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Effect of Nutritional Alterations on Protein Synthesis in Transplantable Hepatomas and Host Livers of Rats¹

Department of Pathology, The George Washington University Medical Center, Washington, D. C. 20037

The effects of selected, short-term, nutritional alterations on female Buffalo rats bearing transplantable hepatomas (5123 and 19) were investigated. In this study, nutritional alterations, which have been tried earlier dealing with the effects on hepatic protein metabolism of normal rats, were utilized. The host livers and hepatomas (intrahepatically transplanted) of tumor-bearing rats revealed little changes in polyribosomal aggregation or in in vitro protein synthesis in fasted animals (2 to 3 days) that were tube-fed a single feeding of a complete diet, a complete amino acid mixture, a protein-free diet, or tryptophan. This is in contrast to the stimulatory effect elicited by these feedings to normal female Buffalo rats without tumors. Rats tube-fed hypertonic NaCl solution (6%) revealed a marked degree of polyribosomal disaggregation and inhibition of protein synthesis in host livers and similar but less marked changes in the intrahepatically transplanted hepatomas. Hepatoma-bearing (s.c. and intrahepatic) rats that were force-fed a threoninedevoid diet for 3 days revealed increased protein synthesis in the host livers and decreased protein synthesis in the hepatomas in comparison with similar rats force-fed a complete diet. Thus, the results of this study reveal that host livers of hepatoma-bearing rats are not responsive to certain nutritional stresses (complete amino acids or diet, protein-free diet, or tryptophan) as is the case with livers of normal rats. Hepatomas are resistent to some of the nutritional stresses studied; with two exceptions, the administration of hypertonic NaCl solution, where the response occurred but was less than that in the host liver, and the force feeding for 3 days of a threonine-devoid diet, where hepatoma protein synthesis was decreased while it became increased in the host liver.

¹ This investigation was supported by USPHS Research Grant CA22997 from the National Cancer Institute.

² To whom requests for reprints should be addressed.

Received 6/ 5/78. Accepted 3/ 2/79.