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Effects of Exogenous Histones upon the Induction of Tryptophan Pyrrolase and Tyrosine Transaminase in Liver and Morris Hepatomas¹

Department of Biochemistry, School of Medicine, University of North Carolina, Chapel Hill, North Carolina 27514 [H. W. S., J. L. I.] and Department of Biochemistry, College of Medicine, Howard University, Washington, D. C. 20001 [H. P. M.]

Morris hepatoma 5123tc in intact or adrenalectomized Buffalo strain rats has a very low basal level of tryptophan pyrrolase (TP) activity and a high basal level of tyrosine transaminase (TKT) activity in comparison with normal liver. Both enzymes are inducible by hydrocortisone injections, but the induced level of TP in the hepatoma is much less than that of liver. Injections i.p. of histones or poly-L-lysine induce increases in TP, but not TKT, in the hepatoma in adrenalectomized rats.

The rate of decline of induced TP activity in the 5123tc hepatoma in the presence of puromycin to prevent further synthesis of the enzyme is identical with the rate of decline in normal liver, and consequently the low basal levels and weak inducibility of TP in this tumor probably should be attributed to a defect in synthesis of TP, rather than to accelerated rate of degradation of this enzyme. Injected histones decrease the rate of decline of TP activity in the hepatoma as well as liver. On the other hand, there is no decline of induced TKT activity in the hepatoma during an 8-hr period after induction, in contrast to normal liver, in which the half-life of TKT is 2.9 hr. Consequently, the high basal level of TKT in this hepatoma probably should be attributed to a low rate of degradation rather than a high rate of synthesis. The rate of degradation of TKT in liver of rats bearing this hepatoma also is greatly decreased in comparison with normal liver; this suggests that the tumor may produce a circulating inhibitor of the degradative system for TKT.

Basal levels of TP and TKT and inducibility by hydrocortisone and poly-L-lysine were studied in four other Morris hepatomas: 5123A, 5123C, 7793, and 7795.

¹ Aided by Grant GM 08318-08 from the National Institute of General Medical Sciences Grant CA-10729 from the National Cancer Institute, NIH, and Grant E-24I from the American Cancer Society. Some of the equipment used in this research was obtained through Department Equipment Grant GB-4577 from the National Science Foundation.

² Predoctoral Research Trainee, supported by Training Grant 5T01GM00404 from the National Institute of General Medical Sciences, NIH.

Received 2/24/69. Accepted 10/16/69.