity in patients is not known from this study. These results suggest that either lower parenteral dose or lower infusion rate of ascorbic acid may be more appropriate for adjuvant therapy in iron-overloaded uremic patients.

Aged↗
PubMed1983

Ascorbic acid and alkaline phosphatase activity.

Ascorbic acid is found strikingly to decrease the activity of bovine kidney alkaline phosphatase in vitro. The inhibition of alkaline phosphatase is a function of ascorbic acid concentration and is time and temperature dependent. The presence of the substrate protects the enzyme against the inhibitory action of the vitamin.

Alkaline Phosphatase↗
PubMed1990

Effect of increasing storage iron on ascorbic acid metabolism in the guinea pig.

Ascorbic acid (AA) metabolism was studied in control and iron-loaded guinea pigs. All animals were fed an AA-deficient diet and given a daily intraperitoneal (ip) dose of 10 mg sodium ascorbate. The control-diet formula contained 0.10 g Fe/kg diet; the experimental diet contained an additional 3.33 g Fe/kg diet as FeSO4. After 14 wk animals were injected (ip) with 9.25 x 10(3) Bq [1-14C]L-ascorbic acid. Blood was collected for 10 d and plasma specific activity of AA was determined. All animals were subsequently killed and selected tissues were analyzed for AA and iron concentrations. In spite of marked elevation of iron concentrations in plasma, spleen, and liver in experimental animals compared with controls, no differences in AA metabolism as determined by tissue AA concentrations and AA half-life, turnover rate, and body-pool size were evident. These results demonstrate that iron loading has no effect on the rate of AA catabolism in guinea pigs.

Animals↗
PubMed1967

Ascorbic acid deficiency in cultured human fibroblasts.

Fibroblasts grown in medium containing less than 1 microg of ascorbic acid per milliliter showed evidence of ascorbic acid deficiency when compared with cells grown in medium containing 50 microg of ascorbic acid per milliliter. This was manifested morphologically by dilated endoplasmic reticulum, a decrease in number, size, and intensity of staining of the mitochondria, by defective intercellular fibril formation, and by easy disaggregation of the cells from the intercellular matrix after treatment with pronase. When 50 microg per milliliter of ascorbic acid was incorporated into the medium, the altered morphology was corrected, banded fibrils were produced which were organized into bundles, and the cells were tightly bound in a matrix which was resistant to disaggregation with a variety of proteolytic enzymes. Collagen and sulfated glycosaminoglycan synthesis were less in the control than in the ascorbic acid supplemented cells. Similar morphological and chemical changes have been reported in the connective tissue of scorbutic animals. The effects of low ascorbic acid concentration on fibroblasts in culture indicate that these cells require ascorbic acid to maintain connective tissue functions.

Amino Sugars↗
PubMed1980

Effect of ascorbic acid in vitro on lymphocyte reactivity to mitogens.

The direct effects of ascorbic acid and dehydroascorbic acid in vitro on human lymphocyte proliferation to phytohemagglutinin (PHA) and concanavalin A (Con A) stimulation were determined. Cells exposed to physiologic and high concentrations of ascorbic acid and dehydroascorbic acid showed poorer tritiated thymidine ([3H]TdR) incorporation than controls without the vitamin. The inhibitory effect was dose-dependent, with the greatest inhibition occurring as the concentration of ascorbic acid and dehydroascorbic acid was increased. At supraoptimal concentrations of PHA and Con A, there was no recovery of the mitogen response, indicating that ascorbic acid did not inhibit the response by competition. Viability studies of cells in culture showed that concentrations of ascorbic acid and dehydroascorbic acid, which consistently inhibited mitogenic stimulation of lymphocytes, were noncytotoxic throughout the culture period. Timed addition of ascorbic acid to PHA-stimulated lymphocytes in culture demonstrated inhibition of [3H]TdR incorporation when ascorbic acid was added as late as 96 hours after initiation of culture. However, the greatest inhibitory effect was observed when ascorbic acid was added at initiation or early in culture. Inhibition was also evident when RNA and protein synthesis were determined. The results suggest that physiologic and high concentrations of ascorbic and dehydroascorbic acid affect early metabolic events in the process of mitogen-stimulated lymphocyte activation.

Ascorbic Acid↗
PubMed1990

Determination of L-ascorbic acid in fruit and vegetable juices by flow injection with immobilised ascorbate oxidase.

Ascorbate oxidase was immobilised on cyanogen bromide activated-Sepharose 4B and incorporated in a flow-injection system with amperometric detection at a glassy carbon electrode at +0.6 V. On passage through the immobilised ascorbate oxidase a fraction of the L-ascorbic acid was converted into dehydroascorbic acid and the decrease in signal was measured. This could be directly related to the amount of L-ascorbic acid present. The calibration graph was linear over the range 0-400 ng ml(-1) with a correlation coefficient of 0.9994. The detection limit (2 sigma) in phosphate buffer (0.08 M, pH 5.5) was 4.0 ng ml(-1). The relative standard deviation for a 200 ng ml(-1) standard was 1.0% (n = 10) and the sampling throughput was 30 samples h(-1). The method was used for the simple and rapid determination of L-ascorbic acid in fruit and vegetable juice.

Ascorbate Oxidase↗
PubMed2003

The microencapsulated ascorbic acid release in vitro and its effect on iron bioavailability.

The present study was carried out to examine the stability of microencapsulated ascorbic acid in simulated-gastric and intestinal situation in vitro and the effect of microencapsulated ascorbic acid on iron bioavailability. Coating materials used were polyglycerol monostearate (PGMS) and medium-chain triacylglycerol (MCT), and core materials were L-ascorbic acid and ferric ammonium sulfate. When ascorbic acid was microencapsulated by MCT, the release of ascorbic acid was 6.3% at pH 5 and 1.32% at pH 2 in simulated-gastric fluids during 60 min. When ascorbic acid was microencapsulated by PGMS, the more ascorbic acid was released in the range of 9.5 to 16.0%. Comparatively, ascorbic acid release increased significantly as 94.7% and 83.8% coated by MCT and PGMS, respectively, for 60 min incubation in simulated-intestinal fluid. In the subsequent study, we tested whether ascorbic acid enhanced the iron bioavailability or not. In results, serum iron content and transferring saturation increased dramatically when subjects consumed milks containing both encapsulated iron and encapsulated ascorbic acid, compared with those when consumed uncapsulated iron or encapsulated iron without ascorbic acid. Therefore, the present data indicated that microencapsulated ascorbic acid with both PGMS and MCT were effective means for fortifying ascorbic acid into milk and for enhancing the iron bioavailability.

Ascorbic Acid↗