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Cytochrome P450 and oxidative DNA damage during liver tumorigenesis by Helicobacter hepaticus

  1. Author:
    Sipowicz, M. A.
    Chomarat, P.
    Diwan, B. A.
    Awasthi, Y. C.
    Ward, J. M.
    Anver, M. A.
    Wild, C. P.
    Rice, J. M.
    Kasprzak, K. S.
    Anderson, L. M.
    1. Year of Conference: 1997
  2. Conference Name: Annual Meeting of the American Association for Cancer Research
    1. 38
    2. Pages: A528
  4. Type of Work: Meeting Abstract
  1. Abstract:

    A recently-discovered bacterium, Helicobacter hepaticus, infects the intrahepatic bile canaliculi of mice, causing a severe chronic hepatitis culminating in liver cancer. It thus affords an animal model for study of bacteria-associated tumorigenesis, including H pylori-related gastric cancer. Reactive oxygen species are often postulated to contribute to this process. We now report that livers of male mice infected with H hepaticus show significant increases in the oxidatively-damaged DNA deoxynucleoside, 8-oxo-2'-deoxyguanosine (8-oxo-dG). Perfusion of infected livers with nitro blue tetrazolium (NBT) revealed that superoxide was produced in the cytoplasm of hepatocytes, especially near portal triads. A potential source of superoxide was up-regulated cytochrome P450 (CYP) isoforms 1A2 and 2A5, both showing pronounced increase concomitant with severe hepatitis. The CYP2A5 immunohistochemical staining co-localized with formazan deposits resulting from NBT reduction. These findings suggest that CYP2A5 contributes to the superoxide generation and 8-oxo-dG formation. Three glutathione S-transferase isoforms, pi, YaYa, and mGSTA4.4, also showed striking increases, evidencing major oxidative stress in these livers.

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