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Binding of Growth Hormone to Rat Liver during Experimental Chemical Hepatocarcinogenesis^*

Departments of Endocrinology and Medical Oncology, City of Hope National Medical Center Duarte, California 91010

Address all correspondence and requests for reprints to: A. Lev-Ran, City of Hope National Medical Center, Duarte, California 91010.

Abstract

Male F-344 rats (180–200 g) received either a single injection of diethylnitrosamine (DEN) or continuous feeding with 2-acetylaminofluorene (AAF). DEN induced a decrease in the binding of human GH (hGH) to its hepatic Golgi receptors in a dose-dependent manner; the changes were due to a decrease in the number of hGH receptors without significant changes in their affinity. Thirty days after DEN, the binding of hGH returned to normal. After the administration of AAF, the binding of hGH increased owing to the greater number of binding sites, and this effect persisted for the 30-day period of the continuous AAF feeding. In three separate hepatocellular carcinomas, the hGH binding to the Golgi fraction of the tumors was only one quarter of the binding to the peritumorous tissues. We conclude that DEN and AAF, administered acutely for a short time, affect hepatic hGH receptors in a different way, but that hepatocellular carcinomas bind much less hGH than peritumorous or normal tissues. The results show that hepatocarcinogenesis encompasses changes in receptors belonging to different classes. (Endocrinology 118: 1869–1871, 1986)

Footnotes

^* This work was supported in part by PHS Grant CA-33572 from the National Cancer Institute.

Received September 18, 1985.