Induction of tyrosine aminotransferase and the amino acid transport system was investigated in livers of non-tumor-bearing Sprague-Dawley and A × C rats, in host livers, and in hepatomas of rats bearing Morris hepatoma 5123C, 7794B, 7800, 9121, or 9618A, under conditions not previously used with hepatomas. The agents used to study the induction of the enzyme and the transport system were: a high-protein diet; dexamethasone alone; glucagon and theophylline, alone and in combination; and glucagon, theophylline, and dexamethasone together. Tyrosine aminotransferase and the amino acid transport system in the hepatomas and host livers responded to the inducing agents to varying degrees and from widely different initial fasting values. Thus a wide diversity in patterns of induction was observed, with no two hepatoma lines or their host livers responding similarly to all inducing agents. Induction of tyrosine aminotransferase was studied in the livers of neonatal rats from 0 to 9 days of age, with the use of glucagon, theophylline, both drugs, or dibutyryl cyclic adenosine 3′,5′-monophosphate. The range of data seen with the hepatomas is paralleled by the wide range exhibited by the changes during the shift from neonatal to adult liver. At the low end of the range, hepatoma 9618A resembles the earliest neonatal liver in terms of its tyrosine aminotransferase activity, whether induced or occurring naturally. At the high end of the scale, other hepatomas may exceed normal adult liver in naturally occurring or induced levels of tyrosine aminotransferase or amino acid transport, while resembling neonatal liver in other respects.

1

Support was provided in part by Departmental Grant CA-07175 and Training Grant T01-CA5002 from the National Cancer Institute, USPHS.

This content is only available via PDF.