Effects of Ethanol on Experimental Hepatocarcinogenesis

Abstract

Although primary hepatoma is not very frequent in alcoholics, the incidence of hepatoma in cases of hepatitis B infection combined with heavy alcohol drinking is high. In the present study, the effects of chronic alcohol administration onthe development of chemicalinduced hepatic cancer in rats were analyzed. In 70% hepatectomized Wistar strain male rats, asingle dose (1 mg per 100 gm body weight) of diethylnitrosamine was injected intraperitoneally. Eight weeks after the injection, 20% alcohol–10% sucrose solution (diethylnitrosamine–alcohol group), 0.1% sodium phenobarbital solution (diethylnitrosamine–phenobarbital group), 10% sucrose solution (diethylnitrosamine–sucrose group) or tap water (diethylnitrosamine–alone group) was given as drinking water for 32 weeks. The numbers of visible nodules per liver were significantly greater in the diethylnitrosamine–alcohol and diethylnitrosamine–phenobarbital groups compared to the diethylnitrosaminealone and diethylnitrosamine–sucrose groups. The numbers of enzyme–altered foci which were positive to γ–glutamyl transpeptidase staining per square centimeter of liver section were also greater in the diethylnitrosamine–alcohol and diethylnitrosamine–phenobarbital groups than in the diethylnitrosamine–alone and diethylnitrosamine–sucrose groups, although the numbers of nodules and enzyme–altered foci were significantly larger in the diethylnitrosamine–phenobarbital group than in the diethylnitrosamine–alcohol group. The enzyme–altered foci areas calculated by γ–glutamyl transpeptidase staining were significantly larger in the diethylnitrosamine–alcohol and diethylnitrosamine–phenobarbital groups than in the diethylnitrosamine–alone and diethylnitrosamine–sucrose groups. Histologically, visible nodules observed in diethylnitrosamine–phenobarbital and diethylnitrosamine–alcohol groups showed characteristic features of neoplastic nodules. These results indicate that alcohol has a promoter action on the development of chemically induced hepatic cancer like phenobarbital.