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PubMed1984

Comparison of blood levels of histamine and total ascorbic acid in pre-eclampsia with normal pregnancy.

Levels of histamine and total ascorbic acid (L-ascorbic acid plus dehydroascorbic acid) in the peripheral blood of women in pre-eclampsia have been measured. The results show that blood histamine is increased both in the moderate and severe form of pre-eclampsia. Blood ascorbic acid on the other hand is increased only in the severe form of pre-eclampsia. The rise in histamine values may be in response to the rising blood pressure in pre-eclampsia. The rise in ascorbic acid values may reflect the reduced maternal blood volume and/or restricted transport of ascorbic acid from maternal to fetal tissues.

Adult↗
PubMed2005

Pharmacologic ascorbic acid concentrations selectively kill cancer cells: action as a pro-drug to deliver hydrogen peroxide to tissues.

Human pharmacokinetics data indicate that i.v. ascorbic acid (ascorbate) in pharmacologic concentrations could have an unanticipated role in cancer treatment. Our goals here were to test whether ascorbate killed cancer cells selectively, and if so, to determine mechanisms, using clinically relevant conditions. Cell death in 10 cancer and 4 normal cell types was measured by using 1-h exposures. Normal cells were unaffected by 20 mM ascorbate, whereas 5 cancer lines had EC(50) values of <4 mM, a concentration easily achievable i.v. Human lymphoma cells were studied in detail because of their sensitivity to ascorbate (EC(50) of 0.5 mM) and suitability for addressing mechanisms. Extracellular but not intracellular ascorbate mediated cell death, which occurred by apoptosis and pyknosis/necrosis. Cell death was independent of metal chelators and absolutely dependent on H(2)O(2) formation. Cell death from H(2)O(2) added to cells was identical to that found when H(2)O(2) was generated by ascorbate treatment. H(2)O(2) generation was dependent on ascorbate concentration, incubation time, and the presence of 0.5-10% serum, and displayed a linear relationship with ascorbate radical formation. Although ascorbate addition to medium generated H(2)O(2), ascorbate addition to blood generated no detectable H(2)O(2) and only trace detectable ascorbate radical. Taken together, these data indicate that ascorbate at concentrations achieved only by i.v. administration may be a pro-drug for formation of H(2)O(2), and that blood can be a delivery system of the pro-drug to tissues. These findings give plausibility to i.v. ascorbic acid in cancer treatment, and have unexpected implications for treatment of infections where H(2)O(2) may be beneficial.

Antioxidants↗
PubMed1980

Role of ascorbic acid in auxin induced cell elongation--a cytochemical study.

Cytochemical detection of ascorbic acid in cultured root tips of Zea mays shows that dividing cells accumulate ascorbic acid in the cytoplasm. The localization pattern alters in the root tip as the cells begin to elongate. In elongating cells ascorbic acid is distinctly localized on cell walls. Ascorbic acid content per cell increases with the onset of cell elongation. Fully elongated cells contain fivefold more ascorbic acid than meristematic cells. Cytophotometric analysis reveals a sharp and positive correlation (r = +0.93) between percentage increase in content of ascorbic acid per cell and corresponding increase in cell size at different phases of cell elongation. IAA treatment to the roots raises the content of ascorbic acid per cell with a parallel increase in size of cell. Involvement of ascorbic acid in IAA induced cell elongation is discussed.

Ascorbic Acid↗
PubMed2002

The effects of ascorbic acid on cartilage metabolism in guinea pig articular cartilage explants.

Ascorbic acid has been associated with the slowing of osteoarthritis progression in guinea pig and man. The goal of this study was to evaluate transcriptional and translational regulation of cartilage matrix components by ascorbic acid. Guinea pig articular cartilage explants were grown in the presence of L-ascorbic acid (L-Asc), D-isoascorbic acid (D-Asc), sodium L-ascorbate (Na L-Asc), sodium D-isoascorbate (Na D-Asc), or ascorbyl-2-phosphate (A2P) to isolate and analyze the acidic and nutrient effects of ascorbic acid. Transcription of type II collagen, prolyl 4-hydroxylase (alpha subunit), and aggrecan increased in response to the antiscorbutic forms of ascorbic acid (L-Asc, Na L-Asc, and A2P) and was stereospecific to the L-forms. Collagen and aggrecan synthesis also increased in response to the antiscorbutic forms but only in the absence of acidity. All ascorbic acid forms tended to increase oxidative damage over control. This was especially true for the non-nutrient D-forms and the high dose L-Asc. Finally, we investigated the ability of chondrocytes to express the newly described sodium-dependent vitamin C transporters (SVCTs). We identified transcripts for SVCT2 but not SVCT1 in guinea pig cartilage explants. This represents the first characterization of SVCTs in chondrocytes. This study confirms that ascorbic acid stimulates collagen synthesis and in addition modestly stimulates aggrecan synthesis. These effects are exerted at both transcriptional and post-transcriptional levels. The stereospecificity of these effects is consistent with chondrocyte expression of SVCT2, shown previously to transport L-Asc more efficiently than D-Asc. Therefore, this transporter may be the primary mechanism by which the L-forms of ascorbic acid enter the chondrocyte to control matrix gene activity.

Aggrecans↗
PubMedDate not supplied

Relationship of ascorbic acid to blood lead levels.

CONTEXT: Some animal studies suggest that orally administered ascorbic acid may chelate lead and decrease the risk of the toxic effects of lead. However, results from several small studies in humans have yielded inconclusive evidence of a beneficial effect of ascorbic acid on lead toxicity. OBJECTIVE: To examine the relationship between serum ascorbic acid levels and prevalence of elevated blood lead levels. DESIGN, SETTING, AND PARTICIPANTS: Cross-sectional analysis of a probability sample of the US population enrolled in the Third National Health and Nutrition Examination Survey, 1988-1994 (4213 youths aged 6-16 years and 15365 adults aged > or =17 years) without a history of lead poisoning. MAIN OUTCOME MEASURES: Elevated and log blood lead levels by serum ascorbic acid level. RESULTS: A total of 22 youths (0.5%) and 57 adults (0.4%) had elevated blood lead levels (defined as > or =0.72 micromol/L [15 microg/dL]) and > or =0.97 micromol/L [20 microg/dL], respectively). After controlling for the effects of age, race, sex, income level, and dietary energy, fat, calcium, iron, and zinc intake, youths in the highest serum ascorbic acid tertile had an 89% decreased prevalence of elevated blood lead levels compared with youths in the lowest serum ascorbic acid tertile (odds ratio, 0.11; 95% confidence interval, 0.04-0.35; P for trend = .002). Adults in the highest 2 serum ascorbic acid tertiles had a 65% to 68% decreased prevalence of elevated blood lead levels compared with adults in the lowest serum ascorbic acid tertile (P for trend = .03). As a continuous predictor, serum ascorbic acid level was independently associated with decreased log blood lead levels among adults (P<.001), but not among youths (P=.14). CONCLUSIONS: Our data suggest that high serum levels of ascorbic acid are independently associated with a decreased prevalence of elevated blood lead levels. If these associations are related causally, ascorbic acid intake may have public health implications for control of lead toxicity.

Adolescent↗
PubMed1997

Effect of supplementation of smoking men with plain or slow release ascorbic acid on lipoprotein oxidation.

OBJECTIVE: To study the effects of two month ascorbic acid supplementation on in vitro lipoprotein oxidation resistance and on in vivo lipid peroxidation, and to compare the absorption of two ascorbic acid preparations. DESIGN: Randomized, single blinded and placebo-controlled clinical trial. SETTING: Men, aged 36-65 y, smoking 11-40 cigarettes daily. SUBJECTS: Sixty-two subjects were recruited by newspaper advertisements and randomized. Fifty-nine subjects completed the study. INTERVENTION: Subjects were randomized into three groups to receive 250 mg BID of plain or slow release ascorbic acid tablets or placebo daily for two months. In the pharmacokinetic part of the study, the absorption of the ascorbic acid preparations was followed for 12 h. MAIN OUTCOME MEASURES: Plasma malondialdehyde (MDA) concentration and the oxidation resistance of VLDL + LDL. For the pharmacokinetic study, the area under the plasma concentration curve (AUC) of ascorbic acid. RESULTS: Plasma reduced ascorbic acid increased by 32% in the plain ascorbate group and by 54% in the slow release group during a two month supplementation. Plasma MDA increased in the plain ascorbic acid group compared with placebo group (P < 0.05), but there were no significant differences in the changes in lipoprotein oxidation reactions induced by copper or by hemin and H2O2. Plasma reduced and total ascorbic acid AUC values were significantly higher in both plain and slow release ascorbate groups compared with placebo group. CONCLUSIONS: Oral supplementation of 500 mg of ascorbic acid daily for two months alone without any other antioxidant does not appear to have protective effect on either in vitro lipoprotein oxidation resistance or in vivo lipid peroxidation in smoking men, but might even promote the formation of MDA.

Adult↗
PubMed1985

Ascorbic acid regulation of norepinephrine biosynthesis in isolated chromaffin granules from bovine adrenal medulla.

The effect of ascorbic acid on the conversion of dopamine to norepinephrine was investigated in isolated chromaffin granules from bovine adrenal medulla. Ascorbic acid was shown to double the rate of [3H]norepinephrine formation from [3H]dopamine, despite no demonstrable accumulation of ascorbic acid into chromaffin granules. The enhancement of norepinephrine biosynthesis by ascorbic acid was dependent on the external concentrations of dopamine and ascorbate. The apparent Km of the dopamine beta-hydroxylation system for external dopamine was approximately 20 microM in the presence or absence of ascorbic acid. However, the apparent maximum velocity of norepinephrine formation was nearly doubled in the presence of ascorbic acid. By contrast, the apparent Km and Vmax of dopamine uptake into chromaffin granules were not affected by ascorbic acid. Norepinephrine formation was increased by ascorbic acid when the concentration of ascorbate was 200 microM or higher; a concentration of 2 mM appeared to induce the maximal effect under the experimental conditions used here. The effect of ascorbic acid on conversion of dopamine to norepinephrine required Mg-ATP-dependent dopamine uptake into chromaffin granules. In contrast to ascorbic acid, other reducing agents such as NADH, glutathione, and homocysteine were unable to enhance norepinephrine biosynthesis. These data suggest that ascorbic acid provides reducing equivalents for hydroxylation of dopamine despite the lack of ascorbate accumulation into chromaffin granules. These findings imply the functional existence of an electron carrier system in the chromaffin granule which transfers electrons from external ascorbic acid for subsequent intragranular norepinephrine biosynthesis.

Adenosine Triphosphate↗
PubMed2002

Enhancement of glutathione-dependent haemin degradation by ascorbic acid.

In the current work, we investigated the effect of ascorbic acid on GSH-mediated haemin degradation. GSH-mediated haemin degradation in the presence of ascorbic acid in phosphate-buffered saline and in erythrocyte ghosts was determined by recording absorbance at 365 and 399nm, respectively. Generation of intracellular H(2)O(2) was measured indirectly in terms of the inactivation of endogenous catalase in erythrocytes in the presence of 3-amino-1,2,4-triazole. Although ascorbic acid itself did not induce haemin degradation, it enhanced GSH-mediated haemin degradation. Experiments with catalase showed that H(2)O(2) was essential in this process. The oxidation of ascorbic acid in the presence of haemin was stimulated by GSH, suggesting that ascorbic acid can alter the mechanism of H(2)O(2) generation observed with GSH and haemin alone. These results suggest that enhancement of GSH-mediated haemin degradation by ascorbic acid may be due to an increase in the production of H(2)O(2) generated by GSH and haemin in the absence of ascorbic acid.

Animals↗
PubMed1978

On the specificity of alcoholic acidic silver nitrate reagent for the histochemical localization of ascorbic acid. A reappraisal.

The specificity of the alcoholic acidic silver nitrate staining method for the histochemical localization of ascorbic acid was reappraised. It was found that the method is by and large better suited for the localization of ascorbic acid in both animal and plant tissues due to its greater specificity, which is ensured by employing reagent made in carbon dioxide saturated glass distilled water as well as by carrying out the reaction at a low temperature (0-4 degrees C) and at a pH of 2-2.5.

Adrenal Glands↗
PubMed1984

Comparison of ascorbic acid concentrations in granulocytes and lymphocytes.

The author measured the ascorbic acid concentration (microgram/10(8) cells) in leukocytes from fourteen healthy male subjects aged 20 to 28 years. The mean values were 10.9 (range 3.7 to 15.8) in granulocytes and 88.5 (range 35.3 to 122.2) in lymphocytes. These findings suggest that ascorbic acid metabolism in lymphocytes differs from that in granulocytes. In the second experiments the changes in ascorbic acid concentrations were measured in the course of an ascorbic acid loading test to a 33-year-old healthy male volunteer, in which increasing doses (1, 3, 5, 10 g/day X 7 days) were weekly loaded for 4 successive weeks and the ascorbic acid concentrations were examined at the end of each week. As the loading dose increased, ascorbic acid concentration in lymphocytes decreased during the 4 week period while the counterpart value in granulocytes stayed essentially constant. The present findings suggest the differences in ascorbic acid metabolism between granulocytes and lymphocytes.

Adult↗
PubMed1989

Ovarian aromatase activity in scorbutic mutant rats unable to synthesize ascorbic acid.

Osteogenic disorder syndrome rats are unable to synthesize ascorbic acid owing to the lack of l-gulonolactone oxidase, and become scorbutic within a few weeks without the supply of ascorbic acid. We studied effects of ascorbic acid deficiency on the ovarian aromatase activity in vivo using osteogenic disorder syndrome rats. The ovarian aromatase activity in ascorbic acid-deficient osteogenic disorder syndrome rats was significantly higher than that in normal or ascorbic acid-supplied osteogenic disorder syndrome rats. The activity in hypophysectomized immature rats was extremely low, but increased after treatment with pregnant mare serum gonadotropin, regardless of the presence or absence of ascorbic acid. The extent of the increase was the same among experimental groups. The present results indicate that ascorbic acid at physiological level lowers the ovarian aromatase activity, whereas it does not impair the responsiveness of the aromatase activity to gonadotropins.

Animals↗
PubMed1980

Effects of ascorbic acid on neutrophil locomotion.

The effects of ascorbic acid on neutrophil locomotion were studied in experimental conditions able to dissociate random from truly directional motility. It was shown that the significant enhancement of chemotaxis achievable with high ascorbic acid concentrations was due to an increase of the true chemotactic response. With lower concentrations of ascorbic acid, chemotactic values were unaffected as the result of an increase in the rate of neutrophil locomotion with a concomitant inhibition of the true chemotactic response. Ascorbic acid appeared to exert its effect on the whole moving cell population.

Ascorbic Acid↗
PubMed2000

L-Ascorbic acid and L-galactose are sources for oxalic acid and calcium oxalate in Pistia stratiotes.

Axenic Pistia stratiotes L. plants were pulse-chase labeled with [14C]oxalic acid, L[1-14C]ascorbic acid, L-6-14C]ascorbic acid, D-[1-14C]erythorbic acid, L-[1-14C]galactose, or [1-14C]glycolate. Specific radioactivities of L-ascorbic acid (AsA), free oxalic acid (OxA) and calcium oxalate (CaOx) in labeled plants were compared. Samples of leaf tissue were fixed for microautoradiography and examined by confocal microscopy. Results demonstrate a biosynthetic role for AsA as precursor of OxA and its crystalline deposition product, CaOx, in idioblast cells of P. stratiotes and support the recent discovery of Wheeler, Jones and Smirnoff (Wheeler, G.L., Jones M.A., & Smirnoff, N. (1998). The biosynthetic pathway of vitamin C in higher plants. Nature, 393, 365-369) that L-galactose is a key intermediate in the conversion of D-glucose to AsA in plants. D-[1-14C]erythorbic acid (a diastereomeric analog of AsA) is utilized also by P. stratiotes as a precursor of OxA and its calcium salt deposition product in idioblasts. Labeled OxA is rapidly incorporated into CaOx in idioblasts, but microautoradiography shows there is also significant incorporation of carbon from OxA into other components of growing cells, contrary to the dogma that OxA is a relatively stable end product of metabolism. Glycolate is a poor substrate for synthesis of OxA and CaOx formation, further establishing AsA as th immediate precursor in the synthesis of OxA used for calcium precipitation in crystal idioblasts.

Ascorbic Acid↗
PubMed1987

Ascorbic acid: a nonradioactive extracellular space marker in canine heart.

The distribution pattern of ascorbic acid and L-[14C]ascorbic acid in myocardial tissue was compared with those of the classical radioactive extracellular space markers [3H]-inulin, [3H]sucrose, and Na82Br. A new polarographic technique was developed for analogue registration of ascorbic acid concentration in coronary venous blood. The kinetic data of the markers were studied in an open-chest canine heart preparation (n = 17 dogs) during a constant tracer infusion of up to 9 min. Distribution volumes were calculated based on the mean transit time method of Zierler (K. L. Zierler, Circ. Res. 10:393-407, 1962). The distribution volume of ascorbic acid (23.6 ml/100 g wet wt) as well as of L-[14C]ascorbic acid (24.5 ml/100 g wet wt) in myocardial tissue agreed closely with those of [3H]inulin (18.6 ml/100 g wet wt) and [3H]sucrose (22.0 ml/100 g wet wt), as well as 82Br- (27.3 ml/100 g wet wt). The obtained kinetic data confirmed that ascorbic acid exhibits the physicochemical properties of an extracellular space marker, though this compound was shown to leak slowly into myocardial cells. Favorable attributes of this indicator are its low molecular weight, high diffusibility in interstitial fluid, low binding affinity to macromolecules, and high transcapillary (1.8 X 10(-5) cm/s) as well as low transplasmalemmal penetration rate (3.7 X 10(-8) cm/s). Therefore, this nonradioactive marker can be applied in a safe and simple fashion, and without untoward side effects in experimental animals as well as in patients.

Animals↗
PubMed1998

Transport of ascorbic acid in gastric epithelial cells in vitro.

The normal human stomach contains high concentrations of ascorbic acid in both the mucosa and gastric juice, but the mechanism of ascorbic acid transport in the stomach is unknown. To understand more, ascorbic acid accumulation in gastric epithelial cell lines was investigated. Ascorbic acid was transported into gastric epithelial cells (Kato III and AGS cell lines) and accumulated up to eight-fold against a concentration gradient, as measured by high-performance liquid chromatography with electrochemical detection. Kinetic analysis using both non-radioactive and radioactive sources of ascorbic acid showed that ascorbic acid accumulation was mediated by one saturable concentration-dependent transport system with a Km of 3-11 micromol/l and Vmax of 0.8-0.9 nmol/10(8) cells/min. These data suggest that ascorbic acid uptake in gastric mucosal cells may be facilitated by a high-affinity saturable transport activity. Loss of intracellular ascorbic acid from Kato III and AGS cells was slower than seen in vivo which may limit the usefulness of these cell lines as a physiological model for the secretion of mucosal ascorbic acid into gastric juice.

Ascorbic Acid↗
PubMed1993

Enzymatic basis for altered ascorbic acid and dehydroascorbic acid levels in diabetes.

Abnormal plasma ascorbic acid (AA) and dehydroascorbic acid (DHAA) levels observed in diabetes may be correlated to a deficiency in the recycling of AA. Ascorbic acid and DHAA levels are altered in diabetic liver in the present study. In addition, a coupling of the hexose monophosphate (HMP) shunt by way of NADPH to glutathione reductase and subsequent DHAA reduction is demonstrated. Ascorbic acid production was assayed directly and by way of the HMPS pathway. Results indicate that AA production from DHAA via the HMPS pathway occurs, and is significantly decreased in diabetic liver. Glucose-6-phosphate dehydrogenase (G6PDH) activity is shown to be decreased in diabetic liver. Since G6PDH is essential in providing NADPH for the reduction of glutathione required for subsequent DHAA reduction, its decreased activity is consistent with altered levels of AA and DHAA observed in diabetic tissues.

Animals↗
PubMed2006

LC-MS display of the total modified amino acids in cataract lens proteins and in lens proteins glycated by ascorbic acid in vitro.

We previously reported chromatographic evidence supporting the similarity of yellow chromophores isolated from aged human lens proteins, early brunescent cataract lens proteins and calf lens proteins ascorbylated in vitro [Cheng, R. et al. Biochimica et Biophysica Acta 1537, 14-26, 2001]. In this paper, new evidence supporting the chemical identity of the modified amino acids in these protein populations were collected by using a newly developed two-dimensional LC-MS mapping technique supported by tandem mass analysis of the major species. The pooled water-insoluble proteins from aged normal human lenses, early stage brunescent cataract lenses and calf lens proteins reacted with or without 20 mM ascorbic acid in air for 4 weeks were digested with a battery of proteolytic enzymes under argon to release the modified amino acids. Aliquots equivalent to 2.0 g of digested protein were subjected to size-exclusion chromatography on a Bio-Gel P-2 column and four major A330nm-absorbing peaks were collected. Peaks 1, 2 and 3, which contained most of the modified amino acids were concentrated and subjected to RP-HPLC/ESI-MS, and the mass elution maps were determined. The samples were again analyzed and those peaks with a 10(4) - 10(6) response factor were subjected to MS/MS analysis to identify the daughter ions of each modification. Mass spectrometric maps of peaks 1, 2 and 3 from cataract lenses showed 58, 40 and 55 mass values, respectively, ranging from 150 to 600 Da. Similar analyses of the peaks from digests of the ascorbylated calf lens proteins gave 81, 70 and 67 mass values, respectively, of which 100 were identical to the peaks in the cataract lens proteins. A total of 40 of the major species from each digest were analyzed by LC-MS/MS and 36 were shown to be identical. Calf lens proteins incubated without ascorbic acid showed several similar mass values, but the response factors were 100 to 1000-fold less for every modification. Based upon these data, we conclude that the majority of the major modified amino acids present in early stage brunescent Indian cataract lens proteins appear to arise as a result of ascorbic acid modification, and are presumably advanced glycation end-products.

Amino Acids↗
PubMed1989

Response of White Leghorn chicks fed ascorbic acid and challenged with Escherichia coli or with corticosterone.

This study was undertaken to assess the effects of dietary ascorbic acid on the growth and immunoresponsiveness of chickens when subjected to particular types of stress. White Leghorn chicks were fed diets containing no supplemental ascorbic acid, and ascorbic-acid diet (330 ppm) for 2 days or for 19 days before challenge. Then, half of the females were inoculated with Escherichia coli; half of the males were challenged with dietary corticosterone (30 ppm) for 12 days; and the remaining chicks were maintained as controls. These chicks, reared under "good" husbandry procedures, did not realize advantages in growth or feed efficiency due to the short- or long-term consumption of diets containing ascorbic acid. Incubation with E. coli resulted in considerably higher heterophil-to-lymphocyte ratios 24 h after inoculation, and E. coli-induced mortality was higher for pullets on short-term ascorbic acid than for those on long-term or no ascorbic acid. Dietary corticosterone caused differences in body weight and the relative weights of certain organs, regardless of dietary levels of ascorbic acid. The antibody response to red-blood-cell antigens from sheep was enhanced in unchallenged cockerels (no dietary corticosterone) fed ascorbic acid on a long-term basis, but dietary corticosterone overshadowed the advantageous effects of dietary ascorbic acid. These data showed that the effects of supplemental ascorbic acid on growth and on immunoresponsiveness were related to the quality of the husbandry, length of supplemental feeding, age of the chicks, endogenous-exogenous balance for ascorbic acid, and the relationship with corticosterone.

Animals↗