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PubMed1977

[Breakdown of linoleic and linolenic acid hydroperoxides in the presence of ascorbic acid analysis of the volatile aldehydes (author's transl)].

Hydroperoxide emulsions with 10(-3) mol ascorbic acid were stored for 19 h at 22 degrees C. Volatile aldehydes were formed in the presence of oxygen and traces of metals. The main compounds were identified as follows (mol-%): 2-pentenal [51] and 2-hexenal [22] from 13-hydroperoxioctadeca-9,11,15-trienoic acid; propanol [38] and 2-hexenal [25] from 9-hydroperoxioctadeca-10,12,15-trienoic acid; hexanal [82] respectively [66] from 13-hydroperoxioctadeca-9,11-respectively 9-hydroperoxioctadeca-10,12-dienoic acid. C9 and C10 aldehydes were only detected in very low concentrations as fragments of the 9-hydroperoxides.

Aldehydes↗
PubMed1983

Effect of peritoneal dialysis on plasma levels of ascorbic acid.

The effect of peritoneal dialysis on plasma ascorbate levels was investigated in 32 patients suffering from end-stage renal disease. Our studies demonstrated a high peritoneal clearance of ascorbic acid resulting in a significant loss into the dialysate. The quantity of ascorbic acid lost by patients undergoing peritoneal dialysis was proportional to the predialysis ascorbic acid levels. Since the ascorbic acid lost from the plasma during peritoneal dialysis is not adequately replaced by dietary consumption of vitamin C, patients undergoing chronic peritoneal dialysis should receive ascorbic acid supplementation as an important part of their therapeutic regimen.

Adult↗
PubMed2006

Relationship between seminal ascorbic acid and sperm DNA integrity in infertile men.

Ascorbic acid has recently been reported to protect sperm DNA from the damage induced by exogenous oxidative stress in vitro. But, there is no report on seminal ascorbic acid and sperm DNA fragmentation in infertile men. In this study, we asked whether sperm DNA damage correlates with seminal ascorbic acid levels. Sperm DNA fragmentation index (DFI) was analysed in 75 men by flow cytometry after acridine orange staining. We also measured the levels of seminal plasma ascorbic acid and total antioxidant capacity. Abnormal sperm DNA integrity (DFI >or= 30%) was observed in 12% of the patients with normal semen parameters and in 52% of the patients with abnormal semen parameters. There were significant correlations between the level of DFI and conventional semen parameters including sperm count, motility and morphology (r = -0.29, -0.55 and -0.53 respectively; p < 0.05). Seminal ascorbic acid level was significantly lower in the patients with leucospermia than the patient with normal semen parameters. Interestingly, a significantly greater percentage of men with abnormal DFI were observed in the patients with low levels of seminal ascorbic acid compared with those with normal or high levels of ascorbic acid (59% vs. 33%, p < 0.05). Men with insufficient seminal ascorbic acid frequently have sperm DNA damage.

Adult↗
PubMed1976

Ascorbic acid and fractures in children with myelomeningocele.

Ascorbic acid intake of sixty-seven patients with myelomeningocele, ages one through eight years, was evaluated in two groups, fracture and non-fracture, to compare their intake of ascorbic acid from food-plus-supplement, food-only, and supplement-only with the recommended allowances. Intake from food-plus-supplement exceeded the allowance for 90 per cent of the fracture and 83 per cent of the non-fractured patients. Intake from food-only exceeded the recommended allowance in 79 per cent of the fracture and 75 per cent of the non-fracture subjects. All supplementations exceeded 100 per cent of the recommended allowance. There was no significant difference in the ascorbic acid intakes of fracture and non-fracture patients. Since there was no apparent correlation between fractures and ascorbic acid intake, we do not recommend ascorbic acid supplementation to prevent fractures. If such high levels are suggested, the potentially harmful effects of excessive ascorbic acid in growing children must be carefully considered.

Adolescent↗
PubMed2001

Requirement for GSH in recycling of ascorbic acid in endothelial cells.

Ascorbic acid may be involved in the defense against oxidant stress in endothelial cells. Such a role requires that the cells effectively recycle the vitamin from its oxidized forms. In this work, we studied the ability of cultured bovine aortic endothelial cells (BAECs) to take up and reduce dehydroascorbic acid (DHA) to ascorbate, as well as the dependence of ascorbate recycling on intracellular GSH. BAECs took up and reduced DHA to ascorbate much more readily than they took up ascorbate. Although BAECs in culture did not contain ascorbate, ascorbate accumulated to concentrations of 2-3 mM in BAECs following incubation with 400 microM DHA. Extracellular ferricyanide oxidized intracellular ascorbate, which was recycled by the cells. Reduction of DHA, either when added to the cells or when generated in response to ferricyanide, caused significant decreases in intracellular GSH concentrations. Depletion of intracellular GSH with 1-chloro-2,4-dinitrobenzene, diethylmaleate, and diamide almost abolished the ability of the cells to reduce DHA to ascorbate. DHA reduction by thioredoxin reductase was evident in dialyzed cell extracts, but occurred at rates far lower than direct GSH reduction of DHA. These results suggest that maximal rates of DHA reduction, and thus recycling of ascorbate from DHA, are dependent upon GSH in these cells.

Animals↗
PubMed1988

Glutathione inhibits the glycation and crosslinking of lens proteins by ascorbic acid.

The incubation of crude extracts of bovine lens with 20 mM ascorbic acid leads to the formation of covalent adducts even in the presence of saturating levels of a metal chelator. When dialysed lens extracts were used both ASA-protein adducts and highly crosslinked lens proteins were observed which are similar to those found in the water insoluble fraction from cataractous lenses. Both adduct formation and protein crosslinking, however, were markedly inhibited if undialysed lens extracts were used or if increasing concentrations of glutathione were added to the incubation mixture. Similar inhibition was seen with cysteine, dithiothreitol and sodium bisulfite, but little effect was observed with the glutathione analog ophthalmic acid or with free radical quenchers. Glutathione was readily oxidized during the incubation and no oxidation of ascorbic acid was observed until all the reduced glutathione was exhausted. No loss of ascorbic acid and no protein crosslinking were observed when oxygen was completely removed from the reaction mixture. These data strongly suggest that the glycating species was an oxidized form of ascorbic acid. Ascorbic acid solutions displayed a rapid oxidation in vitro, which was decreased 80-fold upon the addition of 1 mM chelator and was completely inhibited by both glutathione and chelator. A rapid decrease in the level of dissolved oxygen was seen in the presence of ascorbic acid or ascorbic acid and glutathione, but not with glutathione alone. These data argue that glutathione inhibits glycation by rapidly reducing dehydroascorbic acid back to ascorbic acid, which is not active in protein glycation

Animals↗
PubMed1979

The interaction of L-ascorbic acid with the active center of myrosinase.

Only L-ascorbic acid activated plant myrosinase (thioglucoside glucohydrolase, EC 3.2.3.1), whereas ascorbic acid analogs did not. The enzyme protein was conformationally changed by the addition of L-ascorbic acid to the spectrophotometric analysis, approx. 1.5 amino residues appeared on the surface of the enzyme and about 2.3 tryptophan residues were buried in the molecule when 1 mM L-ascorbic acid was added. Optimum temperature for the myrosinase activity was approx. 55 degrees C without L-ascorbic acid, but with L-ascorbic acid it was about 35 degrees C; that for beta-glucosidase activity was the same (55 degrees C) with or without L-ascorbic acid. The effect of chemical modification of the functional groups of myrosinase on the interaction of L-ascorbic acid was investigated and the interaction of L-ascorbic acid with the active center of the enzyme is proposed.

2-Hydroxy-5-nitrobenzyl Bromide↗
PubMed1986

Possible mechanisms responsible for the increased ascorbic acid content of Plasmodium vinckei-infected mouse erythrocytes.

The possible mechanisms underlying the acquisition of an increased ascorbic acid content by mouse erythrocytes containing the malarial parasite Plasmodium vinckei were investigated. Ascorbic acid was taken up readily by parasitized red blood cells but not by controls, whilst its partly oxidized form, dehydroascorbic acid, entered both. The uptake of both ascorbic acid and dehydroascorbic acid into erythrocytes was increased as a result of malarial infection. Lysates prepared from parasitized red blood cells reduced exogenous dehydroascorbic acid to ascorbic acid at a higher rate than control red blood cell lysates; this difference was abolished following dialysis of the lysates, a process which removes endogenous reduced glutathione (GSH). The rates of chemical and enzymatic reduction of dehydroascorbic acid to ascorbic acid by GSH were of similar magnitude, thus calling into question the existence of a specific dehydroascorbate reductase in erythrocytes and parasites. These observations suggest that the increased uptake of dehydroascorbic acid into parasitized red blood cells may be a result of enhanced dehydroascorbate-reducing capacity, whilst the presence of the parasite induces a selective increase in the permeability of the erythrocyte plasma membrane to ascorbic acid. The endogenous ascorbic acid content of livers obtained from infected mice was 55% below the normal concentration and its relative rate of destruction during incubation in vitro was enhanced in comparison with that of control livers. Furthermore, the capacity of liver homogenates to synthesize ascorbic acid from glucuronic acid was greatly reduced in infected mice. Therefore it is unlikely that the increase in ascorbic acid content of parasitized red blood cells is a consequence of increased biosynthesis and release of ascorbic acid by the host liver. We have not been able to exclude the possibility that the malarial parasite itself may be capable of de novo synthesis of ascorbic acid.

Animals↗
PubMed2001

Effects of ascorbic acid on retinal pigment epithelial cells.

PURPOSE: Evaluation of effects of ascorbic acid on cell characteristics of dedifferentiated porcine retinal pigment epithelial (pRPE) cells. METHODS: pRPE cells were incubated in vitro with increasing concentrations of ascorbic acid (0.25-1.5 mMol). Cell proliferation was assayed by measuring the incorporation of 5-bromo-2'-deoxy-uridine (BrdU) into cellular DNA. Migration and contraction properties were studied on a cell permissive porous membrane and collagen gels, respectively. Phenotypic changes in response to ascorbic acid and its derivative ascorbic acid 2-phophate were evaluated by microscopy and indirect immunofluorescence. RESULTS: Ascorbic acid significantly inhibits cell proliferation, migration, and contraction in concentrations of 1 mMol or more. Under the influence of at least 1 mMol ascorbic acid dedifferentiated pRPE cells exhibited a pigmented status within 24 hours. Addition of 500 U/ml catalase prevented the antiproliferative effect of ascorbic acid and the formation of pigment. Concentrations of 0.5 mMol ascorbic acid as well as 1 mMol ascorbic acid 2-phosphate promoted differentiation of cell phenotype. Furthermore, ascorbic acid 2-phosphate supported the formation of in vivo-like epithelial structures. CONCLUSIONS: Ascorbic acid has an influence on vital cell characteristics such as proliferation, migration, contraction and differentiation of pRPE cells. As dedifferentiation of these cells is an integral part in the development of proliferative vitreoretinopathy (PVR), ascorbic acid should be taken into consideration as a supplement in the clinical management of this disease.

Animals↗
PubMedDate not supplied

The effect of core-to-wall ratio and Span 80 concentration on the properties of ascorbic acid microcapsules.

Ethylcellulose microcapsules containing ascorbic acid were prepared by the emulsification-solvent evaporation technique. The effect of core-to-wall ratios and surfactant concentrations on the dissolution rate and size distribution of the ascorbic acid microcapsules were studied. Span 80 was used as a dispersing agent and light liquid paraffin as a continuous phase. The dissolution of ascorbic acid microcapsules was studied using the USP rotating basket method. A high core-to-wall ratio resulted in an increase of both microcapsule size and drug release rate. For a given core-to-wall ratio a high concentration of Span 80 increased the drug release rate, this was associated with the presence of drug crystals on the microcapsule surface.

Antioxidants↗
PubMed1987

Ascorbic acid as an antioxidant in measurements of catecholamines in plasma.

Sodium metabisulfite, commonly used to prevent the oxidation of catecholamines during extraction from plasma onto alkaline alumina, does not prevent their subsequent degradation in acetic acid eluates. However, ascorbic acid, a potent antioxidant, is extracted with the catecholamines onto the alumina and prevents such destruction. However, ascorbic acid may interfere with the electrochemical measurement of catecholamines, unless sequential oxidation and reduction are used. Other methods of minimizing catecholamine oxidation in acetic acid eluates include refrigerating at 4 degrees C and capping the sample vials to exclude atmospheric oxygen.

Aluminum Oxide↗
PubMed2000

Antioxidant properties of novel lipophilic ascorbic acid analogues.

Structural modifications of ascorbic acid by the introduction of lipophilic moieties has led to derivatives with increased stability against thermal and oxidative degradation. Two series of new lipophilic ascorbic analogues were synthesized to obtain antioxidants devoid of autooxidant properties: 4-benzoyl-3-hydroxyfuran-2(5H)-ones (3a-j) and 4-acetyl-5-aryl-3,4-dihydrofuran-2(5H)ones (5a-f). These compounds were submitted to three different tests: reduction of the stable free radical, 1,1-diphenyl-2-picrylhydrazyl (DPPH); superoxide-anion scavenging assay; and lipid-peroxidation assay. Most compounds interacted with DPPH: at a concentration of 5 x 10(-3) M, the reducing activity of 4-benzoyl derivatives, 3c and 3h, was more than 50%; under the same conditions, the rate of inhibition for 4-acetylbutanolides, 5a and 5f, reached 60.6% and 87.3%, respectively; 93.3% inhibition was observed with ascorbic acid. In the superoxide-anion scavenging assay, at a concentration of 1 mg mL(-1), 4-benzoyl derivatives, 3g and 3i, exhibited a good activity, with IC50 (dose resulting in 50% inhibition) values of 1.45 and 1.35 x 10(-3) M, respectively. 4-Acetylbutanolide, 5f, significantly inhibited the Fe2+/ADP/ascorbate-induced lipid peroxidation of rat liver microsomes with an IC50 of 4.9 x 10(-4) M. This study demonstrates that enol functions in the structure of ascorbic acid analogues are not absolutely essential to bring about antioxidant effects.

Animals↗
PubMed1990

Regulation of ascorbic acid concentration in embryonic chick brain.

The relationship between ascorbic acid concentration and cellular transport mechanisms was studied in chicken embryos (Gallus gallus domesticus). Unincubated (Day 0) fertile eggs did not contain detectable levels of ascorbic acid as assayed by high performance liquid chromatography with electrochemical detection. However, ascorbic acid concentration in brain increased to 5.6 nmol/mg tissue by Day 10 in ovo and then gradually declined 32% before birth. These levels were an order of magnitude greater than in skeletal muscle, where ascorbic acid concentration decreased sixfold between Days 8-20. Uptake of ascorbic acid was measured in brain cells that were either freshly isolated or grown in primary culture. Saturable, temperature- and Na(+)-dependent ascorbic acid transport was evident in freshly isolated cells as early as Day 6 and persisted throughout the period of ontogenic development. Primary cultures of embryonic chick brain cells were observed to take up ascorbic acid through a high-affinity (apparent Km = 37 microM, Vmax = 106 nmol ascorbic acid/g protein/min) mechanism. This transport system may maintain the high concentrations of ascorbic acid observed in the central nervous system during the ontogenic period when the levels of ascorbic acid in peripheral tissues change drastically.

Animals↗