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@ARTICLE{Atkinson:19623,
      author       = {Atkinson, J. and Kapralov, A.A. and Yanamala, N. and
                      Tyurina, Y.Y. and Amoscato, A.A. and Pearce, L. and
                      Peterson, J. and Huang, Z. and Jiang, J. and Samhan-Arias,
                      A.K. and Maeda, A. and Feng, W. and Wasserloos, K. and
                      Belikova, N.A. and Tyurin, V.A. and Wang, H. and Fletcher,
                      J. and Wang, Y. and Vlasova, Il. and Klein-Seetharaman, J.
                      and Stoyanovsky, D.A. and Bayir, H. and Pitt, B.R. and
                      Epperly, M.W. and Greenberger, J.S. and Kagan, V.E.},
      title        = {{A} mitochondrial-targeted inhibitor of cytochrorme c
                      peroxidase mitigates radiation-induced death},
      journal      = {Nature Communications},
      volume       = {2},
      issn         = {2041-1723},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {PreJuSER-19623},
      pages        = {497},
      year         = {2011},
      abstract     = {The risk of radionuclide release in terrorist acts or
                      exposure of healthy tissue during radiotherapy demand potent
                      radioprotectants/radiomitigators. Ionizing radiation induces
                      cell death by initiating the selective peroxidation of
                      cardiolipin in mitochondria by the peroxidase activity of
                      its complex with cytochrome c leading to release of
                      haemoprotein into the cytosol and commitment to the
                      apoptotic program. Here we design and synthesize
                      mitochondria-targeted triphenylphosphonium-conjugated
                      imidazole-substituted oleic and stearic acids that blocked
                      peroxidase activity of cytochrome c/cardiolipin complex by
                      specifically binding to its haem-iron. We show that both
                      compounds inhibit pro-apoptotic oxidative events, suppress
                      cyt c release, prevent cell death, and protect mice against
                      lethal doses of irradiation. Significant
                      radioprotective/radiomitigative effects of
                      imidazole-substituted oleic acid are observed after
                      pretreatment of mice from 1 h before through 24 h after
                      the irradiation.},
      keywords     = {Animals / Cell Death: drug effects / Cell Death: radiation
                      effects / Cytochrome-c Peroxidase: antagonists $\&$
                      inhibitors / Electron Spin Resonance Spectroscopy / Enzyme
                      Inhibitors: chemistry / Enzyme Inhibitors: pharmacology /
                      Female / Mice / Mice, Inbred C57BL / Mitochondria: drug
                      effects / Mitochondria: enzymology / Models, Molecular /
                      Molecular Dynamics Simulation / Radiation-Protective Agents:
                      chemistry / Radiation-Protective Agents: pharmacology /
                      Enzyme Inhibitors (NLM Chemicals) / Radiation-Protective
                      Agents (NLM Chemicals) / Cytochrome-c Peroxidase (NLM
                      Chemicals) / J (WoSType)},
      cin          = {ICS-5},
      ddc          = {500},
      cid          = {I:(DE-Juel1)ICS-5-20110106},
      pnm          = {BioSoft: Makromolekulare Systeme und biologische
                      Informationsverarbeitung},
      pid          = {G:(DE-Juel1)FUEK505},
      shelfmark    = {Multidisciplinary Sciences},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:21988913},
      UT           = {WOS:000296787300010},
      doi          = {10.1038/ncomms1499},
      url          = {https://juser.fz-juelich.de/record/19623},
}