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Chemical Compound Review

DEHYDROASCORBIC ACID     5-(1,2- dihydroxyethyl)oxolane-2,3,4- trione

Synonyms: AGN-PC-00PO2V, CHEMBL174035, SureCN257592, AG-K-73613, CHEBI:17242, ...
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Disease relevance of DEHYDROASCORBIC ACID


Psychiatry related information on DEHYDROASCORBIC ACID


High impact information on DEHYDROASCORBIC ACID


Chemical compound and disease context of DEHYDROASCORBIC ACID

  • The 125-residue Grx domain and the two full-length variants were expressed in E. coli and exhibited GSH-dependent hydroxyethyl disulfide and dehydroascorbate reducing activities [10].
  • When NO-catalyzed degradation of HS was depressed in mouse neuroblastoma cell line (N2a) by using 3-beta[2(diethylamino) ethoxy]androst-5-en-17-one (U18666A), both ascorbate and dehydroascorbic acid restored formation of anMan-positive products that colocalized with Rab7 [11].
  • The contents of catalytic Fe, which is critical for H2O2-dependent hydroxyl radical (OH) production, and the oxidized forms of ascorbate and glutathione pools, dehydroascorbate (DHA) and oxidized glutathione (GSSG), markedly increased, a significant oxidative damage to lipids and proteins took place under the moderate water stress [12].
  • Pretreatment with ABA caused an obvious reduction in the content of catalytic Fe and significant increases in the activities of antioxidant enzymes and the contents of non-enzymatic antioxidants, and then significantly reduced the contents of DHA and GSSG and the degrees of oxidative damage in leaves exposed to the moderate water stress [12].
  • Pretreatment with an ABA biosynthesis inhibitor, tungstate, significantly suppressed the accumulation of ABA induced by water stress, reduced the enhancement in the capacity of antioxidant defense systems, and resulted in an increase in catalytic Fe, DHA and GSSG, and oxidative damage in the water-stressed leaves [12].

Biological context of DEHYDROASCORBIC ACID


Anatomical context of DEHYDROASCORBIC ACID


Associations of DEHYDROASCORBIC ACID with other chemical compounds




Analytical, diagnostic and therapeutic context of DEHYDROASCORBIC ACID


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  2. Human HL-60 myeloid leukemia cells transport dehydroascorbic acid via the glucose transporters and accumulate reduced ascorbic acid. Vera, J.C., Rivas, C.I., Zhang, R.H., Farber, C.M., Golde, D.W. Blood (1994) [Pubmed]
  3. Relationship of dehydroascorbic acid transport to cell lineage in lymphocytes from normal subjects and patients with chronic lymphocytic leukemia. Stahl, R.L., Farber, C.M., Liebes, L.F., Silber, R. Cancer Res. (1985) [Pubmed]
  4. Increased facilitated transport of dehydroascorbic acid without changes in sodium-dependent ascorbate transport in human melanoma cells. Spielholz, C., Golde, D.W., Houghton, A.N., Nualart, F., Vera, J.C. Cancer Res. (1997) [Pubmed]
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  6. Mammalian facilitative hexose transporters mediate the transport of dehydroascorbic acid. Vera, J.C., Rivas, C.I., Fischbarg, J., Golde, D.W. Nature (1993) [Pubmed]
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  10. Cloning and expression of a novel human glutaredoxin (Grx2) with mitochondrial and nuclear isoforms. Lundberg, M., Johansson, C., Chandra, J., Enoksson, M., Jacobsson, G., Ljung, J., Johansson, M., Holmgren, A. J. Biol. Chem. (2001) [Pubmed]
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  23. Stimulation of the pentose phosphate pathway and glutathione levels by dehydroascorbate, the oxidized form of vitamin C. Puskas, F., Gergely, P., Banki, K., Perl, A. FASEB J. (2000) [Pubmed]
  24. Inhibition of human leukocyte 3-hydroxy-3-methylglutaryl coenzyme A reductase activity by ascorbic acid. An effect mediated by the free radical monodehydroascorbate. Harwood, H.J., Greene, Y.J., Stacpoole, P.W. J. Biol. Chem. (1986) [Pubmed]
  25. Protein-disulfide isomerase- and protein thiol-dependent dehydroascorbate reduction and ascorbate accumulation in the lumen of the endoplasmic reticulum. Nardai, G., Braun, L., Csala, M., Mile, V., Csermely, P., Benedetti, A., Mandl, J., Banhegyi, G. J. Biol. Chem. (2001) [Pubmed]
  26. Vitamin C transiently arrests cancer cell cycle progression in S phase and G2/M boundary by modulating the kinetics of activation and the subcellular localization of Cdc25C phosphatase. Thomas, C.G., Vezyraki, P.E., Kalfakakou, V.P., Evangelou, A.M. J. Cell. Physiol. (2005) [Pubmed]
  27. The p38 pathway partially mediates caspase-3 activation induced by reactive oxygen species in Fanconi anemia C cells. Pearl-Yafe, M., Halperin, D., Scheuerman, O., Fabian, I. Biochem. Pharmacol. (2004) [Pubmed]
  28. Ebselen is a dehydroascorbate reductase mimic, facilitating the recycling of ascorbate via mammalian thioredoxin systems. Zhao, R., Holmgren, A. Antioxid. Redox Signal. (2004) [Pubmed]
  29. Characterization of the monomethylarsonate reductase and dehydroascorbate reductase activities of Omega class glutathione transferase variants: implications for arsenic metabolism and the age-at-onset of Alzheimer's and Parkinson's diseases. Schmuck, E.M., Board, P.G., Whitbread, A.K., Tetlow, N., Cavanaugh, J.A., Blackburn, A.C., Masoumi, A. Pharmacogenet. Genomics (2005) [Pubmed]
  30. Identification and characteristics of the structural gene for the Drosophila eye colour mutant sepia, encoding PDA synthase, a member of the Omega class glutathione S-transferases. Kim, J., Suh, H., Kim, S., Kim, K., Ahn, C., Yim, J. Biochem. J. (2006) [Pubmed]
  31. Dehydroascorbate and ascorbate transport in rat liver microsomal vesicles. Bánhegyi, G., Marcolongo, P., Puskás, F., Fulceri, R., Mandl, J., Benedetti, A. J. Biol. Chem. (1998) [Pubmed]
  32. Ascorbic acid and dehydroascorbic acid measurements in human plasma and serum. Dhariwal, K.R., Hartzell, W.O., Levine, M. Am. J. Clin. Nutr. (1991) [Pubmed]
  33. Ascorbic acid assays of individual neurons and neuronal tissues using capillary electrophoresis with laser-induced fluorescence detection. Kim, W.S., Dahlgren, R.L., Moroz, L.L., Sweedler, J.V. Anal. Chem. (2002) [Pubmed]
  34. Purification, cloning and expression of dehydroascorbic acid-reducing activity from human neutrophils: identification as glutaredoxin. Park, J.B., Levine, M. Biochem. J. (1996) [Pubmed]
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