Degradation Of Vitamin C

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Degradation Of Vitamin C Studies

Results for your query on March 22, 1999:: Search all fields for: Vitamin C And degradation; Published in 1966 through 1999; Only select references with abstracts available; Show references published in English only; Show references pertaining to humans

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Number	Title	Comments
...1...	Factors influencing the stability of ascorbic acid in total parenteral nutrition infusions.
...2...	Ascorbic acid in cholesterol metabolism and in detoxification of xenobiotic substances: problem of optimum vitamin C intake.
...3...	Vitamin C depletion is associated with alterations in blood histamine and plasma free carnitine in adults.
...4...	The reversibility of the vitamin C redox system: electrochemical reasons and biological aspects.
...5...	Ascorbic acid and vitamin B12.
...6...	Vitamin C improves endothelium-dependent vasodilation in patients with insulin-dependent diabetes mellitus.
...7...	Total plasma antioxidant capacity predicts thrombosis-prone status in NIDDM patients.
...8...	Vitamin C improves endothelial function of conduit arteries in patients with chronic heart failure.
...9...	Vitamin C improves endothelium-dependent vasodilation in forearm resistance vessels of humans with hypercholesterolemia.
...10...	Antioxidant vitamin C improves endothelial dysfunction in chronic smokers.
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...11...	Influence of natural antioxidants on in vitro lipoprotein oxidation.
...12...	Protection by alpha-tocopherol but not ascorbic acid from hydrogen peroxide induced cell death in normal human breast epithelial cells in culture.
...13...	Vitamin C and cardiovascular disease: a review.
...14...	Effect of dietary antioxidant combinations in humans. Protection of LDL by vitamin E but not by beta-carotene.
...15...	Protective effect of alpha-tocopherol and L-ascorbic acid against the ischemic-reperfusion injury in patients during open-heart surgery.
...16...	Gas phase oxidants of cigarette smoke induce lipid peroxidation and changes in lipoprotein properties in human blood plasma. Protective effects of ascorbic acid.
...17...	Nonenzymatic degradation and salvage of dietary folate: physicochemical factors likely to influence bioavailability.
...18...	Adherence, proliferation and collagen turnover by human fibroblasts seeded into different types of collagen sponges.
...19...	Induction of DNA fragmentation in human myelogenous leukemic cell lines by sodium 5,6-benzylidene-L-ascorbate and its related compounds.
...20...	Stability of sodium 5,6-benzylidene-L-ascorbate.
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...21...	Inhibition of oxidative degradation of hyaluronic acid by uric acid.
...22...	Ascorbate deficiency results in decreased collagen production: under-hydroxylation of proline leads to increased intracellular degradation.
...23...	A critical assessment of the effects of aminoguanidine and ascorbate on the oxidative modification of LDL: evidence for interference with some assays of lipoprotein oxidation by aminoguanidine.
...24...	Bleaching of membrane-bound merocyanine 540 in conjunction with free radical-mediated lipid peroxidation.
...25...	Pentoxifylline. A hydroxyl radical scavenger.	Hydroxyl radical was generated by a mixture of ascorbic acid, H2O2 and Fe(III)-EDTA. We evaluated the iron-dependent degradation of deoxyribose, mediated by hydroxyl radical, in the presence of different concentrations of PTX (from 0.05 to 3 mM), measuring the degradation products of deoxyribose that react with 2-thiobarbituric acid (TBA).
...26...	Ascorbic acid and urate in human seminal plasma: determination and interrelationships with chemiluminescence in washed semen.
...27...	Warfarin causes the degradation of protein C precursor in the endoplasmic reticulum.
...28...	Aggregation and precipitation of human relaxin induced by metal-catalyzed oxidation.	The modification of relaxin by ascorbic acid/CuCl2 solution could be totally inhibited by the presence of EDTA. In contrast, catalase and superoxide dismutase showed no effects on the oxidation process.
...29...	The role of superoxide and hydroxyl radicals in the degradation of hyaluronic acid induced by metal ions and by ascorbic acid.
...30...	Collagen degradation in human lung fibroblasts: extent of degradation, role of lysosomal proteases, and evaluation of an alternate hypothesis.
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...31...	Biochemical, microbiological, and nutritional aspects of kimchi (Korean fermented vegetable products).
...32...	Retinoic acid-induced inhibition of type I collagen gene expression by human lung fibroblasts.
...33...	Iodine-mediated inactivation of lipid- and nonlipid-enveloped viruses in human antithrombin III concentrate.
...34...	The effect of synovial fluid proteins in the degradation of hyaluronic acid induced by ascorbic acid.	Hyaluronic acid was degraded to less than one-third of the original molecular weight in the range of the physiological concentrations of ascorbic acid. Synovial fluid proteins protected against the ascorbate-dependent degradation of hyaluronic acid at their physiological concentrations. It is suggested that the inhibitory activity of ceruloplasmin mainly depends on the ferroxidase activity and that of transferrin is probably due to iron binding property.
...35...	Modulation by sodium ascorbate of the effect of chloroquine on low density lipoprotein retention and degradation in cultured human skin fibroblasts.
...36...	Measurement of ascorbate and dehydroascorbate contents in biological fluids.
...37...	Ascorbic acid stimulates collagen production without altering intracellular degradation in cultured human skin fibroblasts.
...38...	Lipid peroxidation and haemoglobin degradation in red blood cells exposed to t-butyl hydroperoxide. Effects of the hexose monophosphate shunt as mediated by glutathione and ascorbate.
...39...	Stability of rifampin in plasma: consequences for therapeutic monitoring and pharmacokinetic studies.
...40...	High galactose levels in vitro and in vivo impair ascorbate regeneration and increase ascorbate-mediated glycation in cultured rat lens.
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...41...	Lack of effect of ascorbic acid, hippuric acid, and methenamine (urinary formaldehyde) on the copper-reduction glucose test in geriatric patients.
...42...	Differing effects of probucol and vitamin E on the oxidation of lipoproteins, ceroid accumulation and protein uptake by macrophages.
...43...	Induction of collagen synthesis by ascorbic acid. A possible mechanism.
...44...	Ascorbate increases the number of low density lipoprotein receptors in cultured arterial smooth muscle cells.
...45...	Bioavailability in infants of iron from infant cereals: effect of dephytinization.
...46...	Fibroblast-migration in a wound model of ascorbic acid-supplemented three-dimensional culture system: the effects of cytokines and malotilate, a new wound healing stimulant, on cell-migration.
...47...	Ascorbic acid specifically increases type I and type III procollagen messenger RNA levels in human skin fibroblast.
...48...	The interaction between two antioxidants, sodium ascorbate and gallic acid: radical intensity and apoptosis induction.
...49...	Regulation of collagen biosynthesis by ascorbic acid: a review.
...50...	In vivo antineoplastic activity of ascorbic acid for human mammary tumor.
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...51...	Degradation of distinct forms of multimeric vitronectin by human fibroblasts.
...52...	Role of hydrogen peroxide for cell death induction by sodium 5,6-benzylidene-L-ascorbate.
...53...	Effect of physiological fluids on radical intensity of sodium ascorbate and sodium 5,6-benzylidene-L-ascorbate.
...54...	Ultraviolet A decreases epidermal growth factor (EGF) processing in cultured human fibroblasts and keratinocytes: inhibition of EGF-induced diacylglycerol formation.
...55...	Iron deficiency among pregnant Pakistanis in Norway and the content of phytic acid in their diet.
...56...	Iron deficiency among pregnant Pakistanis in Norway and the content of phytic acid in their diet.
...57...	UVA irradiation of human lens proteins produces residual oxidation of ascorbic acid even in the presence of high levels of glutathione.
...58...	Enhancement of cytotoxic activity of ascorbate by Acer nikoense Maxim. Extracts.
...59...	Ascorbic acid promotes prostanoid release in human lung parenchyma.
...60...	Mechanism of interferon-gamma action. Characterization of indoleamine 2,3-dioxygenase in cultured human cells induced by interferon-gamma and evaluation of the enzyme-mediated tryptophan degradation in its anticellular activity.
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...61...	The effect of ascorbic acid and ferric ammonium citrate on iron uptake and storage in lens epithelial cells.
...62...	Administration of antioxidant vitamins does not alter plasma fibrinolytic activity in subjects with central obesity.
...63...	DNA- and protein-scission activities of ascorbate in the presence of copper ion and a copper-peptide complex.
...64...	Gas chromatographic/mass spectrometric measurement of ascorbic acid and analysis of ascorbic acid degradation in solution.	L-Ascorbic acid, DHA, and the oxidized products derived from AA can be accurately measured using GC/MS. Owing to the complex nature of the reactions through which AA proceeds, we believe that GC/MS is currently the procedure of choice in making AA-related measurements. The methods described are useful in defining reactions involving AA. The methods may indicate in vivo oxidative injury and may allow the use of AA-derived products to determine if antioxidant modulations are effective.
...65...	Ascorbic acid as an antioxidant in measurements of catecholamines in plasma.
...66...	Enhancement of radical intensity and cytotoxic activity of ascorbate by hyperthermia.
...67...	Lack of correlation between TBARS production and PUFA degradation during incubation of membrane erythrocytes in an OH. (Fe2+/H2O2) generator system.
...68...	Ascorbic acid and ferritin catabolism.
...69...	Ability of retinoic and ascorbic acid to interfere with the binding of benzo(a)pyrene to DNA in explants from donors with bronchial cancer.
...70...	Quality control of protein C: protein C synthesized in the presence of warfarin is selectively degraded in the endoplasmic reticulum.
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...71...	Effect of metal ions on radical intensity and cytotoxic activity of ascorbate.	Various metal ions were investigated for their ability to modify the radical intensity and cytotoxic activity of sodium ascorbate or ascorbic acid. The addition of metal ions, such as Cu+, Cu2+, Fe2+, Zn2+, Mn2+ and Fe3+, dose-dependently enhanced the ascorbyl radical intensity whereas Na+, K+, Ca2+ and Mg2+ were totally inactive. The enhancement of ascorbyl radical intensity by metal ions was tightly coupled with the accelerated degradation of ascorbate. Addition of either serum or albumin significantly reduced the stimulation effect of Cu2+, and almost completely eliminated that of Fe3+ and Zn2+. The noncytotoxic concentration of Cu2+ significantly enhanced the cytotoxicity of ascorbate against cultured human glioblastoma T98G cell line. The present data suggest the possible role of metal ions in the regulation of the biological activity of ascorbate.
...72...	Formation of carbon dioxide from ascorbate in man.
...73...	Enhancement of radical intensity and cytotoxic activity of ascorbate by PSK and lignins.
...74...	Expression and functional characterization of chimeras between human and bovine vitamin-K-dependent protein-S-defining modules important for the species specificity of the activated protein C cofactor activity.
...75...	Role of ascorbate in the activation of NF-kappaB by tumour necrosis factor-alpha in T-cells.
...76...	Effect of ascorbate oxidase on radical intensity and cytotoxic activity of ascorbate.
...77...	Cupric ion/ascorbate/hydrogen peroxide-induced DNA damage: DNA-bound copper ion primarily induces base modifications.	Dialysis of EDTA-treated genomic DNA purified by standard proteinase K digestion/phenol extraction was necessary to remove low molecular weight species, probably transition metal ions and metal ion chelators, which supported frank strand breaks in the presence of ascorbate + H2O2 without supplemental copper ions.
...78...	A randomized, single-blind, placebo-controlled trial of the effects of 200 mg alpha-tocopherol on the oxidation resistance of atherogenic lipoproteins.
...79...	High density lipoprotein subclasses inhibit low density lipoprotein oxidation.
...80...	Abnormally elevated serum transcobalamin II levels in patients with cerebral malaria.
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...81...	Protection of low density lipoprotein oxidation at chemical and cellular level by the antioxidant drug dipyridamole.
...82...	Antioxidant and prooxidant properties of captopril and enalapril.
...83...	Improvement of some blood coagulation factors in cirrhotic patients treated with low doses of heparin.
...84...	Oxidative structural modifications of low density lipoprotein in homozygous familial hypercholesterolemia.
...85...	Antenatal drugs affecting vitamin K status of the fetus and the newborn.
...86...	Oxidative stress on lens and cataract formation: role of light and oxygen.
...87...	Protein modification by the degradation products of ascorbate: formation of a novel pyrrole from the Maillard reaction of L-threose with proteins.
...88...	Protein C.
...89...	Inactivation of human coagulation factor V by activated protein C.
...90...	Bone mineral density measured by dual-energy x-ray absorptiometry and novel markers of bone formation and resorption in patients on antiepileptic drugs.
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...91...	Different agonist- and antagonist-induced conformational changes in retinoic acid receptors analyzed by protease mapping.
...92...	Protein C, an antithrombotic protein, is reduced in hospitalized patients with intravascular coagulation.
...93...	Reconstruction of parodontal tissue with chitosan.
...94...	Effect of intravenous calcitriol on secondary hyperparathyroidism in chronic hemodialysis patients.
...95...	Biochemical markers for assessing skeletal growth.
...96...	17-beta estradiol protects neurons from oxidative stress-induced cell death in vitro.
...97...	Investigation of ascorbate-Cu (II) induced cleavage of DNA by scanning tunneling microscopy.
...98...	Determination of serum retinol by reversed-phase high-performance liquid chromatography.
...99...	The stability of retinol, alpha-tocopherol, trans-lycopene, and trans-beta-carotene in liquid-frozen and lyophilized serum.
...100...	Vitamin D metabolism in human colon adenocarcinoma-derived Caco-2 cells: expression of 25-hydroxyvitamin D3-1alpha-hydroxylase activity and regulation of side-chain metabolism.

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NLM database Documents

Record 1 from database: MEDLINE
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Title: Factors influencing the stability of ascorbic acid in total parenteral nutrition infusions.
Author: Allwood MC
Address
Source: J Clin Hosp Pharm, 1984 Jun, 9:2, 75-85
Abstract: Ascorbic acid stability in TPN infusions in 3-litre plastic bags was examined. Vitamin C was found to degrade slowly in mixtures which do not contain trace elements. In the presence of copper, degradation proceeds rapidly until dissolved oxygen is depleted. Reducing the copper concentration had only a minor influence on degradation rate. However, this copper-catalyzed reaction was prevented if cysteine was present in the TPN regimen. The amount of ascorbic acid degraded depended on the dissolved oxygen content of the infusion, the amount of residual air in the bag after filling and the permeability of the plastic to oxygen. In the absence of copper, 20-30 mg ascorbic acid was broken down within 24 h at ambient temperatures, but if copper was present, 150-200 mg was degraded within 2-4 h. The contribution of dehydroascorbic acid to the amount of vitamin C delivered to the patient was negligible. It is concluded that either vitamin C and trace element injections containing copper should not be added to the same bag, or an adequate coverage of ascorbic acid must be included to allow for losses by oxidation before and during administration.
Language of Publication: English
Unique Identifier: 84265330

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MeSH Heading (Major): Ascorbic Acid|AD/*ME/PD; Parenteral Nutrition|*/AE; Parenteral Nutrition, Total|*/AE
MeSH Heading: Cold; Copper|PD; Cysteine|PD; Dehydroascorbic Acid|ME; Drug Packaging; Drug Stability; Drug Storage; Human; Oxygen|AN/PD; Plastics|PD; Solutions

Publication Type: JOURNAL ARTICLE
ISSN: 0143-3180
Country of Publication: ENGLAND

Record 2 from database: MEDLINE
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Title: Ascorbic acid in cholesterol metabolism and in detoxification of xenobiotic substances: problem of optimum vitamin C intake.
Author: Ginter E
Address: Research Institute of Human Nutrition, Bratislava, Czechoslovakia.
Source: Nutrition, 1989 Nov, 5:6, 369-74
Abstract: There are extreme contradictions in the question of an optimum intake of vitamin C. The Recommended Dietary Allowances (RDA) in the USA, Great Britain, and many other countries range from 30 to 60mg for an adult man or woman, whereas the proponents of megadoses recommend as much as 18,000mg per day. Critical opinions against both the official RDA and the hypothesis of megadoses are summarized. Ideal RDA should be based on studies with increasing vitamin C doses in which the efficiency of the ascorbate-dependent systems would be correlated with the vitamin C concentration in the target tissues. On the basis of correlations of the hepatic vitamin C levels in guinea pigs with the rate of cholesterol degradation and the activity of microsomal detoxification systems, it is suggested that such intake of ascorbic acid is optimum that ensures a maximum body pool and maximum steady-state levels of vitamin C in the tissues. It is probable that in healthy adults, such a dose ranges from 100 to 200mg and that in stress conditions, it exceeds 200mg per day.
Language of Publication: English
Unique Identifier: 92199820

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MeSH Heading (Major): Ascorbic Acid|*AD/ME
MeSH Heading: Animal; Ascorbic Acid Deficiency|DT/ME; Cholesterol|ME; Cytochrome P-450|ME; Human; Metabolic Detoxication, Drug; Nutritional Requirements; Stress|DT/ME; Xenobiotics|ME

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0899-9007
Country of Publication: UNITED STATES

Record 3 from database: MEDLINE
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Title: Vitamin C depletion is associated with alterations in blood histamine and plasma free carnitine in adults.
Author: Johnston CS; Solomon RE; Corte C
Address: Department of Family Resources and Human Development, Arizona State University, Tempe 85287-2502, USA.
Source: J Am Coll Nutr, 1996 Dec, 15:6, 586-91
Abstract: OBJECTIVE: The purpose of this study was to determine whether carnitine metabolism or histamine degradation would be useful parameters for investigating the optimal requirement for vitamin C. METHODS: Twenty-two non-scorbutic subjects with subnormal vitamin C status (plasma vitamin C < 28 mumol/L) were placed on a metabolic diet low in vitamin C for 3 weeks and repleted with graded doses of vitamin C: 10, 30 and 60 mg vitamin C daily (group 1) or 10,125 and 250 mg vitamin C daily (group 2) for weeks 1, 2 and 3, respectively. Fasting blood samples were collected weekly and analyzed for plasma vitamin C, plasma free carnitine and blood histamine. RESULTS: Group 1 subjects remained in a subnormal vitamin C state throughout the 3-week study, and blood histamine and plasma free carnitine were not impacted by the experimental treatment. Plasma vitamin C in group 2 subjects rose significantly during the study, and these subjects finished the study with an ample vitamin C status indicative of vitamin C intakes above the recommended dietary allowance. Both blood histamine and plasma free carnitine were inversely related to vitamin C status in group 2 subjects. CONCLUSIONS: These data indicate that blood histamine and plasma free carnitine are altered in individuals with subnormal, non-scorbutic vitamin C status and provide evidence that metabolic changes independent of collagen metabolism occur prior to the manifestation of scurvy. Thus utilizing scurvy as an end-point to determine vitamin C requirements may not provide adequate vitamin C to promote optimal health and well-being.
Language of Publication: English
Unique Identifier: 97109456

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MeSH Heading (Major): Ascorbic Acid Deficiency|*BL/UR; Histamine|*BL
MeSH Heading: Adult; Ascorbic Acid|AD/BL/UR; Carnitine|BL; Female; Human; Male; Scurvy|BL; Support, Non-U.S. Gov't

Publication Type: JOURNAL ARTICLE
ISSN: 0731-5724
Country of Publication: UNITED STATES

Record 4 from database: MEDLINE
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Title: The reversibility of the vitamin C redox system: electrochemical reasons and biological aspects.
Author: Sapper H; Kang SO; Paul HH; Lohmann W
Address
Source: Z Naturforsch [C], 1982 Oct, 37:10, 942-6
Abstract: The biological efficacy of vitamin C depends on its redox abilities as given by the relations between ascorbic acid, semidehydroascorbic acid, and dehydroascorbic acid. It is shown by means of proton magnetic resonance spectroscopy that the enzymatic (by ascorbate oxidase) as well as non-enzymatic (by iodine) oxidation of ascorbic acid is, in principle, reversible despite the hydration and structural changes during the formation of dehydroascorbic acid. The strong redox activity of semidehydroascorbic acid which results in a fast disproportionation to ascorbic acid and dehydroascorbic acid is inferred from an inversion of the electrochemical potentials of the vitamin C redox system. The capacity of this is maintained by a fast reduction of dehydroascorbic acid e.g. by reduced glutathione, preventing its delactonization and further degradation.
Language of Publication: English
Unique Identifier: 83095669

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MeSH Heading (Major): Ascorbic Acid|BL/*ME
MeSH Heading: Animal; Ascorbate Oxidase|ME; Dehydroascorbic Acid; Glutathione; Human; Nuclear Magnetic Resonance; Oxidation-Reduction

Publication Type: JOURNAL ARTICLE
Country of Publication: GERMANY, WEST

Record 5 from database: MEDLINE
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Title: Ascorbic acid and vitamin B12.
Author: Newmark HL; Scheiner JM; Marcus M; Prabhudesai M
Address
Source: JAMA, 1979 Nov, 242:21, 2319-20
Abstract: Using extraction procedures in which the extracted vitamin B12 was protected by cyanide or metabisulfite, several investigators found no change in vitamin B12 when meals were incubated in the presence of ascorbic acid for 30 minutes at 37 degrees C. A previous report suggested degradation of vitamin B12 under these conditions, but this was apparently caused by incomplete protection of the extracted vitamin B12 in the assay procedure. If incubation at 37 degrees C for 30 minutes is a laboratory mimic of the gastric environment, one must conclude that high doses of ascorbic acid do not affect the stability of vitamin B12 in vivo.
Language of Publication: English
Unique Identifier: 80029992

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MeSH Heading (Major): Ascorbic Acid|AE/*AN; Food Analysis|*/MT; Vitamin B 12|AI/*AN/ME
MeSH Heading: Human

Publication Type: JOURNAL ARTICLE
ISSN: 0098-7484
Country of Publication: UNITED STATES

Record 6 from database: MEDLINE
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Title: Vitamin C improves endothelium-dependent vasodilation in patients with insulin-dependent diabetes mellitus.
Author: Timimi FK; Ting HH; Haley EA; Roddy MA; Ganz P; Creager MA
Address: Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Source: J Am Coll Cardiol, 1998 Mar, 31:3, 552-7
Abstract: OBJECTIVES: We sought to determine whether the antioxidant vitamin C improves endothelium-dependent vasodilation of forearm resistance vessels in patients with insulin-dependent diabetes mellitus. BACKGROUND: Endothelium-dependent vasodilation is impaired in patients with diabetes mellitus. Oxidatively mediated degradation of endothelium-derived nitric oxide contributes to abnormal endothelium-dependent vasodilation in animal models of diabetes mellitus. METHODS: The study group included 10 patients with insulin-dependent diabetes mellitus and 10 age-matched control subjects. Forearm blood flow was determined by venous occlusion plethysmography. Endothelium-dependent vasodilation was assessed by intraarterial infusion of methacholine (0.3 to 10 microg/min). Endothelium-independent vasodilation was assessed by intraarterial infusion of nitroprusside (0.3 to 10 microg/min). Forearm blood flow dose-response curves were determined for each drug infusion before and during concomitant infusion of vitamin C (24 mg/min). RESULTS: In diabetic subjects, endothelium-dependent vasodilation was augmented by the concomitant infusion of vitamin C (p = 0.001). Endothelium-independent vasodilation was not affected by the concomitant infusion of vitamin C (p = NS). In control subjects, vitamin C infusion did not affect endothelium-dependent vasodilation (p = NS). CONCLUSIONS: Vitamin C selectively restores the impaired endothelium-dependent vasodilation in the forearm resistance vessels of patients with insulin-dependent diabetes mellitus. These findings indicate that nitric oxide degradation by oxygen-derived free radicals contributes to abnormal vascular reactivity in humans with insulin-dependent diabetes mellitus.
Language of Publication: English
Unique Identifier: 98161741

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MeSH Heading (Major): Ascorbic Acid|AD/*PD; Diabetes Mellitus, Insulin-Dependent|*PP; Endothelium, Vascular|*DE/PP; Free Radical Scavengers|AD/*PD; Vascular Resistance|*DE; Vasodilation|*DE
MeSH Heading: Adult; Drug Administration Schedule; Female; Forearm|BS; Human; Infusions, Intra-Arterial; Male; Middle Age; Support, U.S. Gov't, P.H.S.; Treatment Outcome

Publication Type: JOURNAL ARTICLE
ISSN: 0735-1097
Country of Publication: UNITED STATES

Record 7 from database: MEDLINE
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Title: Total plasma antioxidant capacity predicts thrombosis-prone status in NIDDM patients.
Author: Ceriello A; Bortolotti N; Pirisi M; Crescentini A; Tonutti L; Motz E; Russo A; Giacomello R; Stel G; Taboga C
Address: Department of Medicine and Pathology, Clinical and Experimental, University of Udine, Italy.
Source: Diabetes Care, 1997 Oct, 20:10, 1589-93
Abstract: OBJECTIVE: To explore the hypothesis that a relationship exists between free radical activity and abnormalities in hemostasis in NIDDM. RESEARCH DESIGN AND METHODS: The use of the total radical-trapping antioxidant parameter (TRAP) has very recently been proposed to explore the antioxidant property of a plasma and their mutual cooperation. In the present study, TRAP, vitamin E, vitamin C, vitamin A, uric acid, protein-bound SH (thiol) groups, fibrinogen, prothrombin fragments F1 + 2, and D-dimer have been evaluated in 46 NIDDM patients and 47 healthy matched control subjects. RESULTS: In NIDDM patients, TRAP, vitamin A, SH groups, and uric acid were significantly reduced, whereas the level of vitamin E was significantly increased. Vitamin C was similar in the two groups. Fibrinogen, prothrombin fragment 1 + 2, and D-dimer were increased in diabetic patients. TRAP, but no single other antioxidant, had a strong inverse association with fibrinogen, prothrombin fragment 1 + 2, and D-dimer. CONCLUSIONS: These findings are consistent with the hypothesis that oxidative stress may condition coagulation activation in diabetics. However, the data suggest that it is the total antioxidant capacity rather than any single plasma antioxidant that is the most relevant parameter.
Language of Publication: English
Unique Identifier: 97460215

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MeSH Heading (Major): Antioxidants|*AN; Diabetes Mellitus, Non-Insulin-Dependent|*BL; Diabetic Angiopathies|*EP; Thrombosis|*EP
MeSH Heading: Ascorbic Acid|BL; Case-Control Studies; Female; Fibrin Fibrinogen Degradation Products|AN; Fibrinogen|AN; Hemostasis; Human; Male; Middle Age; Peptide Fragments|AN; Predictive Value of Tests; Protein Precursors|AN; Prothrombin|AN; Reference Values; Regression Analysis; Risk Factors; Uric Acid|BL; Vitamin A|BL; Vitamin E|BL

Publication Type: JOURNAL ARTICLE
ISSN: 0149-5992
Country of Publication: UNITED STATES

Record 8 from database: MEDLINE
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Title: Vitamin C improves endothelial function of conduit arteries in patients with chronic heart failure.
Author: Hornig B; Arakawa N; Kohler C; Drexler H
Address: Abteilung Kardiologie, Medizinische Hochschule Hannover, Germany.
Source: Circulation, 1998 Feb, 97:4, 363-8
Abstract: BACKGROUND: Chronic heart failure (CHF) is associated with endothelial dysfunction including impaired endothelium-mediated, flow-dependent dilation (FDD). There is evidence for increased radical formation in CHF, raising the possibility that nitric oxide is inactivated by radicals, thereby impairing endothelial function. To test this hypothesis, we determined the effect of the antioxidant vitamin C on FDD in patients with CHF. METHODS AND RESULTS: High-resolution ultrasound and Doppler was used to measure radial artery diameter and blood flow in 15 patients with CHF and 8 healthy volunteers. Vascular effects of vitamin C (25 mg/min IA) and placebo were determined at rest and during reactive hyperemia (causing endothelium-mediated dilation) before and after intra-arterial infusion of N-monomethyl-L-arginine (L-NMMA) to inhibit endothelial synthesis of nitric oxide. Vitamin C restored FDD in patients with heart failure after acute intra-arterial administration (13.2+/-1.7% versus 8.2+/-1.0%; P<.01) and after 4 weeks of oral therapy (11.9+/-0.9% versus 8.2+/-1.0%; P<.05). In particular, the portion of FDD mediated by nitric oxide (ie, inhibited by L-NMMA) was increased after acute as well as after chronic treatment (CHF baseline: 4.2+/-0.7%; acute: 9.1+/-1.3%; chronic: 7.3+/-1.2%; normal subjects: 8.9+/-0.8%; P<.01). CONCLUSIONS: Vitamin C improves FDD in patients with CHF as the result of increased availability of nitric oxide. This observation supports the concept that endothelial dysfunction in patients with CHF is, at least in part, due to accelerated degradation of nitric oxide by radicals.
Language of Publication: English
Unique Identifier: 98127728

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MeSH Heading (Major): Ascorbic Acid|AD/*TU; Cardiac Output, Low|*DT/PP/US; Endothelium, Vascular|*DE/*PP/US; Radial Artery|*DE/*PP/US
MeSH Heading: omega-N-Methylarginine|PD; Administration, Oral; Adult; Chronic Disease; Enzyme Inhibitors|PD; Human; Injections, Intra-Arterial; Male; Middle Age; Regional Blood Flow|DE/PH; Support, Non-U.S. Gov't; Time Factors; Treatment Outcome; Vasodilation|DE/PH

Publication Type: CLINICAL TRIAL; JOURNAL ARTICLE
ISSN: 0009-7322
Country of Publication: UNITED STATES

Record 9 from database: MEDLINE
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Title: Vitamin C improves endothelium-dependent vasodilation in forearm resistance vessels of humans with hypercholesterolemia.
Author: Ting HH; Timimi FK; Haley EA; Roddy MA; Ganz P; Creager MA
Address: Vascular Medicine and Atherosclerosis Unit, Brigham and Women's Hospital, Boston, MA 02115, USA.
Source: Circulation, 1997 Jun, 95:12, 2617-22
Abstract: BACKGROUND: Endothelium-dependent vasodilation is impaired in humans with hypercholesterolemia. Oxidative degradation of endothelium-derived nitric oxide plays a major role in endothelial dysfunction in animal models of hypercholesterolemia. To assess whether this mechanism is relevant to humans, we studied the effect of vitamin C, an antioxidant, on vasodilator function in forearm resistance vessels of patients with hypercholesterolemia. METHODS AND RESULTS: We studied 11 hypercholesterolemic and 12 healthy control subjects. Forearm blood flow was determined by venous occlusion plethysmography. Endothelium-dependent vasodilation was assessed by intra-arterial infusion of methacholine (0.3 to 10 micrograms/min). Endothelium-independent vasodilation was measured by intra-arterial infusion of nitroprusside (0.3 to 10 micrograms/min) and verapamil (10 to 300 micrograms/min). Forearm blood flow dose-response curves were determined for each drug before and during coadministration of vitamin C (24 mg/min). In hypercholesterolemic subjects, endothelium-dependent vasodilation to methacholine was augmented by coinfusion of vitamin C (P = .001); in contrast, endothelium-independent vasodilation to nitroprusside and verapamil were not affected by coinfusion of vitamin C (P = .8 and P = .3, respectively). In control subjects, vitamin C administration did not alter endothelium-dependent vasodilation (P = .2). CONCLUSIONS: We conclude that vitamin C improves endothelium-dependent vasodilation in the forearm resistance vessels of patients with hypercholesterolemia. These findings suggest that nitric oxide degradation by oxygen-derived free radicals contributes to abnormal vascular reactivity in hypercholesterolemic humans.
Language of Publication: English
Unique Identifier: 97336682

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MeSH Heading (Major): Ascorbic Acid|*TU; Endothelium, Vascular|*PP; Forearm|*BS; Hypercholesterolemia|*DT/*PP; Vascular Resistance|*; Vasodilation|*DE
MeSH Heading: Adult; Female; Human; Male; Middle Age; Regional Blood Flow|DE; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Vehicles|PD

Publication Type: CLINICAL TRIAL; JOURNAL ARTICLE
ISSN: 0009-7322
Country of Publication: UNITED STATES

Record 10 from database: MEDLINE
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Title: Antioxidant vitamin C improves endothelial dysfunction in chronic smokers.
Author: Heitzer T; Just H; Münzel T
Address: Medizinische Klinik III, Kardiologie, UniversitÂat Freiburg, Germany.
Source: Circulation, 1996 Jul, 94:1, 6-9
Abstract: BACKGROUND: Chronic smoking is associated with endothelial dysfunction, an early stage of atherosclerosis. It has been suggested that endothelial dysfunction may be a consequence of enhanced degradation of nitric oxide secondary to formation of oxygen-derived free radicals. To test this hypothesis, we investigated the effects of the antioxidant vitamin C on endothelium-dependent responses in chronic smokers. METHODS AND RESULTS: Forearm blood flow responses to the endothelium-dependent vasodilator acetylcholine (7.5, 15, 30, and 60 micrograms/min) and the endothelium-independent vasodilator sodium nitroprusside (1, 3, and 10 micrograms/min) were measured by venous occlusion plethysmography in 10 control subjects and 10 chronic smokers. Drugs were infused into the brachial artery, and forearm blood flow was measured for each drug before and during concomitant intra-arterial infusion of the antioxidant vitamin C (18 mg/min). In control subjects, vitamin C had no effect on forearm blood flow in response to acetylcholine and sodium nitroprusside. In contrast, in chronic smokers the attenuated forearm blood flow responses to acetylcholine were markedly improved by concomitant administration of vitamin C, whereas the vasodilator responses to sodium nitroprusside were not affected. CONCLUSIONS: The present studies demonstrate that the antioxidant vitamin C markedly improves endothelium-dependent responses in chronic smokers. This observation supports the concept that endothelial dysfunction in chronic smokers is at least in part mediated by enhanced formation of oxygen-derived free radicals.
Language of Publication: English
Unique Identifier: 96266946

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MeSH Heading (Major): Antioxidants|*TU; Ascorbic Acid|*TU; Endothelium, Vascular|*DE/*PP; Smoking|*AE
MeSH Heading: Acetylcholine|TU; Forearm|BS; Human; Injections, Intra-Arterial; Middle Age; Nitroprusside|TU; Reference Values; Regional Blood Flow|DE; Time Factors

Publication Type: CLINICAL TRIAL; JOURNAL ARTICLE
ISSN: 0009-7322
Country of Publication: UNITED STATES

Record 11 from database: MEDLINE
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Title: Influence of natural antioxidants on in vitro lipoprotein oxidation.
Author: Dobreanu M; Módy E
Address: Department of Clinical Biochemistry-Laboratory, TÈargu-MureÀs University of Medicine and Pharmacy, Romania.
Source: Rom J Intern Med, 1997 Jan, 35:1-4, 55-62
Abstract: Susceptibility of low-density lipoproteins (LDL) to oxidation might be a critical risk factor in the development and progression of atherosclerosis. The oxidation involves the degradation of polyunsaturated fatty acids, the formation of lysolecithin, oxysterols and aldehyde modification of lysine residues on Apo B100. The oxidation products have a number of biological activities such as cytotoxicity, atherogenesis, and carcinogenesis. The aim of this study was to investigate the in vitro antioxidant effects of vitamins E, A, and C on LDL. LDL was isolated from plasma by density gradient high-speed centrifugation and used as 0.1 microM/l isotonic solution. LDL oxidation was triggered by simple incubation with Cu2+ (1, 2, 5, 10, 12, 20 microM/l), in absence or presence of lipid-soluble or water-soluble antioxidants in different concentrations (tocopherols--0.5, 1, 2, and 4 microM/l; cerotenoids--0.1, 0.2, and 0.4 microM/l; ascorbate--2.5, 5, and 10 microM/l). The LDL oxidability was measured by continuous spectrophotometrical monitoring at 234 nm of the increased formation of conjugated diene hydroperoxides. The oxidation curves showed a profile with an inhibition period followed by a propagation period and were quantitatively characterized by two parameters: lag-phase (expressed in minutes), and propagation rate (expressed in changes of absorbance--delta E234nm/min). Lag-phase--the period of inhibition oxidation--was attributed to the ability of LDL (by antioxidants) to resist oxidation in vitro. LDL lag-phase decreased and propagation rate increased with the increasing of copper concentration. In conclusion: 1) susceptibility of LDL to oxidation depends on both the concentration of pro-oxidant stimuli and the entity and concentrations of antioxidants; 2) antioxidants retard the process through which LDL undergo oxidation in vitro when exposed to copper ions; 3) a synergistic effect may also be involved, as water-soluble vitamin C keeps the fat-soluble vitamin E and vitamin A within LDL.
Language of Publication: English
Unique Identifier: 98223746

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MeSH Heading (Major): Antioxidants|*PD; Lipid Peroxidation|*DE; Lipoproteins, LDL|*DE/IP/ME
MeSH Heading: Ascorbic Acid|PD; Comparative Study; Copper|PD; Dose-Response Relationship, Drug; Human; In Vitro; Isotonic Solutions; Time Factors; Vitamin A|PD; Vitamin E|PD

Publication Type: JOURNAL ARTICLE
ISSN: 1220-4749
Country of Publication: ROMANIA

Record 12 from database: MEDLINE
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Title: Protection by alpha-tocopherol but not ascorbic acid from hydrogen peroxide induced cell death in normal human breast epithelial cells in culture.
Author: Dabrosin C; Ollinger K
Address: Department of Obstetrics and Gynaecology, Faculty of Health Sciences, University Hospital, LinkÂoping, Sweden. lotda@ihm.liu.se
Source: Free Radic Res, 1998 Sep, 29:3, 227-34
Abstract: Alpha-tocopherol and ascorbic acid have been suggested to play a role in breast cancer prevention due to their antioxidative capacity. Increased exposure to endogenous and exogenous sex steroids is a known risk factor for breast cancer. We have studied the effects of alpha-tocopherol and ascorbic acid on hydrogen peroxide induced cell death in sex hormone treated normal breast epithelial cells in culture. We found that alpha-tocopherol but not ascorbic acid alone protected the cells. The effect of alpha-tocopherol increased when ascorbic acid was added to the cultures. The hydrogen peroxide degradation rate decreased in cultures treated with alpha-tocopherol alone and in combination with ascorbic acid compared to cells grown in medium or with ascorbic acid only. Oestradiol and progesterone treatment did not influence the results. Possible beneficial effects of combining various antioxidants, endogenous as well as exogenous, on human breast tissue need to be investigated further both in vivo and in vitro.
Language of Publication: English
Unique Identifier: 99017540

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MeSH Heading (Major): Ascorbic Acid|AN/*PD; Breast|*CY/DE; Epithelial Cells|*DE; Hydrogen Peroxide|ME/*TO; Vitamin E|AN/*PD
MeSH Heading: Cell Death|DE; Cells, Cultured; Estradiol|PD; Female; Human; Lactate Dehydrogenase|ME; Progesterone|PD; Support, Non-U.S. Gov't

Publication Type: JOURNAL ARTICLE
ISSN: 1071-5762
Country of Publication: SWITZERLAND

Record 13 from database: MEDLINE
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Title: Vitamin C and cardiovascular disease: a review.
Author: Simon JA
Address: Prevention Sciences Group of the University of California, San Francisco, School of Medicine.
Source: J Am Coll Nutr, 1992 Apr, 11:2, 107-25
Abstract: Vitamin C functions as a regulator of the catabolism of cholesterol to bile acids in the guinea pig and has been demonstrated to be an important factor in lipid regulation of the guinea pig, rabbit and rat. Correlation studies in humans have shown an inverse relationship between vitamin C intake and cardiovascular disease mortality. Observational and experimental studies in humans have yielded inconsistent results, but taken together indicate that for individuals with high total cholesterol concentrations, greater than or equal to 5.20 mmol/L (200 mg/dl) and less than full tissue saturation, increasing the concentration of vitamin C may have a salutary effect on total cholesterol. Vitamin C's effect on promoting the production and inhibiting the degradation of prostacyclin is reviewed, as are implications of these findings regarding thrombosis and atherogenesis. Evidence indicative of a protective effect on lipid peroxidation by vitamin C is examined. Analysis of the literature regarding groups at high risk for coronary heart disease reveals that men, the elderly, smokers, diabetics, hypertensives and perhaps oral estrogen-containing contraceptive users have lowered plasma vitamin C levels. Evidence linking vitamin C to human cardiovascular disease is largely circumstantial, but taken in total, is suggestive of an association. Further examination of the relationship between vitamin C and cardiovascular disease is warranted.
Language of Publication: English
Unique Identifier: 92251056

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MeSH Heading (Major): Ascorbic Acid|*PH/TU; Cardiovascular Diseases|ET/*PC; Cholesterol|*ME
MeSH Heading: Animal; Blood Pressure; Hemostasis; Human; Lipid Peroxidation; Risk Factors

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
ISSN: 0731-5724
Country of Publication: UNITED STATES
CAS Registry/EC Number: 50-81-7 (Ascorbic Acid); 57-88-5 (Cholesterol)

Record 14 from database: MEDLINE
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Title: Effect of dietary antioxidant combinations in humans. Protection of LDL by vitamin E but not by beta-carotene.
Author: Reaven PD; Khouw A; Beltz WF; Parthasarathy S; Witztum JL
Address: Department of Medicine, University of California, San Diego, La Jolla 92093-0682.
Source: Arterioscler Thromb, 1993 Apr, 13:4, 590-600
Abstract: Experimental and epidemiological evidence supports the hypothesis that oxidation of low density lipoprotein (LDL) appears to be important in mediating the atherogenicity of LDL. To test this hypothesis in humans, it will be necessary to perform intervention studies in large populations. We performed two studies to assess the effectiveness of supplementation with beta-carotene and vitamin E, used alone and in combination with each other, and with vitamin C, to protect LDL from oxidation. In phase 1, after a placebo period, eight subjects were given beta-carotene (60 mg/day) for 3 months, then beta-carotene plus vitamin E (1,600 mg/day) for another 3 months, and then beta-carotene plus vitamin E plus vitamin C (2 g/day) for 3 months. During phase 2, beta-carotene and vitamin C were discontinued, and subjects took only vitamin E for 5 months. During each period, LDL samples were isolated, and measurements of susceptibility to oxidation were performed. beta-Carotene levels in LDL increased nearly 20-fold, but LDL susceptibility to oxidation did not change. Addition of vitamin E increased LDL vitamin E levels nearly 2.5-fold, and this decreased LDL oxidation 30-40%. During the vitamin C supplementation period, plasma levels of beta-carotene and vitamin E rose, but only beta-carotene increased in LDL. However, the susceptibility of LDL to oxidation in this period was not decreased further. During phase 2, when subjects took only vitamin E, LDL susceptibility to oxidation was decreased by 50% as measured by thiobarbituric acid-reactive substances, conjugated dienes, and lipid peroxide formation as well as by macrophage degradation. Thus, long-term supplementation with large doses of vitamin E alone, but not beta-carotene, conferred increased protection to LDL in in vitro assays of oxidation. These data should be useful in planning therapeutic strategies to test the antioxidant hypothesis in humans.
Language of Publication: English
Unique Identifier: 93222138

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MeSH Heading (Major): Carotene|*PD; Lipoproteins, LDL|*ME; Oxidation-Reduction|*/DE; Vitamin E|*PD
MeSH Heading: Adult; Aged; Ascorbic Acid|PD; Diet; Drug Combinations; Female; Human; Macrophages|ME; Male; Middle Age; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Thiobarbituric Acid Reactive Substances|ME

Publication Type: JOURNAL ARTICLE
ISSN: 1049-8834
Country of Publication: UNITED STATES
CAS Registry/EC Number: 0 (Drug Combinations); 0 (Lipoproteins, LDL); 0 (Thiobarbituric Acid Reactive Substances); 1406-18-4 (Vitamin E); 36-88-4 (Carotene); 50-81-7 (Ascorbic Acid); 7235-40-7 (Beta Carotene)

Record 15 from database: MEDLINE
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Title: Protective effect of alpha-tocopherol and L-ascorbic acid against the ischemic-reperfusion injury in patients during open-heart surgery.
Author: Barta E; Pechán I; Cornák V; Luknárová O; Rendeková V; Verchovodko P
Address: Institute for Cardiovascular Diseases, Medical Faculty, Comenius University, Bratislava, CSFR.
Source: Bratisl Lek Listy, 1991 Mar-Apr, 92:3-4, 174-83
Abstract: The purpose of the investigation was: 1. to examine the effect of cardiopulmonary bypass (CPB) on the generation of cytotoxic oxygen-derived radicals and 2. to determine if the pretreatment of patients with vitamins E and C will combat generation of such radicals. Twenty patients undergoing CPB for treatment of cardiac disease were entered into the study and randomized to one of two groups. Group 1 (n = 9) served as control. Group 2 (n = 11) consisted of patients pretreated with 2000 IU of vitamin E 12 h prior to surgical intervention and 2 g of vitamin C given in the morning on the day of operation. Blood samples from arterial and mixed venous blood for analysis were obtained at the following intervals: 1. before anesthesia, 2. before sternotomy, 3. at the start of CPB, 4. at the end of CPB, 5. at the time of skin closure, 6. in the morning of the following day. Blood specimens from the coronary sinus were withdrawn A--before aortic cross-clamping, B--immediately after aortic declamping, C--in the 5th min, and D--in the 15th min of reperfusion. The concentration of inorganic phosphate as well as of uric acid was significantly higher in the control group what might indicate that vitamins E and C attenuate the degradation of adenine nucleotides. The most important difference between treated and control groups was observed in plasma concentration of malondialdehyde--a marker of lipid peroxidation--which was significantly lower in pretreated patients. A similar pattern of changes was found in the level of the lysosomal enzyme N-acetyl-glucosaminidase. Finally, pretreatment with vitamins E and C inhibited the decrease of catalase, observed in controls.
Language of Publication: English
Unique Identifier: 91230471

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MeSH Heading (Major): Ascorbic Acid|AD/*TU; Heart Surgery|*; Myocardial Reperfusion Injury|BL/*PC; Vitamin E|AD/*TU
MeSH Heading: Animal; Cardiopulmonary Bypass; Drug Therapy, Combination; Female; Hamsters; Human; Male; Middle Age; Phosphates|BL; Random Allocation; Uric Acid|BL

Publication Type: CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
ISSN: 0006-9248
Country of Publication: CZECHOSLOVAKIA
CAS Registry/EC Number: 0 (Phosphates); 1406-18-4 (Vitamin E); 50-81-7 (Ascorbic Acid); 69-93-2 (Uric Acid)

Record 16 from database: MEDLINE
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Title: Gas phase oxidants of cigarette smoke induce lipid peroxidation and changes in lipoprotein properties in human blood plasma. Protective effects of ascorbic acid.
Author: Frei B; Forte TM; Ames BN; Cross CE
Address: Division of Biochemistry and Molecular Biology, University of California, Berkeley 94720.
Source: Biochem J, 1991 Jul 1, 277 ( Pt 1):, 133-8
Abstract: Cigarette smoke (CS) is known to contain a large number of oxidants. In order to assess the oxidative effects of CS on biological fluids, we exposed human blood plasma to filtered (gas phase) and unfiltered (whole) CS, and determined the rate of utilization of endogenous antioxidants in relation to the appearance of lipid hydroperoxides. Lipid peroxidation was measured with a specific and sensitive assay that can detect lipid hydroperoxides at plasma levels as low as 10 nM. We found that exposure of plasma to the gas phase of CS, but not to whole CS, induces lipid peroxidation once endogenous ascorbic acid has been oxidized completely. In addition, CS exposure caused oxidation of plasma protein thiols and albumin-bound bilirubin, whereas uric acid and alpha-tocopherol were not consumed at significant rates. In plasma exposed to the gas phase of CS, low-density lipoprotein exhibited slightly increased electrophoretic mobility, but there was no apparent degradation of apolipoprotein B. Our results support the concept of an increased vitamin C utilization in smokers, and suggest that lipid peroxidation induced by oxidants present in the gas phase of CS leads to potentially atherogenic changes in lipoproteins.
Language of Publication: English
Unique Identifier: 91307512

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MeSH Heading (Major): Ascorbic Acid|*PD; Lipid Peroxidation|*/DE; Lipoproteins|*BL/IP; Smoke|*AN; Smoking|*BL
MeSH Heading: Adult; Antioxidants; Electrophoresis, Polyacrylamide Gel; Human; Kinetics; Male; Middle Age; Support, U.S. Gov't, P.H.S.

Publication Type: JOURNAL ARTICLE
ISSN: 0264-6021
Country of Publication: ENGLAND
CAS Registry/EC Number: 0 (Antioxidants); 0 (Lipoproteins); 50-81-7 (Ascorbic Acid)

Record 17 from database: MEDLINE
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Title: Nonenzymatic degradation and salvage of dietary folate: physicochemical factors likely to influence bioavailability.
Author: Lucock MD; Priestnall M; Daskalakis I; Schorah CJ; Wild J; Levene MI
Address: Department of Clinical Medicine, University of Leeds, United Kingdom.
Source: Biochem Mol Med, 1995 Jun, 55:1, 43-53
Abstract: We investigated the oxidative degradation pathway of 5CH3-H4PteGlu, the main extracellular folate and the predominant form of the vitamin found in food and blood. 5CH3-H4PteGlu is oxidized to 5CH3-5,6-H2PteGlu which subsequently undergoes C9-N10 bond cleavage yielding a pteridine residue and P-ABG, the latter step resulting in irreversible loss of vitamin activity. Under moderately acid conditions typical of the postprandial gut (pH 3.5) 5CH3-H4PteGlu is fairly stable (t1/2 = 273.6 min), while 5CH3-5,6-H2PteGlu is rapidly degraded (t1/2 = 16.9 min). In a neutral environment (pH 6.4) stability is reversed; 5CH3-H4PteGlu t1/2 = 12.0 mins, 5CH3-5,6-H2PteGlu t1/2 = 1504.6 min. Ascorbic acid was efficacious in the facile salvage of 5CH3-H4PteGlu from 5CH3-5,6-H2PteGlu which occurred rapidly and with significant efficiency (100% conversion) under acid (pH 3.5) conditions, t1/2 = 1.3 min (1 mmol/liter ascorbate), but was less efficient under neutral (pH 6.4) conditions t1/2 = 273.6 min (36% conversion). The presence of zinc and iron broadly maintains the pattern of effect, but increases all reaction rates. PteGlu was stable under all conditions studied. These results obtained in an artificial environment were supported by findings in human gastric juice: at a gastric pH of 1.47 with low endogenous ascorbate (7.0 mumol/liter), 5CH3-5,6-H2PteGlu and 5CH3-H4PteGlu both degrade instantly via C9-N10 bond cleavage to yield an equimolar amount of P-ABG. If the same gastric juice is spiked at 58.0 mumol/liter ascorbate (moderate endogenous concentration), 5CH3-H4PteGlu is stable (t1/2 = 334.7 min), while 5CH3-5,6-H2PteGlu is instantly salvaged to 5CH3-H4PteGlu with 43.3% efficiency, and the remaining 5CH3-5,6-H2PteGlu is degraded to P-ABG. In gastric juice with an elevated pH of 7.0 and no endogenous ascorbate, 5CH3-5,6-H2PteGlu and 5CH3-H4PteGlu are both stable, with no C9-N10 bond cleavage. This, for 5CH3-H4PteGlu, is in apparent contrast to findings at pH 6.4 in an artificial environment. The same gastric juice spiked to 50 mumol/liter ascorbate did not result in 5CH3-H4PteGlu salvage from 5CH3-5,6-H2PteGlu.(ABSTRACT TRUNCATED AT 400 WORDS)
Language of Publication: English
Unique Identifier: 96028633

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MeSH Heading (Major): Tetrahydrofolates|CH/*ME/PK
MeSH Heading: Ascorbic Acid|ME/PD; Biological Availability; Chemistry, Physical; Diet; Folic Acid|AA/ME; Gastric Juice|ME; Human; Hydrogen-Ion Concentration; In Vitro; Kinetics; Oxidation-Reduction; Support, Non-U.S. Gov't

Publication Type: JOURNAL ARTICLE
ISSN: 1077-3150
Country of Publication: UNITED STATES

Record 18 from database: MEDLINE
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Title: Adherence, proliferation and collagen turnover by human fibroblasts seeded into different types of collagen sponges.
Author: Middelkoop E; de Vries HJ; Ruuls L; Everts V; Wildevuur CH; Westerhof W
Address: Department of Cell Biology and Histology, Academic Medical Center, Amsterdam, The Netherlands.
Source: Cell Tissue Res, 1995 May, 280:2, 447-53
Abstract: We describe an in vitro model that we have used to evaluate dermal substitutes and to obtain data on cell proliferation, the rate of degradation of the dermal equivalent, contractibility and de novo synthesis of collagen. We tested three classes of collagenous materials: (1) reconstituted non-crosslinked collagen, (2) reconstituted collagen that was chemically crosslinked with either glutaraldehyde, aluminium alginate or acetate, and (3) native collagen fibres, with or without other extracellular matrix molecules (elastin hydrolysate, hyaluronic acid or fibronectin). The non-crosslinked reconstituted collagen was degraded rapidly by human fibroblasts. The chemically crosslinked materials proved to be cytotoxic. Native collagen fibres were stable. In the absence of ascorbic acid, the addition of elastin hydrolysate to this type of matrix reduced the rate of collagen degradation. Both elastin hydrolysate and fibronectin partially prevented fibroblast-mediated contraction. Hyaluronic acid was only slightly effective in reducing the collagen degradation rate and more fibroblast-mediated contraction of the material was found than for the native collagen fibres with elastin hydrolysate and fibronectin. In the presence of ascorbate, collagen synthesis was enhanced in the native collagen matrix without additions and in the material containing elastin hydrolysate, but not in the material with hyaluronic acid. These results are indicative of the suitability of tissue substitutes for in vivo application.
Language of Publication: English
Unique Identifier: 95300193

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MeSH Heading (Major): Collagen|*/DE/ME; Fibroblasts|*CY/ME; Skin, Artificial|*; Surgical Sponges|*; Tissue Culture|*IS
MeSH Heading: Ascorbic Acid|PD; Cell Adhesion; Cell Division; Cells, Cultured; Cross-Linking Reagents|PD; Elastin|PD; Extracellular Matrix|ME; Fibronectins|PD; Human; Hyaluronic Acid|PD; Microscopy, Electron, Scanning; Support, Non-U.S. Gov't

Publication Type: JOURNAL ARTICLE
ISSN: 0302-766X
Country of Publication: GERMANY

Record 19 from database: MEDLINE
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Title: Induction of DNA fragmentation in human myelogenous leukemic cell lines by sodium 5,6-benzylidene-L-ascorbate and its related compounds.
Author: Kuribayashi N; Sakagami H; Sakagami T; Niimi E; Shiokawa D; Ikekita M; Takeda M; Tanuma S
Address: First Department of Biochemistry, School of Medicine, Showa University, Tokyo, Japan.
Source: Anticancer Res, 1994 May, 14:3A, 969-76
Abstract: High-performance liquid chromatography revealed that sodium 5,6-benzylidene-L-ascorbate (SBA), dissolved in distilled water, was gradually decomposed into ascorbic acid and benzaldehyde. Among these three compounds, ascorbic acid showed the most potent cytotoxic activity. The cytotoxic activity of each compound was significantly reduced during degradation in culture medium. Agarose gel electrophoresis and fluorometric determination of DNA revealed that ascorbic acid, as well as SBA, induced DNA fragmentation into nucleosomal oligomers in human myelogenous leukemic cell lines, but not in freshly isolated human peripheral blood cells. The results suggest that antitumor activity of SBA might be at least in part mediated by the action of ascorbic acid, a degradation product of SBA.
Language of Publication: English
Unique Identifier: 94354633

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MeSH Heading (Major): Antineoplastic Agents|*PD; Ascorbic Acid|*AA/ME/PD; Benzylidene Compounds|ME/*PD; DNA|*ME
MeSH Heading: Animal; Benzaldehydes|ME; Cell Line; Cell Survival|DE; Human; Leukemia, Myeloid|ME/PA; Mice; Support, Non-U.S. Gov't

Publication Type: JOURNAL ARTICLE
ISSN: 0250-7005
Country of Publication: GREECE

Record 20 from database: MEDLINE
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Title: Stability of sodium 5,6-benzylidene-L-ascorbate.
Author: Sakagami H; Yamamura TS; Takahashi H; Shibuya I; Takeda M
Address: First Department of Biochemistry, School of Medicine, Showa University, Tokyo, Japan.
Source: Anticancer Res, 1995 Jul, 15:4, 1269-74
Abstract: The stability of sodium 5,6-benzylidene-L-ascorbate (SBA), consisting of two diastereomers, was investigated by high-performance liquid chromatography. In extensively acidic buffer, the acetal in SBA was immediately cleaved to liberate ascorbic acid and benzaldehyde. At higher pH, the cleavage of SBA was significantly reduced, but the degradation (due to possible opening of the lactone ring) of SBA was stimulated. The degradation rate of SBA was significantly increased with increasing temperature, and was higher than that of ascorbic acid or benzaldehyde. SBA was degraded with incubation time in culture medium, with accompanying loss of its biological activity, but only a marginal concentration of benzaldehyde, but not of ascorbic acid, was produced from SBA. The amount of SBA extracted from the apoptosing leukemic cells by 70% acetonitrile amounted to about 0.04% of that present in the medium fraction. These data suggest that SBA itself, but not contaminating ascorbic acid nor benzaldehyde, is responsible for the antitumor activity of SBA.
Language of Publication: English
Unique Identifier: 95382569

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MeSH Heading (Major): Antineoplastic Agents|*CH; Ascorbic Acid|*AA/CH/PD; Benzylidene Compounds|*CH/PD
MeSH Heading: Chromatography, High Pressure Liquid; Drug Stability; Human; Hydrogen-Ion Concentration; Stereoisomerism; Support, Non-U.S. Gov't

Publication Type: JOURNAL ARTICLE
ISSN: 0250-7005
Country of Publication: GREECE

Record 21 from database: MEDLINE
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Title: Inhibition of oxidative degradation of hyaluronic acid by uric acid.
Author: Liu KM; Swann D; Lee P; Lam KW
Address
Source: Curr Eye Res, 1984 Aug, 3:8, 1049-53
Abstract: It has been postulated that glycosaminoglycans in the trabeculum have an influence on aqueous humor drainage. Ascorbate reduces the viscosity of hyaluronic acid, and also increases outflow facility. Our recent observation of high urate concentrations in some glaucomatous eyes led us to study the influence of urate on oxidative degradation of hyaluronic acid by ascorbate. The viscosity of rooster comb hyaluronic acid was reduced slowly by ascorbate. Cupric sulfate accelerated ascorbate oxidation and also enhanced hyaluronic acid degradation. Urate inhibited ascorbate oxidation and prevented the copper catalyzed oxidative degradation of rooster comb hyaluronic acid. The range of urate concentrations used in this study was within the range of urate concentrations observed in glaucomatous eyes. The partially purified umbilical cord hyaluronic acid had lower viscosity than rooster comb hyaluronic acid, and rapidly degraded in the presence of ascorbate. The ascorbate effect on umbilical cord hyaluronic acid was partially prevented by urate.
Language of Publication: English
Unique Identifier: 85026249

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MeSH Heading (Major): Aqueous Humor|*ME; Glaucoma|*ME; Hyaluronic Acid|AI/*ME/PD; Trabecular Meshwork|*ME; Uric Acid|*ME/PD
MeSH Heading: Animal; Ascorbic Acid|AI/PD; Chickens; Copper|PD; Drug Interactions; Female; Human; In Vitro; Male; Oxidation-Reduction|DE; Pregnancy; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Umbilical Cord; Viscosity

Publication Type: JOURNAL ARTICLE
ISSN: 0271-3683
Country of Publication: ENGLAND

Record 22 from database: MEDLINE
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Title: Ascorbate deficiency results in decreased collagen production: under-hydroxylation of proline leads to increased intracellular degradation.
Author: Berg RA; Steinmann B; Rennard SI; Crystal RG
Address
Source: Arch Biochem Biophys, 1983 Oct, 226:2, 681-6
Abstract: Collagen production by cultured human lung fibroblasts was examined when the cells were made deficient in ascorbate. Cells grown in the absence of ascorbate produced 30% less collagen during a 6-h labeling period than cells incubated with as little as 1 microgram/ml ascorbate during the labeling period. Cells grown without ascorbate produced under-hydroxylated collagen which was subject to increased intracellular degradation from a basal level of 16% to an enhanced level of 49% of all newly synthesized collagen. The likely mechanism for increased intracellular degradation is the inability of under-hydroxylated collagen to assume a triple-helical conformation causing it to be susceptible to intracellular degradation. Measurement of collagen production by enzyme linked immunoassay (ELISA) using antibodies directed against triple-helical determinants of collagen showed that both types I and III collagens were affected. In contrast, another connective tissue component, fibronectin, was not affected. Analysis by ELISA showed a greater decrease in collagen production than did analysis by the collagenase method, suggesting that some non-helical collagen chains (detected by collagenase but not by ELISA) were secreted in the absence of ascorbate. These results provide a mechanism to account, in part, for the deficiency of collagen in connective tissues which occurs in a state of ascorbate deficiency.
Language of Publication: English
Unique Identifier: 84051275

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MeSH Heading (Major): Ascorbic Acid Deficiency|*ME; Collagen|BI/*ME; Lung|*ME; Proline|*ME
MeSH Heading: Ascorbic Acid|PD; Cells, Cultured; Fibroblasts|DE/ME; Human; Hydroxyproline|ME; Kinetics; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.

Publication Type: JOURNAL ARTICLE
ISSN: 0003-9861
Country of Publication: UNITED STATES

Record 23 from database: MEDLINE
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Title: A critical assessment of the effects of aminoguanidine and ascorbate on the oxidative modification of LDL: evidence for interference with some assays of lipoprotein oxidation by aminoguanidine.
Author: Scaccini C; Chiesa G; Jialal I
Address: Center for Human Nutrition, University of Texas, Southwestern Medical Center at Dallas 75235.
Source: J Lipid Res, 1994 Jun, 35:6, 1085-92
Abstract: Several lines of evidence support a role for oxidized low density lipoprotein (LDL) in the genesis of the atherosclerotic lesion. Hence, the effect of compounds with antioxidant properties on LDL oxidation assumes great significance. Ascorbate, a potent water-soluble chain-breaking antioxidant, has been shown to inhibit LDL oxidation. Aminoguanidine (AMG) is a pharmacological inhibitor of advanced non-enzymatic glycosylation. Recently it has been suggested that aminoguanidine might have an inhibitory effect on LDL oxidation, but total lipid peroxidation assayed by conjugated diene formation was not inhibited. Thus, in this study, we compared the effect of aminoguanidine with ascorbate to obtain a better appreciation of the effect of AMG on Cu(2+)-catalyzed LDL oxidation. Oxidative modification of LDL was monitored by assaying intermediates and end products of lipid peroxidation, conjugated dienes (CD), lipid peroxides (LPO), and relative electrophoretic mobility (REM). Apolipoprotein B-100 modification (increased fluorescence, fragmentation on SDS-PAGE, and 125I-labeled LDL degradation by human macrophages) was also measured. Ascorbate (100 microM) inhibited LDL oxidation by > 95%, as evidenced by all of the selected indices. Aminoguanidine (20 mM) substantially decreased thiobarbituric acid-reactive substances (TBARS) activity and lipid peroxide formation, but only partially prevented the increase of REM (-55%), apoB fluorescence (-39%), and degradation by macrophages (-54%). Unlike ascorbate, AMG failed to preserve alpha-tocopherol in LDL, prevent apoB-100 fragmentation, or inhibit conjugated diene formation during LDL oxidation. Furthermore, incubation of AMG with already oxidized LDL resulted in a significant decrease in TBARS activity and LPO, and 26.9% decrease in the REM of LDL.(ABSTRACT TRUNCATED AT 250 WORDS)
Language of Publication: English
Unique Identifier: 94358639

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MeSH Heading (Major): Ascorbic Acid|*PD; Guanidines|AD/*PD; Lipid Peroxidation|*DE; Lipoproteins, LDL|*ME
MeSH Heading: Apolipoproteins B|ME; Copper|ME; Dose-Response Relationship, Drug; Electrophoresis, Polyacrylamide Gel; Human; Kinetics; Macrophages|ME; Oxidation-Reduction; Support, Non-U.S. Gov't; Thiobarbituric Acid Reactive Substances|ME

Publication Type: JOURNAL ARTICLE
ISSN: 0022-2275
Country of Publication: UNITED STATES

Record 24 from database: MEDLINE
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Title: Bleaching of membrane-bound merocyanine 540 in conjunction with free radical-mediated lipid peroxidation.
Author: Pintar TJ; Lin F; Girotti AW
Address: Department of Biochemistry, Medical College of Wisconsin, Milwaukee 53226.
Source: Free Radic Biol Med, 1994 May, 16:5, 603-12
Abstract: The lipophilic dye merocyanine 540 (MC540) can photosensitize potentially lethal cell membrane damage as well as its own degradation (bleaching). Photobleaching in a test membrane, the human erythrocyte ghost has been examined. White light irradiation of MC540-sensitized ghosts resulted in lipid hydroperoxide (LOOH) formation, low-level thiobarbituric acid (TBA) reactivity, and dye bleaching (A568 decay). When the reaction was carried out in the presence of ascorbate (AH-), and added Fe3+, there was a large enhancement of TBA reactivity (indicative of free radical-mediated lipid peroxidation) and concomitant increase in the rate of photobleaching. Rapid bleaching also occurred when MC540 was incubated in the dark with ghosts that had been photoperoxidized with another dye (a phthalocyanine) and then exposed to AH-. The extent of bleaching in this system was found to be proportional to the starting level of LOOH. Like the wave of free radical lipid peroxidation that accompanied it, dye bleaching in AH(-)-treated, preperoxidized ghosts was stimulated by supplemental Fe3+, inhibited by desferrioxamine or butylated hydroxytoluene (BHT), but unaffected by catalase or superoxide dismutase. From this and related evidence, we deduce that: (1) in the absence of Fe3+/AH-, photoperoxidation and photobleaching occur independently and are nonradical, singlet oxygen-mediated processes; and (2) in the presence of Fe3+/AH-, 1-electron reduction of photogenerated LOOHs results in a surge of lipid peroxidation that amplifies dye loss via free radical processes. MC540 bleaching might be exploited as a relatively simple and sensitive indicator of lipid autoxidation in isolated membranes and cells.
Language of Publication: English
Unique Identifier: 94299217

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MeSH Heading (Major): Erythrocyte Membrane|DE/*ME; Lipid Peroxidation|*; Pyrimidinones|*ME/PD
MeSH Heading: Antioxidants; Ascorbic Acid|PD; Comparative Study; Ferric Compounds|PD; Free Radicals; Human; Photochemistry; Photosensitizing Agents|ME; Support, U.S. Gov't, P.H.S.; Thiobarbituric Acid Reactive Substances|ME

Publication Type: JOURNAL ARTICLE
ISSN: 0891-5849
Country of Publication: UNITED STATES

Record 25 from database: MEDLINE
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Title: Pentoxifylline. A hydroxyl radical scavenger.
Author: Freitas JP; Filipe PM
Address: ClÆinica DermatolÆogica UniversitÆaria, Faculdade de Medicina de Lisboa, Portugal.
Source: Biol Trace Elem Res, 1995 Jan, 47:1-3, 307-11
Abstract: Pentoxifylline (PTX), a tri-substituted purine and xanthine derivative, has been used for several years to improve microcirculation because of its hemorheological properties. PTX has also antifibrotic and anti-inflammatory effects. We studied the reaction of PTX with the hydroxyl radical and superoxide anion. Hydroxyl radical was generated by a mixture of ascorbic acid, H2O2 and Fe(III)-EDTA. We evaluated the iron-dependent degradation of deoxyribose, mediated by hydroxyl radical, in the presence of different concentrations of PTX (from 0.05 to 3 mM), measuring the degradation products of deoxyribose that react with 2-thiobarbituric acid (TBA). The reaction of PTX with hydroxyl radical occurred with a rate constant of (1.1 +/- 0.2) x 10(10) M-1/s. These results support the properties of PTX as a hydroxyl radical scavenger. Some authors verified that PTX decreases the release of superoxide anion from activated neutrophils. We studied the effect of PTX as a scavenger of superoxide generated in vitro by a hypoxanthine-xanthine oxidase system. PTX was not a superoxide anion scavenger in this system.
Language of Publication: English
Unique Identifier: 95298509

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MeSH Heading (Major): Free Radical Scavengers|*/PD; Hydroxyl Radical|*; Pentoxifylline|*/PD
MeSH Heading: Ascorbic Acid; Comparative Study; Edetic Acid; Ferric Compounds; Human; Hydrogen Peroxide; Iron Chelating Agents; Kinetics; Neutrophils|DE/PH; Superoxides; Xanthine Oxidase|ME; Xanthines|ME

Publication Type: JOURNAL ARTICLE
ISSN: 0163-4984
Country of Publication: UNITED STATES

Record 26 from database: MEDLINE
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Title: Ascorbic acid and urate in human seminal plasma: determination and interrelationships with chemiluminescence in washed semen.
Author: Thiele JJ; Friesleben HJ; Fuchs J; Ochsendorf FR
Address: Zentrum der Dermatologie und Venerologie, Abteilung II, Frankfurt/M, Germany.
Source: Hum Reprod, 1995 Jan, 10:1, 110-5
Abstract: Peroxidative damage induced by reactive oxygen species (ROS) has been proposed as one of the major causes of defective sperm function. The ROS detected in semen reflect an imbalance between ROS generation and degradation. The objective of the present study was to investigate the relationship between the oxidative and anti-oxidative potential in semen of infertile patients and healthy donors. Specimens were obtained from 28 patients and 18 healthy donors (controls). A conventional spermiogram, measurement of luminol-chemiluminescence (CL) in washed semen, and high performance liquid chromatography determination of ascorbic acid and urate concentrations in seminal plasma were performed. Oligozoospermic patients exhibited higher CL signals than controls (P < 0.001). Normozoospermic patients showed lower ascorbic acid (mean +/- SE: 491 +/- 46 microM, P < 0.04) and urate concentrations (320 +/- 22 microM, P < 0.009) than controls (612 +/- 35 and 426 +/- 26 microM respectively). Seminal plasma ascorbic acid was negatively correlated with the CL signals (P < 0.0006) and positively correlated with the percentage of spermatozoa with normal morphology (P < 0.006). This is the first report of a correlation between the anti-oxidant ascorbic acid in seminal plasma and ROS generation in human semen. Furthermore, the reduced ascorbic acid/urate concentrations found in semen of normozoospermic patients might be indicative of a reduced anti-oxidative protection.
Language of Publication: English
Unique Identifier: 95263752

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MeSH Heading (Major): Ascorbic Acid|*ME; Infertility, Male|*ME; Semen|*ME; Uric Acid|*ME
MeSH Heading: Adult; Antioxidants|ME; Chemiluminescence; Human; Male; Oligospermia|ME; Oxidation-Reduction; Reactive Oxygen Species|ME; Support, Non-U.S. Gov't

Publication Type: CLINICAL TRIAL; CONTROLLED CLINICAL TRIAL; JOURNAL ARTICLE
ISSN: 0268-1161
Country of Publication: ENGLAND

Record 27 from database: MEDLINE
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