Abstract

Hepatic carcinogenesis was studied first in castrated rats and second in castrated male rats given testosterone ingesting 0·025 per cent N- 2-fluorenyldiacetamide (F-diAA) † † Chemical Abstracts' nomenclature: N, N-diacetyl-2-fluorenamine or N, N-diacetyl-2-aminofluorene. . Rats were 12 or 52 weeks of age. The incidence of carcinomas and the number of rats with large carcinomas, multiple carcinomas, and metastases, as well as the degree and incidence of cirrhosis, was highest in the younger castrated male rats given testosterone. Twelve-week-old castrated male rats developed more hyperplastic nodules, carcinomas and cirrhosis than 52-week-old castrated male rats. Testosterone increased only slightly the incidence of carcinomas, hyperplastic nodules and cirrhosis in 52-week-old castrated male animals. Testosterone is important in F-diAA-hepatic carcinogenesis, particularly in young adult male rats. It is concluded that the restoration of the level of sex hormone in aged rats will not restore the susceptibility to hepatic carcinogenesis comparable to that of younger rats.

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