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PubMed2002

Vitamin C suppresses TNF alpha-induced NF kappa B activation by inhibiting I kappa B alpha phosphorylation.

Extracellular stimuli signal for activation of the transcription factor NFkappaB, leading to gene expression regulating processes involved in immune responses, inflammation, and cell survival. Tumor necrosis factor-alpha (TNFalpha) activates NFkappaB via a well-defined kinase pathways involving NFkappaB-inducing kinase (NIK), which activates downstream multisubunit IkappaB kinases (IKK). IKK in turn phosphorylates IkappaB, the central regulator of NFkappaB function. We found that intracellular vitamin C inhibits TNFalpha-induced activation of NFkappaB in human cell lines (HeLa, monocytic U937, myeloid leukemia HL-60, and breast MCF7) and primary endothelial cells (HUVEC) in a dose-dependent manner. Vitamin C is an important antioxidant, and most cells accumulate ascorbic acid (AA) intracellularly by transporting the oxidized form of the vitamin, dehydroascorbic acid (DHA). Because ascorbic acid is a strong pro-oxidant in the presence of transition metals in vitro, we loaded cells with vitamin C by incubating them with DHA. Vitamin C-loaded cells showed significantly decreased TNFalpha-induced nuclear translocation of NFkappaB, NFkappaB-dependent reporter transcription, and IkappaBalpha phosphorylation. Our data point to a mechanism of vitamin C suppression of NFkappaB activation by inhibiting TNFalpha-induced activation of NIK and IKKbeta kinases independent of p38 MAP kinase. These results suggest that intracellular vitamin C can influence inflammatory, neoplastic, and apoptotic processes via inhibition of NFkappaB activation.

Active Transport, Cell Nucleus↗
PubMed1979

[Effects of ingestion of an antioxidant, BHT, on the metabolism of ascorbic acid and vitamin A in rats].

The antioxidant foor additive, BHT, was fed to male rat for 28 days at a 0.5% concentration in a diet containing ascorbic acid or not. BHT intake had no effect on ascorbic and dehydroascorbic acid contents in the adrenals, spleen or liver, whether or not the diet contained ascorbic acid. When the ration included 100 mg/kg of ascorbic acid, BHT intake caused a sharp rise in urinary excretion of this compound. This data confirm the work of other authors studying an ascorbic acid-poor diet. These results indicate that BHT intake leads to increased synthesis of ascorbic acid. This augmentation would be the result of stimulating the biosynthesis pathway of uridyl-di-phospho-glucuronic acid, which is necessary to the elimination of BHT in the form of glucuroconjugate. BHT intake in an ascorbic acid-rich diet reduces hepatic vitamin A concentration by 44 p. 100 and the hepatic reserve of this vitamin by 22 p. 100. BHT detoxication, as that of other exogenous compounds, thus seems to cause increased vitamin A utilization.

Adrenal Glands↗
PubMed1997

Glutathione dependent reduction of alloxan to dialuric acid catalyzed by thioltransferase (glutaredoxin): a possible role for thioltransferase in alloxan toxicity.

Recombinant pig liver thioltransferase (rPLTT) catalyzes the reduction of alloxan to dialuric acid by glutathione (GSH). This is the second non-disulfide substrate, after dehydroascorbic acid, described for thioltransferase. The reaction kinetics, measured by a coupled assay including glutathione disulfide reductase and NADPH yielded a Km = 82 microM for alloxan, a k(cat) = 37 s(-1), and a k(cat)/Km = 4.5 x 10(5) M(-1) s(-1). The presence of rPLTT suppressed the competitive formation of compound 305, an alloxan-GSH conjugate of unknown structure, and at GSH concentrations between 0.05 mM and 1.5 mM, oxygen consumption was greater than that recorded in the uncatalyzed reaction. Both superoxide dismutase and catalase inhibited oxygen consumption in 1.0 mM GSH and 0.2 mM alloxan in the presence of rPLTT. This study suggests that thioltransferase (glutaredoxin) plays a significant role in the cytotoxicity of alloxan in vulnerable tissues.

Alloxan↗
PubMed1984

An in vitro effect of ascorbate on the spontaneous reduction of sodium nitrite concentration in a reaction mixture.

Nitrite is known to react with free amines to form nitrosamines which may have carcinogenic activity. The present study provides evidence showing that addition of ascorbic acid in a reaction mixture results in a spontaneous decrease in nitrite concentration. The nitrite lowering effect of ascorbic acid appears to correlate with the rate of oxidation of the vitamin to dehydroascorbic acid, suggesting that ascorbic acid may be involved in the reduction of nitrite to nitrogen oxide.

Ascorbic Acid↗
PubMed1990

Mammalian thioltransferase (glutaredoxin) and protein disulfide isomerase have dehydroascorbate reductase activity.

Homogeneous native and recombinant porcine liver thioltransferase (glutaredoxin), bovine thymus and human placenta thioltransferase (glutaredoxin) were examined for dehydroascorbate reductase activity (EC 1.8.5.1) involving the direct catalytic reduction of dehydroascorbic acid (DHA) by glutathione. Each enzyme had substantial activity with apparent Km and Vmax for dehydroascorbate between 0.2 and 2.2 mM and 6-27 nmol min-1, respectively, and for gluathione between 1.6 and 8.7 mM and 11-30 nmol min-1, respectively. In the presence of purified bovine liver thioredoxin reductase, homogeneous bovine liver thioredoxin failed to reduce DHA to ascorbic acid as measured by NADPH oxidation. Highly purified bovine liver protein disulfide isomerase (PDI) reacted directly with DHA and GSH to catalyze the reduction of DHA to ascorbic acid. The apparent Km for DHA was 1.0 mM and the Vmax was 8 nmol min-1, and for GSH were 3.9 mM and 14 nmol min-1, respectively. These results suggest that thioltransferase and PDI contribute to the regeneration of oxidized ascorbic acid in mammalian cells, and based on their cellular location, thioltransferase is proposed to be the major cytoplasmic activity, whereas interaction of DHA with microsomal membrane PDI may catalyze regeneration of ascorbic acid and initiate oxidation of intralumenal protein thiols to disulfides.

Animals↗
PubMed1975

[Determination of GSH-DH activity (E.C.1.8.5.1) presence of the enzyme in different wheat varieties (author's transl)].

2,6-dichlorophenol-indophenol is more stable in 75% ethanol than in aqueous solution and ascorbic acid reacts considerably faster in this media than glutathione. The activity determination of glutathione: dehydroascorbic acid oxidoreductase was based on these observations by a photometric measurement of the ascorbic acid resulting from the catalysis. Extracts from various types of wheat were tested and relatively high enzyme activities were found.

Ascorbic Acid↗
PubMed1989

Preventive action of vitamin C on nitrosamine formation.

N-Nitroso compounds are known to form endogenously in the human stomach from the precursors nitrite as well as secondary and tertiary amines. Ascorbic acid has been found to be an effective blocking agent for this process of formation of carcinogenic substances, both in vitro and in vivo. The mechanism by which ascorbic acid reacts is chemical in nature and results in the formation of NO and dehydroascorbic acid. Since NO can be recycled in the presence of O2 to form [NO]x, which is capable of additional nitrosation, greater than stoichrometric amounts of ascorbate are required for effective inhibition in vivo. The efficacy of ascorbic acid for inhibition of nitrosamine formation in humans has been demonstrated both clinically and epidemiologically through the use of "Nitrosoproline Test"--of Ohshima and Bartsch.

Ascorbic Acid↗
PubMed1980

The soluble components of chromaffin granules. A carbon-13 NMR survey.

Carbon-13 NMR spectra of the reconcentrated chromaffin granule lysate have been obtained at 50 MHz and 62.9 MHz. The spectrum contains a number of assignable resonances in addition to those of the main soluble components (catecholamines, adenine nucleotides and chromogranin). Guanine and uridine nucleotides are present at levels of 0.13 and 0.08 mol/mol adenine nucleotides, respectively. Concentrations of cytidine nucleotides and NAD+ are below the detection limit (0.02 mol/mol adenine nucleotides). An unidentified low molecular weight species, thought to be an adenine-containing oligonucleotide, is also present. Ascorbic acid was observed at a concentration of 0.14 mol/mol adenine nucleotides, but both dopamine and dehydroascorbic acid were below the detection limit. Protein resonances agree well with the reported amino acid composition of chromogranin A, with the exception of tryptophan and glutamine which have not previously been measured. The concentrations of these residues are estimated to be 12 +/- 3 and 39 +/- 5 residues per 77 000 dalton unit of chromogranin A. Substantial intensity due to unsaturated fatty acid side-chains in solubilized lipid is seen in the olefinic carbon region and in the methylene region, suggesting the presence of lipoprotein. Unassigned carbohydrate resonances are also present, but are largely obscured by sucrose in the isolation medium.

Adenine Nucleotides↗
PubMed2006

Preventive effects of phosphorylated ascorbate on ultraviolet-B induced apoptotic cell death and DNA strand cleavage through enrichment of intracellular vitamin C in skin epidermal keratinocytes.

Mortality of mouse keratinocytes Pam212 that were irradiated with ultraviolet-B (UVB) was shown to be repressed by pre-irradiated administration with L-ascorbic acid (Asc) or more markedly with Asc-2-O-phosphate (Asc2P), but not with dehydroascorbic acid (DehAsc) or Asc-2-O-alpha-glucoside (Asc2G), although not repressed by post-irradiated administration. The cytoprotection by Asc2P was restricted against UVB below 5-20 mJ/cm2, and exhibited markedly by administration for a period over 2 h, which may be caused by intracellular Asc that was accumulated via dephosphorylation of Asc2P and was increased, 6-24 h after, to levels above twice as abundant as those of Asc-administration. Pre-irradiated Asc2P-administration slightly repressed a DNA ladder-like electrophoretic pattern for UVB-irradiated keratinocytes, containing the histone-bound DNA fragments as shown by ELISA assay, and appreciably repressed the DNA-3'OH cleavage terminals as shown by terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) stain. Thus, prevention of UVB-induced cell death by Asc2P was shown to occur concurrently with inhibition of DNA cleavages and enrichment of intracellular Asc.

Animals↗
PubMed1994

Determination of glycation crosslinking by the sugar-dependent incorporation of [14C]lysine into protein.

A simple, quantitative assay has been established to determine the glycation-dependent crosslinking ability of any sugar by measuring the incorporation of [14C]-lysine into protein. The assay was shown to be both sugar-dependent and protein-dependent and was completely inhibited by sodium cyanoborohydride, 2-aminoguanidine, and semicarbazide. A typical 1.0-ml reaction mixture contained 5 mg lysozyme, 20 mumol threose, and 5 microCi of [14C]lysine and exhibited an incorporation of 8 x 10(5) cpm (1.6 nmol of lysine) after 7 days of incubation. A comparison of the crosslinking ability of a variety of sugars showed glyceraldehyde and dihydroxyacetone to be twice as active as erythrose and threose and eight times more reactive than ribose. Little or no crosslinking could be demonstrated with three different hexoses as well as their phosphorylated derivatives. The dicarbonyl sugars 3-deoxyglucosone and xylosone were at least as effective as ribose in crosslinking, as were the oxidation products of ascorbic acid. Several amine-containing compounds were tested as inhibitors of crosslinking; however, 2-aminoguanidine was the most effective. The rate of synthesis of Lys-Lys, Lys-Arg, and Lys-His crosslinks was determined by measuring the incorporation of [14C]lysine into specific amino acid homopolymers. The relative incorporation was polylysine > polyarginine > polyhistidine with threose, but polyarginine > polyhistidine > polylysine with dehydroascorbic acid, suggesting a different crosslinking mechanism for these two compounds.

Amino Acids↗
PubMed2000

Ascorbic acid reduction of residual active chlorine in potable water prior to halocarboxylate determination.

In studies on the formation of disinfection byproducts (DBPs), it is necessary to scavenge residual active (oxidizing) chlorine in order to fix the chlorination byproducts (such as haloethanoates) at a point in time. Such research projects often have distinct needs from requirements for regulatory compliance monitoring. Thus, methods designed for compliance monitoring are not always directly applicable, but must be adapted. This research describes an adaptation of EPA Method 552 in which ascorbic acid treatment is shown to be a satisfactory means for reducing residual oxidizing chlorine, i.e., HOCl, ClO-, and Cl2, prior to determining concentrations of halocarboxylates. Ascorbic acid rapidly reduces oxidizing chlorine compounds, and it has the advantage of producing inorganic halides and dehydroascorbic acid as opposed to halogenated organic molecules as byproducts. In deionized water and a sample of chlorinated tap water, systematic biases relative to strict adherence to Method 552 were precise and could be corrected for using similarly treated standards and analyte-fortified (spiked) samples. This was demonstrated for the quantitation of chloroethanoate, bromoethanoate, 2,2-dichloropropanoate (dalapon), trichloroethanoate, bromochloroethanoate, and bromodichlorocthanoate when extracted, as the acids, into tert-butyl methyl ether (MTBE) and esterified with diazomethane prior to gas chromatography with electron capture detection (GC-ECD). Recoveries for chloroethanoate, bromoethanoate, dalapon, dichloroethanoate, trichloroethanoate, bromochloroethanoate, bromodichloroethanoate, dibromoethanoate, and 2-bromopropanoate at concentrations near the lower limit of detection were acceptable. Ascorbic acid reduction appears to be the best option presently available when there is a need to quench residual oxidants fast in a DBP formation study without generating other halospecies but must be implemented cautiously to ensure no untoward interactions in the matrix.

Ascorbic Acid↗
PubMed2002

Increased oxidative damage in vitamin C deficiency is accompanied by induction of ascorbic acid recycling capacity in young but not mature guinea pigs.

Ascorbic acid (AA) recycling, i.e. the intracellular regeneration of AA from its oxidized forms semidehydroascorbyl radical and dehydroascorbic acid (DHA), presumably has a key function in maintaining redox homeostasis. Like humans, guinea pigs cannot synthesize AA. In the present paper, the effects of severe AA deficiency on the AA recycling capacity in erythrocytes (RBCs) and liver homogenates were studied in young and mature guinea pigs. Twelve animals of each age category were divided into weight-matched groups of six animals and fed either an AA deficient or sufficient diet. After 5 weeks, they were sacrificed and RBC and liver ascorbate recycling was estimated along with glutathione, tocopherols, AA, SOD, and malondialdehyde (MDA). For young animals, AA recycling capacity was significantly increased in RBCs from the deficient group as compared to the controls (p < 0.001). RBC MDA was not increased by incubation with t-butylhydroperoxide (TBH) while the initial MDA level was significantly elevated (p < 0.001). In mature animals, neither RBC recycling nor MDA levels depended on AA status. Liver recycling capacity was not affected by age or diet, while liver MDA was significantly higher in young but not in mature deficient animals compared to respective controls (p < 0.01). In young animals, incubation with TBH resulted in significant MDA formation in the deficient compared to sufficient animals in both liver and RBCs (p < 0.05). RBC glutathione was not significantly changed by age or diet indicating that the observed changes in recycling capacity are enzyme dependent. The results suggest that young guinea pigs may have a more adaptable antioxidant defense system compared to mature animals while also being more susceptible to oxidative stress.

Aging↗
PubMed2001

Blood transfusion increases radical promoting non-transferrin bound iron in preterm infants.

BACKGROUND: Blood transfusion has been recognised as a risk factor for the development of retinopathy of prematurity (ROP) or chronic lung disease (CLD) in preterm infants, but the precise mechanism involved is not understood. AIM: To investigate the level of non-transferrin bound "free" iron, which has the potential to promote the generation of reactive oxygen species, and its redox status in the plasma of preterm infants immediately before and after blood transfusion. METHODS: Twenty one preterm infants with a median gestational age and birth weight of 27 weeks and 1021 g respectively were prospectively enrolled in the study. Sixteen of the 21 infants developed ROP and/or CLD. The infants were transfused with concentrated red blood cells at a median age of 32 days. The plasma concentration of total bleomycin detectable iron (BDI) was measured and also the ferrous iron (Fe(2+)) activity by bleomycin-iron complex dependent degradation of DNA. RESULTS: Even before blood transfusion, BDI was detectable in one third of the blood samples, and all but one sample had ferrous iron activity. After transfusion, both BDI and ferrous iron activity were significantly increased, in contrast with the situation in full term infants. Plasma ascorbic acid (AA) concentration was significantly decreased after blood transfusion, whereas the level of its oxidation product, dehydroascorbic acid (DHAA), and the DHAA/AA ratio were significantly increased compared with before the transfusion. The activity of plasma ferroxidase, which converts iron from the ferrous to the ferric state, was appreciably decreased in preterm infants, as expected from their very low plasma caeruloplasmin concentration. CONCLUSIONS: Plasma non-transferrin bound iron was significantly increased in preterm infants after blood transfusion and existed partly in the ferrous form, because of the low ferroxidase activity and the reduction of ferric iron (Fe(3+)) by ascorbic acid. This finding was specific to preterm infants and was not observed in full term infants after blood transfusion. Non-transferrin bound "free" iron may catalyse the generation of reactive oxygen species, which may be responsible for the clinical association of blood transfusion with ROP and CLD.

Anti-Bacterial Agents↗
PubMed1993

Effects of air pollutants on the growth and antioxidative system of Norway spruce exposed in open-top chambers.

Grafted Norway spruce trees were subjected to exposure beginning in April 1988, to one of four different air treatments in open-top chambers: Charcoal filtered air (CF), non-filtered air (NF), non-filtered air with the addition of O(3) during summer (NFO), and SO(2) plus NO(2) during winter (NFOSN). CF trees were considered as the reference group. No effects on growth parameters were observed. Samples of the two youngest needle year classes were taken late in November 1989 for enzyme determinations. The activity of ascorbic acid peroxidase (A-POD) increased the same level in all treatments, and activities of catalase and dehydroascorbic acid reductase (DHA-R) increased only in NF and NFO treatments. A higher level of activity in the NFOSN treatment was observed only for glucose-6-phosphate-dehydrogenase (Glc-6-P-DH) and non-specific peroxidase (POD). Isoelectric focusing of POD showed a changed pattern in the NFOSN treatment. Neither activity nor isoelectric focusing of superoxidase dismutase (SOD) was changed in any of the treatments.

Journal Article↗
PubMed1991

The behavior of L-ascorbic acid in the healing process of dorsal wounds in guinea pigs.

The behavior of L-ascorbic acid (AsA) in the healing process of wounds in guinea pigs was investigated by determining AsA and dehydroascorbic acid (DAsA) levels. Dorsal skin wounds of guinea pigs fed AsA-deficient diets for 10 days were surgically induced, and the animals were intraperitoneally supplemented with 0, 0.5, 5, 50 mg/day of AsA for 4 days, respectively. The animals were sacrificed, and the amounts of AsA and DAsA in healing skin wound and intact skin were determined by high-performance liquid chromatography (HPLC). It was found that total AsA levels in the healing wound of the animals in AsA-supplemented groups were almost similar to those in intact skin, respectively. However, DAsA levels in the healing wounds on day 4 of the healing period are significantly higher than those not only in the intact skin but also in the completely regenerated skin on day 14 of the healing period. From these results, it was suggested that the wound healing process was accompanied by the oxidation of AsA, moreover, the reduction of DAsA to AsA did not sufficiently occur in vivo.

Animals↗
PubMed1996

An automated, specific, spectrophotometric method for measuring ascorbic acid in plasma (EFTSA).

OBJECTIVE: To evaluate an automated enzyme linked, ferric-tripyridyltriazine spectrophotometric assay (EFTSA) for plasma ascorbic acid. DESIGN AND METHODS: Using aqueous ascorbic acid solutions and plasma containing native and/or added ascorbic acid, the following were assessed: reaction kinetics, dose response relationships, recovery of added ascorbic acid, specificity, precision. RESULTS: Performing the test on a Cobas Fara centrifugal analyser, the test is linear at least to 400 micromol/L; within-run CVs at 20, 50, 140, and 300 micromol/L ascorbic acid, in both pure aqueous solutions and in plasma, were <5.5%; 99-105% of added ascorbic acid (from 30-130 micromol/L) was recovered. The reaction of ascorbic acid is virtually instantaneous; other native antioxidants do not appear to interfere, and there is no interference by dehydroascorbic acid when readings are taken within a 15-60-s reaction time window. CONCLUSION: EFTSA appears suitable for the routine measurement of ascorbic acid in plasma.

Adult↗
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↗