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Original

Mitochondria-targeted antioxidants do not prevent tumour necrosis factor-induced necrosis of L929 cells

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Pages 1041-1046 | Received 02 May 2007, Published online: 07 Jul 2009

References

  • Fiers W, Beyaert R, Declercq W, Vandenabeele P. More than one way to die: apoptosis, necrosis and reactive oxygen damage. Oncogene 1999; 18: 7719–7730
  • Chen G, Goeddel DV. TNF-R1 signaling: a beautiful pathway. Science 2002; 296: 1634–1635
  • Chan FK, Shisler J, Bixby JG, Felices M, Zheng L, Appel M, Orenstein J, Moss B, Lenardo MJ. A role for tumor necrosis factor receptor-2 and receptor-interacting protein in programmed necrosis and antiviral responses. J Biol Chem 2003; 278: 51613–51621
  • Lin Y, Choksi S, Shen HM, Yang QF, Hur GM, Kim YS, Tran JH, Nedospasov SA, Liu ZG. Tumor necrosis factor-induced nonapoptotic cell death requires receptor-interacting protein-mediated cellular reactive oxygen species accumulation. J Biol Chem 2004; 279: 10822–10828
  • Holler N, Zaru R, Micheau O, Thome M, Attinger A, Valitutti S, Bodmer JL, Schneider P, Seed B, Tschopp J. Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule. Nat Immunol 2000; 1: 489–495
  • Garg AK, Aggarwal BB. Reactive oxygen intermediates in TNF signaling. Mol Immunol 2002; 39: 509–517
  • Schulze-Osthoff K, Bakker AC, Vanhaesebroeck B, Beyaert R, Jacob WA, Fiers W. Cytotoxic activity of tumor necrosis factor is mediated by early damage of mitochondrial functions. J Biol Chem 1992; 267: 5317–5323
  • Denecker G, Vercammen D, Declercq W, Vandenabeele P. Apoptotic and necrotic cell death induced by death domain receptors. Cell Mol Life Sci 2001; 58: 356–370
  • Hennet T, Richter C, Peterhans E. Tumour necrosis factor-α- induces superoxide anion generation in mitochondria of L929 cells. Biochem J 1993; 289: 587–592
  • Meier B, Radeke HH, Selle S, Younes M, Sies H, Resch K, Habermehl GG. Human fibroblasts release reactive oxygen species in response to interleukin-1 or tumour necrosis factor-α. Biochem J 1989; 263: 539–545
  • O'Donnell VB, Spycher S, Azzi A. Involvement of oxidants and oxidant-generating enzyme(s) in tumour-necrosis-factor-α-mediated apoptosis: role for lipoxygenase pathway but not mitochondrial respiratory chain. Biochem J 1995; 310: 133–141
  • Goossens V, Grooten J, De Vos K, Fiers W. Direct evidence for tumor necrosis factor-induced mitochondrial reactive oxygen intermediates and their involvement in cytotoxicity. Proc Natl Acad Sci USA 1995; 92: 8115–8119
  • Hehner SP, Hofmann TG, Ratter F, Dumont A, Dröge W, Schmitz ML. Tumor necrosis factor-α-induced cell killing and activation of transcription factor NF-κB are uncoupled in L929 cells. J Biol Chem 1998; 273: 18117–18121
  • Schulze-Osthoff K, Beyaert R, Vandevoorde V, Haegeman G, Fiers W. Depletion of the mitochondrial electron transport abrogates the cytotoxic and gene-inductive effects of TNF. EMBO J 1883; 12: 3095–3104
  • Gardner PR, White CW. Failure of tumor necrosis factor and interleukin-1 to elicit superoxide production in the mitochondrial matrices of mammalian cells. Arch Biochem Biophys 1996; 334: 158–162
  • Halliwell B, Whiteman M. Measuring reactive species and oxidative damage in vivo and in cell culture: how should you do it and what do the results mean?. Br J Pharmacol 2004; 142: 231–255
  • Mikkelsen RB, Wardman P. Biological chemistry of reactive oxygen and nitrogen and radiation-induced signal transduction mechanisms. Oncogene 2003; 22: 5734–5754
  • Burkitt MJ, Wardman P. Cytochrome C is a potent catalyst of dichlorofluorescin oxidation: implications for the role of reactive oxygen species in apoptosis. Biochem Biophys Res Commun 2001; 282: 329–333
  • James AM, Sharpley MS, Manas AR, Frerman FE, Hirst J, Smith RAJ, Murphy MP. Interaction of the mitochondria-targeted antioxidant MitoQ with phospholipid bilayers and ubiquinone oxidoreductases. J Biol Chem 2007; 282: 14708–14718
  • Asin-Cayuela J, Manas AR, James AM, Smith RA, Murphy MP. Fine-tuning the hydrophobicity of a mitochondria-targeted antioxidant. FEBS Lett 2004; 571: 9–16
  • Murphy MP, Echtay KS, Blaikie FH, Asin-Cayuela J, Cochemé HM, Green K, Buckingham J, Taylor ER, Hurrell F, Hughes G, Miwa S, Cooper CE, Svistunenko DA, Smith RAJ, Brand MD. Superoxide activates uncoupling proteins by generating carbon-centered radicals and initiating lipid peroxidation. J Biol Chem 2003; 278: 48534–48545
  • Pastorino JG, Simbula G, Yamamoto K, Glascott PA, Jr, Rothman RJ, Farber JL. The cytotoxicity of tumor necrosis factor depends on induction of the mitochondrial permeability transition. J Biol Chem 1996; 271: 29792–29798
  • Humphreys DT, Wilson MR. Modes of L929 cell death induced by TNF-α and other cytotoxic agents. Cytokine 1999; 11: 773–782
  • Fusi F, Sgaragli G, Murphy MP. Interaction of butylated hydroxyanisole with mitochondrial oxidative phosphorylation. Biochem Pharmacol 1992; 43: 1203–1208
  • Cauwels A, Janssen B, Waeytens A, Cuvelier C, Brouckaert P. Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2. Nat Immunol 2003; 4: 387–393
  • Li M, Beg AA. Induction of necrotic-like death by tumor necrosis factor alpha and caspase inhibitors: novel mechanism for killing virus-infected cells. J Virol 2000; 74: 7470–7477
  • Murphy MP, Smith RAJ. Targeting antioxidants to mitochondria by conjugation to lipophilic cations. Annu Rev Pharmacol Toxicol 2007; 47: 15.11–15.28
  • Goossens V, De Vos K, Vercammen D, Steemans M, Vancompernolle K, Fiers W, Vandenabeele P, Grooten J. Redox regulation of TNF signaling. BioFactors 1999; 10: 145–156
  • Festjens N, Kalai M, Smet J, Meeus A, Van Coster R, Saelens X, Vandenabeele P. Butylated hydroxyanisole is more than a reactive oxygen species scavenger. Cell Death Differ 2006; 13: 166–169
  • Goossens V, Grooten J, Fiers W. The oxidative metabolism of glutamine. J Biol Chem 1996; 271: 192–196

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