The role of duck hepatitis B virus and aflatoxin B-1 in the induction of oxidative stress in the liver

The aim of our study was to use the Pekin duck model to investigate the int eractions between hepadnaviral infection and aflatoxin B-1 (AFB(1)) exposur e including the role of both factors in the induction of oxidative stress i n the liver. AFB(1) exposure of duck hepatitis B virus (DHBV) infected Peki n ducks induced a significant increase in viral replication associated with an intense biliary ductular cells proliferation. Interestingly, extremely high levels of AFB(1)-DNA adducts (40-120 pmol AFB(1)-Fapy/mg DNA) and AFB( 1)-albumin adducts (1,500-3,000 pg AFB(1)-lys Eq/mg albumin) were detected in duck liver and serum respectively, as compared to other animal species e xposed to a similar AFB(1) dose. DHBV infection was found to induce a non-s ignificant increase in AFB(1)-albumin adduct levels in duck serum. During t he treatment duration there was no effect on formation of oxidative base da mage within DNA and no effect on oxidative lipid peroxidation following eit her viral infection or AFB(1) exposure. In terms of hepatic antioxidant enz ymes (catalase, superoxide dismutase (SOD), glutathione peroxidase) a signi ficant increase in SOD activity occurred following AFB(1) exposure, but not DHBV infection. but this was observed only after the cessation of treatmen t, when biliary ductular cells proliferation was reduced.