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@ARTICLE{Brta:119616,
      author       = {F. Bárta and K. Levová and E. Frei$^*$ and H.
                      Schmeiser$^*$ and V. M. Arlt and M. Stiborová},
      title        = {{T}he effect of aristolochic acid {I} on expression of
                      {NAD}({P}){H}:quinone oxidoreductase in mice and rats--a
                      comparative study.},
      journal      = {Mutation research / Genetic toxicology and environmental
                      mutagenesis},
      volume       = {768},
      issn         = {1383-5718},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {DKFZ-2017-00247},
      pages        = {1 - 7},
      year         = {2014},
      abstract     = {Aristolochic acid is the cause of aristolochic acid
                      nephropathy (AAN) and Balkan endemic nephropathy (BEN) and
                      their associated urothelial malignancies. Using Western
                      blotting, we investigated the expression ofquinone
                      oxidoreductase (NQO1), the most efficient cytosolic enzyme
                      that reductively activates aristolochic acid I (AAI) in mice
                      and rats. In addition, the effect of AAI on the expression
                      of the NQO1 protein and its enzymatic activity in these
                      experimental animal models was examined. We found that NQO1
                      protein levels in cytosolic fractions isolated from liver,
                      kidney and lung of mice differed from those expressed in
                      these organs of rats. In mice, the highest levels of NQO1
                      protein and NQO1 activity were found in the kidney, followed
                      by lung and liver. In contrast, the NQO1 protein levels and
                      enzyme activity were lowest in rat-kidney cytosol, whereas
                      the highest amounts of NQO1 protein and activity were found
                      in lung cytosols, followed by those of liver. NQO1 protein
                      and enzyme activity were induced in liver and kidney of
                      AAI-pretreated mice compared with those of untreated mice.
                      NQO1 protein and enzyme activity were also induced in rat
                      kidney by AAI. Furthermore, the increase in hepatic and
                      renal NQO1 enzyme activity was associated with AAI
                      bio-activation and elevated AAI-DNA adduct levels were found
                      in ex vivo incubations of cytosolic fractions with DNA and
                      AAI. In conclusion, our results indicate that AAI can
                      increase its own metabolic activation by inducing NQO1,
                      thereby enhancing its own genotoxic potential.},
      keywords     = {Aristolochic Acids (NLM Chemicals) / Carcinogens (NLM
                      Chemicals) / aristolochic acid I (NLM Chemicals) / NAD(P)H
                      Dehydrogenase (Quinone) (NLM Chemicals) / NQO1 protein, rat
                      (NLM Chemicals) / Nqo1 protein, mouse (NLM Chemicals)},
      cin          = {C016 / E030},
      ddc          = {570},
      cid          = {I:(DE-He78)C016-20160331 / I:(DE-He78)E030-20160331},
      pnm          = {315 - Imaging and radiooncology (POF3-315)},
      pid          = {G:(DE-HGF)POF3-315},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24769487},
      doi          = {10.1016/j.mrgentox.2014.01.012},
      url          = {https://inrepo02.dkfz.de/record/119616},
}