Dehydroascorbic acid as pre-conditioner: Protection from lipopolysaccharide induced mitochondrial damage

References

• Porter SB. Current status of clinical trials with anti-TNF. Chest 1997;112:339S–341S.
   Google Scholar
• Shapiro N, Howell MD, Michael D, Bates, DW, Angus DC, Ngo L, Talmor D. The association of sepsis syndrome and organ dysfunction with mortality in emergency department patients with suspected infection. Ann Emerg Med 2006;48:583–590.
   PubMedGoogle Scholar
• Svistunenko DA, Davies N, Brealey D, Singer M, Cooper CE. Mitochondrial dysfunction in patients with severe sepsis: an EPR interrogation of individual respiratory chain components. Biochim Biophys Acta Bioenerget 2006;1757:262–272.
   PubMed Web of Science ®Google Scholar
• Levy RJ. Mitochondrial dysfunction, bioenergetic impairment and metabolic down regulation in sepsis. Shock 2007;28:24–28.
   PubMed Web of Science ®Google Scholar
• Galley HF, Howdle PD, Walker BE, Webster NR. The effects of intravenous antioxidants in patients with septic shock. Free Radic Biol Med 1997;23:768–774.
   PubMed Web of Science ®Google Scholar
• de Vega JMA, Diaz J, Serrano E, Carbonell LF. Oxidative stress in critically ill patients with systemic inflammatory response syndrome. Crit Care Med 2002;30:1782–1786.
   Google Scholar
• Cowley HC, Bacon PJ, Goode HF, Webster NR, Jones JG, Menon DK. Plasma antioxidant potential in severe sepsis: a comparison of survivors and nonsurvivors. Crit Care Med 1996;24:1179–1183.
   PubMed Web of Science ®Google Scholar
• Ogilvie AC, Groeneveld ABJ, Straub JP, Thijs LG. Plasma-lipid peroxides and antioxidants in human septic shock. Intensive Care Med 1991;17:40–44.
   Google Scholar
• Galley HF, Davies MJ, Webster NR. Xanthine oxidase activity and free radical generation in patients with sepsis syndrome. Crit Care Med 1996;24:1649–1653.
   PubMed Web of Science ®Google Scholar
• Brealey D, Brand M, Hargreaves I, Heales S, Land J, Smolenski R, Davies NA, Cooper CE, Singer M. Association between mitochondrial dysfunction and severity and outcome of septic shock. Lancet 2002;360:219–223.
   PubMed Web of Science ®Google Scholar
• Yassen K, Galley HF, Lee A, Webster NR. Mitochondrial redox state in the critically ill. Br J Anaesth 1999;83:325–327.
   PubMed Web of Science ®Google Scholar
• Vanhorebeek I, De Vos R, Mesotten D, Wouters PJ, De Wolf-Peeters C, Van den Berghe G. Protection of hepatocyte mitochondrial ultrastructure and function by strict blood glucose control with insulin in critically ill patients. Lancet 2005;365:53–55.
   PubMed Web of Science ®Google Scholar
• Zapelini PH, Rezin GT, Cardoso MR. Antioxidant treatment reverses mitochondrial dysfunction in a sepsis animal model. Mitochondrion 2008;8:211–218.
   PubMed Web of Science ®Google Scholar
• Wilson JX. The physiological role of dehydroascorbic acid. FEBS Lett 2002;527:5–9.
   PubMed Web of Science ®Google Scholar
• Vera JC, Rivas CI, Zhang RH, Golde DW. Colony-stimulating factors signal for increased transport of vitamin C in human host defense cells. Blood 1998;91:2536–2546.
   PubMedGoogle Scholar
• Ng LL, Ngkeekwong FC, Quinn PA, Davies JE. Uptake mechanisms for ascorbate and dehydroascorbate in lymphob-lasts from diabetic nephropathy and hypertensive patients. Diabetologia 1998;41:435–442.
   Google Scholar
• Rumsey SC. Glucose transporter isoforms GLUT1 and GLUT3 transport dehydroascorbic acid. J Biol Chem 1997;272:18982–18991.
   PubMed Web of Science ®Google Scholar
• Puskas F, Gergely P, Banki K, Perl A. Stimulation of the pentose phosphate pathway and glutathione levels by dehydroascorbate, the oxidized form of vitamin C. FASEB J 2000;14:1352–1361.
   PubMed Web of Science ®Google Scholar
• Song JH, Shin, SH, Ross GM. Oxidative stress induced by ascorbate causes neuronal damage in an in vitro system. Brain Res 2001;895:66–72.
   PubMed Web of Science ®Google Scholar
• Brown S, Georgatos M, Reifel C, Song JH, Shin SH, Hong M. Recycling processes of cellular ascorbate generate oxidative stress in pancreatic tissues in in vitro system. Endocrine 2002;18:91–96.
   PubMedGoogle Scholar
• Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia—a delay of lethal cell injury in ischemic myocardium. Circulation 1986;74:1124—1136.
   PubMed Web of Science ®Google Scholar
• Chen Y, Yu AD, Saari JT, Kang YJ. Repression of hypoxia-reoxygenation injury in the catalase-overexpressing heart of transgenic mice. Proc Natl Acad Sci USA 1997;216:112–116.
   Google Scholar
• Pang CY, Neligan P, Xu H, He W, Zhong AG, Hopper R, Forrest CR. Role of ATP-sensitive K+ channels in ischemic preconditioning of skeletal muscle against infarction. Am J Physiol Heart Circ Physiol 1997;273:H44–H51.
   Google Scholar
• Islam CF, Mathie RT, Dinneen MD, Kiely EA, Peters AM, Grace PA. Ischaemia-reperfusion injury in the rat kidney: the effect of preconditioning. Br J Urol 1997;79:842–847.
   PubMedGoogle Scholar
• Tsukaguchi H, Tokui T, Mackenzie B, Berger UV, Chen XZ, Wang YX, Brubaker RF, Hediger MA. A family of mammalian Na+−dependent L-ascorbic acid transporters. Nature 1999; 399:70–75.
   PubMed Web of Science ®Google Scholar
• Fu YC, Maianu L, Melbert BR, Garvey WT. Facilitative glucose transporter gene expression in human lymphocytes, monocytes, and macrophages: a role for GLUT isoforms 1, 3, and 5 in the immune response and foam cell formation. Blood Cells Mol Dis 2004;32:182–190.
   PubMed Web of Science ®Google Scholar
• Levine M, Conry Cantilena C, Wang YH, Welch RW, Washko PW, Dhariwal KR, Park JB, Lazarev A, Graumlich JF, King J, Cantilena LR. Vitamin C pharmacokinetics in healthy volunteers: Evidence for a recommended dietary allowance. Proc Natl Acad Sci USA 1996;93:3704–3709.
   PubMed Web of Science ®Google Scholar
• Vera JC, Rivas CI, Zhang RH, Golde DW. Colony-stimulating factors signal for increased transport of vitamin C in human host defense cells. Blood 1998;91:2536–2546.
   PubMedGoogle Scholar
• Perez-Cruz I, Carcamo JM, Golde DW. Vitamin C inhibits FAS-induced apoptosis in monocytes and U937 cells. Blood 2003;102:336–343.
   PubMed Web of Science ®Google Scholar
• Messer HH, Murray EJ, Goebel NK. Removal of trace-metals from culture media and sera for in vitro deficiency studies. J Nutrit 1982;112:652–657.
   PubMedGoogle Scholar
• Halliwell B. Oxidative stress in cell culture: an under-appreciated problem? FEBS Lett 2003;540:3–6.
   PubMed Web of Science ®Google Scholar
• Prass K, Ruscher K, Karsch M, Isaev N, Megow D, Priller J, Scharff A, Dirnagl U, Meisel A. Desferrioxamine induces delayed tolerance against cerebral ischemia in vivo and in vitro. J Cereb Blood Flow Metab 2002;22:520–525.
   PubMed Web of Science ®Google Scholar
• Song JH, Simons C, Cao L, Shin SH, Hong M, Chung IM. Rapid uptake of oxidized ascorbate induces loss of cellular glutathione and oxidative stress in liver slices. Exp Mol Med 2003;35:67–75.
   PubMed Web of Science ®Google Scholar
• Puskas F, Gergely P, Nil B, Banki K, Perl A. Differential regulation of hydrogen peroxide and Fas-dependent apoptosis pathways by dehydroascorbate, the oxidized form of vitamin C. Antiox Redox Sig 2002;3:357–369.
   Google Scholar
• May JM, Mendiratta S, Qu ZC, Loggins E. Vitamin C recycling and function in Human monocytic U-937 cells. Free Radic Biol Med 1999;26:1513–1523.
   Google Scholar
• Kim EJ, Park YG, Baik EJ, Jung SJ, Won R, Nahm TS, Lee BH. Dehydroascorbic acid prevents oxidative cell death through a glutathione pathway in primary astrocytes. J Neur Res 2005;79:670–679.
   PubMedGoogle Scholar
• Huang J, Agus DB, Winfree CJ, Kiss S, Mack WJ, McTaggart RA, Choudhri TF, Kim LJ, Mocco J, Pinsky DJ, Fox WD, Israel RJ, Boyd TA, Golde DW, Connolly ES. Dehydroascorbic acid, a blood–brain barrier transportable form of vitamin C, mediates potent cerebroprotection in experimental stroke. Proc Natl Acad Sci USA 2001;98:11720–11724.
   PubMed Web of Science ®Google Scholar
• Leon OS, Menendez S, Merino N, Castillo R, Sam S, Perez L, Cruz E, Bocci V. Ozone oxidative preconditioning: a protection against cellular damage by free radicals. Med Inflam 1998;7:289–294.
   PubMed Web of Science ®Google Scholar
• Sharma A, Singh M. Protein kinase C activation and cardio-protective effect of preconditioning with oxidative stress in isolated rat heart. Mol Cell Biochem 2001;219:1–6.
   Google Scholar
• Catani MV, Savini I, Duranti G, Caporossi D, Ceci R, Sabatini S, Avigliano L. Nuclear factor kappa B and activating protein 1 are involved in differentiation-related resistance to oxidative stress in skeletal muscle cells. Free Radic Biol Med 2004;37:1024–1036.
   PubMed Web of Science ®Google Scholar
• Portoles MT, Catala A, Pagini R. Hepatic response to oxidative stress induced by E. coli endotoxin: glutathione as an index of the acute phase during the endotoxic shock. Mol Cell Biochem 1996;159:115–121.
   PubMedGoogle Scholar
• Yasmineh WG, Parkin JL, Caspers JI, Theologides A. Tumor necrosis factor/cachectin decreases catalase activity of rat liver. Cancer Res 1991;51:3990–3995.
   Google Scholar
• Chen ZY, Siu B, Ho YS, Vincent R, Chua CC, Hamdy RC, Chua BHL. Overexpression of MnSOD protects against myocardial ischemia/reperfusion injury in transgenic mice. J Mol Cell Cardiol 1998;30:2281–2289.
   PubMed Web of Science ®Google Scholar
• Lecour S, Owira P, Opie LH. Ceramide-induced preconditioning involves reactive oxygen species. Life Sci 2006;78: 1702–1706.
   Google Scholar
• Guaiquil VH, Vera JC, Golde DW. Mechanism of vitamin C inhibition of cell death induced by oxidative stress in glutathione-depleted HL-60 cells. J Biol Chem 2001;276:40955–40961.
   PubMed Web of Science ®Google Scholar
• Gruss-Fischer T, Fabian I. Protection by ascorbic acid from denaturation and release of cytochrome c, alteration of mitochondrial membrane potential and activation of multiple caspases induced by H2O2, in human leukemia cells. Biochem Pharmacol 2002;63:1325–1335.
   Google Scholar
• Halestrap AP, Kerr PM, Javadov S, Woodfield KY. Elucidating the molecular mechanism of the permeability transition pore and its role in reperfusion injury of the heart. Biochim Biophys Acta Bioenerg 1998;1366:79–94.
   PubMed Web of Science ®Google Scholar
• Castilho RF, Kowaltowski AJ, Meinicke AR, Bechara EJH, Vercesi AE. Permeabilization of the inner mitochondrial-membrane by Ca2+ ions is stimulated by t-butyl hydroperoxide and mediated by reactive oxygen species generated by mitochondria. Free Radic Biol Med 1995;18:479–186.
   PubMed Web of Science ®Google Scholar
• Kowaltowski A, Vercesi AE, Fiskum G. Bcl-2 prevents mitochondrial permeability transition and cytochrome c release via maintenance of reduced pyridine nucleotides. Cell Death Diff 2000;7:903–910.
   PubMedGoogle Scholar
• Li X, Cobb CE, May JM. Mitochondrial recycling of ascorbic acid from dehydroascorbic acid: dependence on the electron transport chain. Arch Biochem Biophys 2002;403:103–110.
   PubMed Web of Science ®Google Scholar
• Bruce-Keller AJ, Begley IG, Fu WM, Butterfield DA, Bredesen DE, Hutchins JB, Hensley K, Mattson MP. Bcl-2 protects isolated plasma and mitochondrial membranes against lipid peroxidation induced by hydrogen peroxide and amyloid beta-peptide. J Neurochem 1998;70:31–39.
   PubMed Web of Science ®Google Scholar
• Hausenloy DJ, Yellon DM. Survival kinases in ischemic preconditioning and postconditioning. Cardiol Res 2006;70:240–253.
   Google Scholar
• Hanley PJ, Daut J. K-ATP channels and preconditioning: a re-examination of the role of mitochondrial K-ATP channels and an overview of alternative mechanisms. J Mol Cell Cardiol 2005;39:17–50.
   PubMed Web of Science ®Google Scholar
• Wang YG, Kudo M, Xu MF, Ayub A, Ashraf M. Mitochondrial K-ATP channel as an end effector of card ioprotection during late preconditioning: triggering role of nitric oxide. J Mol Cell Cardiol 2001;33:2037–2046.
   PubMed Web of Science ®Google Scholar
• Liu Y, Yang XM, Iliodromitis EK, Kremastinos DT, Dost T, Cohen MV, Downey JM. Redox signalling at reperfusion is required for protection from ischemic preconditioning but not from a direct PKC activator. Basic Res Cardiol 2008;103: 54–59.
   PubMed Web of Science ®Google Scholar