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    The environmental pollutant and carcinogen 3-nitrobenzanthrone induces cytochrome P450 1A1 and NAD(P)H:quinone oxidoreductase in rat lung and kidney, thereby enhancing its own genotoxicity.

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    Authors
    Stiborova, Marie
    Dracinska, Helena
    Mizerovska, Jana
    Frei, Eva
    Schmeiser, Heinz H.
    Hudecek, Jiri
    Hodek, Petr
    Phillips, David H.
    Arlt, Volker M.
    Issue Date
    2008-05-02
    
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    Abstract
    3-Nitrobenzanthrone (3-NBA) is a carcinogen occurring in diesel exhaust and air pollution. Using the (32)P-postlabelling method, we found that 3-NBA and its human metabolite, 3-aminobenzanthrone (3-ABA), are activated to species forming DNA adducts by cytosols and/or microsomes isolated from rat lung, the target organ for 3-NBA carcinogenicity, and kidney. Each compound generated identical five DNA adducts. We have demonstrated the importance of pulmonary and renal NAD(P)H:quinone oxidoreductase (NQO1) to reduce 3-NBA to species that are further activated by N,O-acetyltransferases and sulfotransferases. Cytochrome P450 (CYP) 1A1 is the essential enzyme for oxidative activation of 3-ABA in microsomes of both organs, while cyclooxygenase plays a minor role. 3-NBA was also investigated for its ability to induce NQO1 and CYP1A1 in lungs and kidneys, and for the influence of such induction on DNA adduct formation by 3-NBA and 3-ABA. When cytosols from rats treated i.p. with 40mg/kg bw of 3-NBA were incubated with 3-NBA, DNA adduct formation was up to 2.1-fold higher than in incubations with cytosols from control animals. This increase corresponded to an increase in protein level and enzymatic activity of NQO1. Incubations of 3-ABA with microsomes of 3-NBA-treated rats led to up to a fivefold increase in DNA adduct formation relative to controls. The stimulation of DNA adduct formation correlated with the potential of 3-NBA to induce protein expression and activity of CYP1A1. These results demonstrate that 3-NBA is capable to induce NQO1 and CYP1A1 in lungs and kidney of rats thereby enhancing its own genotoxic and carcinogenic potential.
    Citation
    Toxicology 2008, 247 (1):11-22
    Journal
    Toxicology
    URI
    http://hdl.handle.net/10146/38100
    DOI
    10.1016/j.tox.2008.01.018
    PubMed ID
    18329153
    Additional Links
    http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TCN-4RSBYD9-1&_user=1843694&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000055040&_version=1&_urlVersion=0&_userid=1843694&md5=7c1b12339732dfcf1de6505de2d42026
    Type
    Article
    Language
    en
    ISSN
    0300-483X
    Sponsors
    This work was supported in part by Grant Agency of the Czech Republic, grant 303/05/2195, Ministry of Education of the Czech Republic, grant MSM0021620808 and by Cancer Research UK. V.M. Arlt and D.H. Phillips are partners of ECNIS (Environmental Cancer Risk, Nutrition and Individual Susceptibility), a network of excellence operating within the European Union 6th Framework Program, Priority 5: “Food Quality and Safety” (Contract No. 513943).
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.tox.2008.01.018
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