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Retention of Metabolic Regulation in the Hyperplastic Hepatic Nodule Induced by N-2-Fluorenylacetamide¹

Department of Pathology, New York University Medical Center, New York, New York 10016

Studies of the Morris hepatomas have revealed that none of these tumors possesses a normal complement of enzyme-regulatory mechanisms. The current experiments sought to determine whether abnormalities of enzyme regulation characteristic of malignant tumors were already present in a preneoplastic population prior to recognizable malignant transformation.

The experiments were performed during a 12-week period of N-2-fluorenylacetamide (2-FAA) feeding to male rats. This induced hyperplastic hepatic nodules, which nodules precede the appearance of hepatocellular carcinomas by several months, and evidence has been presented that the malignant cells derive from the cells of the nodules.

The enzyme-regulatory mechanisms studied in these experiments were all mediated by corticosteroid. The rise in glucose 6-phosphatase activity following a 24-hr starvation period, a function of endogenous steroid, and induction of glucose 6-phosphatase activity by pharmacological doses of exogenous steroid were both studied. The induction of tyrosine transaminase and tryptophan pyrrolase by exogenous corticosteroid was also studied. Female rats fed an identical diet were used as controls for the toxic effect of 2-FAA. Although susceptible to the carcinogenic effects of 2-FAA in high dosages, at the dose levels used in the current experiments, they developed no pathological changes of significance in the liver. The results of these experiments reveal that the corticosteroid-mediated enzyme-regulatory mechanisms are intact in the hyperplastic hepatic nodule induced by 2-FAA.

¹ These studies were supported by Grant CA 10978-01 from the USPHS and Grant 8-0144-724 from the American Cancer Society.

Received 8/13/69. Accepted 10/28/69.