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@ARTICLE{Schmitz:256597,
      author       = {Schmitz, Sabine and Oskamp, Dominik and Pomplun, Ekkehard
                      and Kriehuber, Ralf},
      title        = {{C}hromosome aberrations induced by the {A}uger electron
                      emitter 125{I}},
      journal      = {Mutation research / Genetic toxicology and environmental
                      mutagenesis},
      volume       = {793},
      issn         = {1383-5718},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {FZJ-2015-06470},
      pages        = {64 - 70},
      year         = {2015},
      abstract     = {DNA-associated Auger electron emitters (AEE) cause cellular
                      damage leading to high-LET type cell survivalcurves
                      indicating an enhanced relative biological effectiveness.
                      Double strand breaks (DSBs) induced
                      byIodine-125-deoxyuridine (125I-UdR) decays are claimed to
                      be very complex. To elucidate the assumedgenotoxic potential
                      of125I-UdR, chromatid aberrations were analysed in exposed
                      human peripheral bloodlymphocytes (PBL).PBL were stimulated
                      with medium containing phytohaemagglutinin (PHA). After 24
                      h, cultures werelabelled with125I-UdR for 18 h (activity
                      concentration 1–45 kBq) during the S-phase. Following
                      stan-dard cytogenetic procedure, at least 100 metaphases
                      were analysed microscopically for each
                      activityconcentration. Cell death was measured by apoptosis
                      assay using flow cytometry. Radiation doses weredetermined
                      by using point kernel calculations.After 18 h labelling
                      with125I-UdR the cell cycle distribution is severely
                      disturbed. About $40\%$ of PBL arefully labelled and $20\%$
                      show a moderate labelling of125I-UdR, whereas $40\%$ of
                      cells remain un-labelled. Thedose-response relationship fits
                      to a polynomial curve in the low dose range, whereas a
                      linear fit suppliesa better estimation in the high dose
                      range. Even the lowest dose of 0.2 Gy leads to a 13-fold
                      increaseof aberrations compared to the controls. On average
                      every fifth125I-decay produces a single chromatidaberration
                      in PBL. Additionally, a dose-dependent increase of cell
                      death is observed.125I-UdR has a very strong genotoxic
                      capacity in human PBL, even at 0.2 Gy. Efficiently labelled
                      cellsdisplaying a prolonged cell cycle compared to
                      moderately labelled cells and cell death contribute
                      substan-tially to the desynchronisation of the cell cycle.
                      Our data, showing for the first time, that
                      one125I-decayinduces ∼ 0.2 chromatid aberrations, are in
                      very good accordance to DSB data, stating that ∼0.26 DSB
                      areinduced per decay, indicating that approximately every
                      DSB is converted into a chromatid aberration.},
      cin          = {S-US},
      ddc          = {570},
      cid          = {I:(DE-Juel1)S-US-20090406},
      pnm          = {899 - ohne Topic (POF3-899)},
      pid          = {G:(DE-HGF)POF3-899},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000364898400010},
      doi          = {10.1016/j.mrgentox.2015.08.007},
      url          = {https://juser.fz-juelich.de/record/256597},
}