PHENYLALANINE HYDROXYLASE ACTIVITY IN ISOLATED, PERFUSED LIVER OF RATS BEARING RHODAMINE SARCOMA, HEPATOMA, AND NODULAR HYPERPLASIA

• Published in: GANN Japanese Journal of Cancer Research Vol. 58; no. 2; pp. 185 - 191
• Main Authors: TERAWAKI, Asaharu, SATO, Minoru, YAMANOUCHI, Masataka, FUKUYAMA, Toetu, ITO, Nobuyuki, NAKAJIMA, Saichi
• Format: Journal Article
• Language: English
• Published: Japan The Japanese Cancer Association 01.01.1967
• Subjects: Animals; Carcinoma 256, Walker - enzymology; Hyperplasia; In Vitro Techniques; Liver - enzymology; Liver Diseases - enzymology; Liver Regeneration; Male; Oxidoreductases - metabolism; Perfusion; Phenylalanine - metabolism; Rats; Sarcoma, Experimental - enzymology; Tryptophan - pharmacology; Tyrosine - pharmacology
• ISSN: 0016-450X
• DOI: 10.20772/cancersci1959.58.2_185

Using isolated perfused liver of rats bearing Rhodamine sarcoma, hepatoma, or nodular hyperplasia, phenylalanine hydroxylase activity and its response to tyrosine and tryptophan were examined. In regenerating rat liver, the initial level of phenylalanine hydroxylase (L-phenylalanine, tetrahydropteridine: oxygen oxidoreductase, EC 1. 14.3.1) and its decrease in response to perfusion with tyrosine and tryptophan solutions were the same as in normal rat liver. However, unlike regenerating rat liver, in ethionineinduced hepatoma and in N-(2-fluorenyl)acetamide-inducedn odular hyperplasia, phenylalanine hydroxylase activity was much lower than that of normal liver and the decrease in response to tyrosine and tryptophan was much less. In host liver, the decrease in response to amino acids was also low, whereas enzyme activity was within the normal range. These results suggest the existence of a disturbance in the intrahepatic regulation of the level of phenylalanine hydroxylase activity in host liver, hepatoma, and nodular hyperplasia, and a difference between the mechanism causing lower activity of phenylalanine hydroxylase and that causing a decreased response to amino acids.