The influence of a prolonged low level of administration to rats and mice of the potent hepatocarcinogen, B1(aflatoxin B1) on liver nuclear acid DNAase was investigated. For comparison, the effects of 3′-methyl-N,N-dimethylaminoazobenzene (3′-MeDAB) (a potent hepatocarcinogen) and 2-methyl-N,N-dimethylaminoazobenzene (2-MeDAB) (a weak hepatocarcinogen) were also studied. Rats were dosed weekly with B1equivalent to frsol|1/5 of the LD50and mice were fed a diet containing 2 mg/kg feed. Both MeDAB carcinogens were fed to rats at the rate of 0.64 g/kg feed. Groups from each treatment were killed at 3 weekly intervals until the appearance of neoplasia and the levels of acid DNAase in hepatic nuclei were assayed. Histological alterations were studied throughout the period of treatment. Both B1and 3′-MeDAB rapidly induced transient increases in the specific activity of acid DNAase in rats. After several months, markedly elevated levels were found, which suddenly declined to normal levels immediately prior to malignant transformation. Histologically, early toxic damage to the liver, seemed to be associated with moderate increases, but the appearance of regenerative nodules was accompanied by marked and sustained increases. In contrast, the weak carcinogen, 2-MeDAB induced only slight changes in the acid DNAase activity of rats. B1induced no changes in the mouse, which is resistant to its carcinogenic effects. © 1973.
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