A Reduction in Mixed Function Oxidases and in Tumor Promoting Effects of Ethanol in a NDEA-Initiated Hepatocarcinogenesis Model

Abstract

Epidemiologic studies associate an increased cancer risk with chronic alcohol consumption [for example, Hakulinen et al., 1974; Breslow and Enstrom, 1974; Feldman et al., 1985; Williams and Horn, 1977; Schottenfeld, 1979; Kono and Ikeda, 1979; Tnyns, 1979; Doll and Peta, 1981]. However, the experimental evidence for this association is not clear. While a number of studies indicate that ethanol, the active ingredient of alcoholic beverages, increases the incidence of chemically induced tumors [for example, Gibel, 1967; Griciute et al., 1982; Gabriel et al., 1982; McCoy et al., 1986], other studies do not show such an effect [Schmahl et al., 1965; Sehmahl, 1976; Habs and Sehmahl, 1981; Teschke et al., 1983]. We recently reported studies that showed that ethanol increased tumor incidence only when administered as a tumor promoter after treatment with an esophagus specific carcinogen, N-nitrosomethylbenzlamine (NMB_zA) was completed [Mufti et al., 1989]. In these studies we wanted to determine the effect of ethanol when given as a tumor promoter on liver carcinogenesis induced by N-nitrosodiethylamine (NDEA). The paper offers an explanation for the negative results obtained in these studies.