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  • Anti-Genotoxic Potential of Bilirubin In Vivo: Damage to DNA in Hyperbilirubinemic Human and Animal Models

    Author(s)
    Wallner, Marlies
    Antl, Nadja
    Rittmannsberger, Barbara
    Schreidl, Stephanie
    Najafi, Khatereh
    Muellner, Elisabeth
    Moelzer, Christine
    Ferk, Franziska
    Knasmueller, Siegfried
    Marculescu, Rodrig
    Doberer, Daniel
    Poulsen, Henrik E
    Vitek, Libor
    Bulmer, Andrew C
    Wagner, Karl-Heinz
    Griffith University Author(s)
    Bulmer, Andrew C.
    Year published
    2013
    Metadata
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    Abstract
    The bile pigment bilirubin is a known antioxidant and is associated with protection from cancer and cardiovascular disease (CVD) when present in too strong concentrations. Unconjugated bilirubin (UCB) might also possess anti-genotoxic potential by preventing oxidative damage to DNA. Moderately elevated bilirubin levels are found in individuals with Gilbert syndrome and more severe in the hyperbilirubinemic Gunn rat model. This study was therefore aimed to assess the levels of oxidative damage to DNA in Gilbert syndrome subjects and Gunn rats compared to matched controls. Seventy-six individuals (age- and sex-matched) were ...
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    The bile pigment bilirubin is a known antioxidant and is associated with protection from cancer and cardiovascular disease (CVD) when present in too strong concentrations. Unconjugated bilirubin (UCB) might also possess anti-genotoxic potential by preventing oxidative damage to DNA. Moderately elevated bilirubin levels are found in individuals with Gilbert syndrome and more severe in the hyperbilirubinemic Gunn rat model. This study was therefore aimed to assess the levels of oxidative damage to DNA in Gilbert syndrome subjects and Gunn rats compared to matched controls. Seventy-six individuals (age- and sex-matched) were allocated into Gilbert syndrome (UCB =17.1 孯l/L; n = 38) or control groups (UCB < 17.1 孯l/L; n = 38). In addition, 40 Gunn rats were used to support the results of the human trial. Single-cell gel electrophoresis (SCGE) assay measuring standard conditions (strand breaks, apurinic/apyrimidinic sites) and formamidopyrimidine glycosylase (FPG)-sensitive sites was conducted in human peripheral blood mononuclear cells (PBMC) and rat PBMCs, colon, and hepatocytes. Furthermore, urinary 8-oxo-2'-deoxyguanosine (8oxodGuo, DNA oxidation) and 8-oxo-guanosine (8oxoGuo, RNA oxidation) were measured in humans. The Gilbert syndrome and Gunn rat groups had significantly higher UCB levels (P < 0.001) than the corresponding controls. No further differences in damage to DNA or RNA were detected between the two groups, except higher strand breaks (PBMCs) in Gunn rats when compared with controls. However, when demographic effects were analyzed, lower 8oxodGuo concentrations were detected in the human group with a BMI =25 kg/m2 (1.70 ᠰ.67 vs. 1.38 ᠰ.43 nmol/mmol creatinine, P < 0.05), although this group showed lower UCB levels than normal weight subjects. This study suggests that the disease preventative effect of UCB is unrelated to DNA oxidation/strand breaks in human and animal models of hyperbilirubinaemia.
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    Journal Title
    Cancer Prevention Research
    Volume
    6
    Issue
    10
    DOI
    https://doi.org/10.1158/1940-6207.CAPR-13-0125
    Subject
    Clinical sciences
    Oncology and carcinogenesis
    Publication URI
    http://hdl.handle.net/10072/58529
    Collection
    • Journal articles

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