A comparison of the effects of aflatoxin B 1 on the livers of rats and duck hepatitis B virus–infected and noninfected ducks

A need exists for an appropriate animal model for the involvement of both hepatitis B virus infection and ingestion of aflatoxins in the etiology of liver cancer. Duck hepatitis B virus–infected ducks, on the basis of hepatoma development in the wild in China, appear to offer this possibility. The duck has been reexamined as a model system, and key metabolic processes have been assayed in comparison with the rat model for hepatocarcinogenesis. Aflatoxin B 1 was found to be more actively metabolized by hepatic microsomes isolated from Pekin ducks in vitro to the aflatoxin B 1 ‐8,9‐epoxide than corresponding fractions from the rat, and in vivo , higher levels of aflatoxin B 1 ‐guanine adduct were formed in hepatic DNA than in the livers of the aflatoxin B 1 –sensitive F344 rat. Repair of this DNA lesion in the duck and the subsequent formation of the ring‐opened aflatoxin B 1 ‐FAPy adduct paralleled that in the rat. No effect of duck hepatitis B virus infection was found on any of these biochemical processes. The formation of hepatic lesions was also studied, and lesions were compared with those seen in the aflatoxin B 1 ‐treated rat. Histological analysis of necropsy specimens from ducks, 20 mo after the ducks received doses of aflatoxin B 1 (25 and 50 μg/kg body wt), showed almost complete regression of the early acute lesions, with no evidence of neoplasia. Male F344 rats treated with aflatoxin B 1 150 μg/kg 5 days/wk for 4 wk had extensive bile duct hyperplasia at the end of the treatment period and 100% incidence of hepatocellular carcinoma after 52 wk. The possible basis for the relative sensitivity of ducks and rats to the carcinogenic action of aflatoxin B 1 is discussed. (H EPATOLOGY 1993;18:188–197).