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@ARTICLE{Vallucci:266788,
      author       = {Vallucci, Maeva and Boutin, Jean A and Janda, Elzbieta and
                      Blandel, Florence and Musgrove, Ruth and Di Monte, Donato
                      and Ferry, Gilles and Michel, Patrick P and Hirsch, Etienne
                      C},
      title        = {{T}he specific {NQO}2 inhibitor, {S}29434, only marginally
                      improves the survival of dopamine neurons in
                      {MPTP}-intoxicated mice.},
      journal      = {Journal of neural transmission},
      volume       = {131},
      number       = {1},
      issn         = {0375-9245},
      address      = {Wien [u.a.]},
      publisher    = {Springer},
      reportid     = {DZNE-2024-00046},
      pages        = {1 - 11},
      year         = {2024},
      abstract     = {Over the years, evidence has accumulated on a possible
                      contributive role of the cytosolic quinone reductase NQO2 in
                      models of dopamine neuron degeneration induced by
                      parkinsonian toxin, but most of the data have been obtained
                      in vitro. For this reason, we asked the question whether
                      NQO2 is involved in the in vivo toxicity of MPTP, a
                      neurotoxin classically used to model Parkinson
                      disease-induced neurodegeneration. First, we show that NQO2
                      is expressed in mouse substantia nigra dopaminergic cell
                      bodies and in human dopaminergic SH-SY5Y cells as well. A
                      highly specific NQO2 inhibitor, S29434, was able to reduce
                      MPTP-induced cell death in a co-culture system of SH-SY5Y
                      cells with astrocytoma U373 cells but was inactive in
                      SH-SY5Y monocultures. We found that S29434 only marginally
                      prevents substantia nigra tyrosine hydroxylase+ cell loss
                      after MPTP intoxication in vivo. The compound produced a
                      slight increase of dopaminergic cell survival at day 7 and
                      21 following MPTP treatment, especially with 1.5 and 3 mg/kg
                      dosage regimen. The rescue effect did not reach statistical
                      significance (except for one experiment at day 7) and tended
                      to decrease with the 4.5 mg/kg dose, at the latest time
                      point. Despite the lack of robust protective activity of the
                      inhibitor of NQO2 in the mouse MPTP model, we cannot rule
                      out a possible role of the enzyme in parkinsonian
                      degeneration, particularly because it is substantially
                      expressed in dopaminergic neurons.},
      keywords     = {Mice / Humans / Animals / Dopaminergic Neurons: metabolism
                      / MPTP Poisoning / Neuroblastoma / Substantia Nigra:
                      metabolism / Dopamine: metabolism / Mice, Inbred C57BL /
                      Disease Models, Animal / MPTP (Other) / NQO2 (Other) /
                      Neuroprotection (Other) / Parkinson disease (Other) / S29434
                      (Other) / NRH - quinone oxidoreductase2 (NLM Chemicals) /
                      N-(2-(2-methoxy-6H-dipyrido(2,3-a-3,2-e)pyrrolizin-11-yl)ethyl)-2-furamide
                      (NLM Chemicals) / Dopamine (NLM Chemicals)},
      cin          = {AG Di Monte},
      ddc          = {610},
      cid          = {I:(DE-2719)1013008},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37851107},
      doi          = {10.1007/s00702-023-02709-3},
      url          = {https://pub.dzne.de/record/266788},
}