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Phenobarbital given together with the hepatocarcinogen, 4-(dimethylamino) azobenzene or with N-2-fluorenylacetamide (AAF), decreased the carcinogenic effect of the chemicals.1,4) On the other hand, phenobarbital given after the carcinogen treatment enhanced the hepatocarcinogenesis with AAF or with diethylnitrosamine (DEN).4,6,7) Phenobarbital also enhanced spontaneous hepatic tumorigenesis in mice.5) We now examined the enhancing effect of phenobarbital in azo-dye carcinogenesis, because there is some uniqueness in morphological and/or biochemical aspects in the liver during carcinogenesis and in the carcinomas induced by azo dyes compared with those by AAF or DEN.3) The effect of phenobarbital was studied by checking the number and size of resulting carcinomas and also ATPase-deficient islands during carcinogenesis. The latter study seemed important since evidence so far suggests that phenobarbital most likely enhances the expression of preneoplastic lesions.6) ATPasedeficient islands (or hyperplastic areas and nodules) have been considered the most possible preneoplastic change.2) Male Donryu rats at 21 days of age were fed a diet containing 0.06% 3'-methyl-4-(dimethylamino) azobenzene (3'-Me-DAB) for 3 weeks. After 2 weeks on basal diet, the rats were divided into 2 groups. The rats in group 1 were fed a diet containing 0.05% phenobarbital throughout the experimental course. The rats in group 2 were kept on the basal

Enhancement of azo-dye hepatocarcinogenesis with dietary phenobarbital in rats.