Published in Cancer Detection and Prevention 2001; 25(2):192-201.

The Role of Duck Hepatitis B Virus and Aflatoxin B1, in the Induction of Oxidative Stress in the Liver

Luc Barrauda, Thierry Doukib, Sylviane Guerretc, Michele Chevallierc, Catherine Jamarda, Christian Trepoa, Christopher P Wildd, Jean Cadetb and Lucyna Covaa

aINSERM U271, 151 Cours Albert Thomas, F-69424 Lyon, and bCENDRFMC, 5dB/LAN, 17, rue des Martyrs, F-38054 Grenoble Cedex 9; cInstitut Merieux, Avenue Tony Gamier, F-69365 Lyon, France; and dMolecular Epidemiology Unit, Epidemiology and Health Services Research, Algernon Firth Building, School of Medicine, University of Leeds, LS2 9JT, UK

Address all correspondence and reprint requests to: Lucyna Cova, PhD, INSERM, Unit 271, 151 Cours Albert Thomas, F-69424, Lyon cedex 03, France.

ABSTRACT: The aim of our study was to use the Pekin duck model to investigate the interactions between hepadnaviral infection and aflatoxin B1 (AFB1) exposure including the role of both factors in the induction of oxidative stress in the liver. AFB1 exposure of duck hepatitis B virus (DHBV) infected Pekin ducks induced a significant increase in viral replication associated with an intense biliary ductular cells proliferation. Interestingly, extremely high levels of AFB1-DNA adducts (40-120 pmol AFB1-Fapy/mg DNA) and AFB1-albumin adducts (1,500-3,000 pg AFB1-lys Eq/mg albumin) were detected in duck liver and serum respectively, as compared to other animal species exposed to a similar AFB1 dose. DHBV infection was found to further induce a nonsignificant increase in AFB1-albumin adduct levels in duck serum. During the treatment duration there was no effect on formation of oxidative base damage within DNA and no effect on oxidative lipid peroxidation following either viral infection or AFB1 exposure. In terms of hepatic antioxidant enzymes—catalase, superoxide dismutase (SOD), glutathione peroxidase—AFB1 exposure, but not DHBV infection, resulted in a significant increase in SOD activity but this was observed only after the cessation of treatment, when biliary ductular cells proliferation was reduced.

KEY WORDS: aflatoxin B1, duck hepatitis B virus infection, hepatitis B virus, liver pathology, oxidative stress.