Effects of ethanol on experimental hepatocarcinogenesis

Hepatology. 1986 Jan-Feb;6(1):65-72. doi: 10.1002/hep.1840060113.

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 on the development of chemical-induced hepatic cancer in rats were analyzed. In 70% hepatectomized Wistar strain male rats, a single 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 diethylnitrosamine-alone and diethylnitrosamine-sucrose groups. The numbers of enzyme-altered foci which were positive to gamma-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 gamma-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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carcinogens
  • Cocarcinogenesis*
  • Diethylnitrosamine
  • Ethanol / toxicity*
  • Liver Neoplasms, Experimental / chemically induced*
  • Liver Neoplasms, Experimental / enzymology
  • Male
  • Phenobarbital / toxicity
  • Rats
  • Rats, Inbred Strains
  • gamma-Glutamyltransferase / metabolism

Substances

  • Carcinogens
  • Diethylnitrosamine
  • Ethanol
  • gamma-Glutamyltransferase
  • Phenobarbital