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The Effect of Hepatocarcinogenesis upon 5-Hydroxytryptophan Decarboxylase and Serotonin Deaminase

( Biomedical Division of The Samuel Roberts Noble Foundation, Inc., Ardmore, Okla.)

Enzymes associated with the catabolism of 5-hydroxytryptophan (5-HT) were assayed in transplanted hepatomas, in primary lesions induced with 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB), and in 3'-Me-DAB precancerous rat liver. Among six transplanted rat hepatomas, 5-HT decarboxylase activity was essentially absent in five, whereas the Morris hepatoma 5123 manifested activity equivalent to that observed in rat liver. Mouse Hepatoma 134 retained slight but measurable activity, but no appreciable activity was observed in Hepatoma 129. When animals were fed diets containing 3'-Me-DAB for 12 weeks, the 5-HT decarboxylase activity of the liver was significantly depressed as early as 2 weeks. At 4 and 8 weeks the activity was about half the value observed in control animals, but at 12 weeks the activity was essentially the same as that of controls. When primary lesions developed, no 5-HT decarboxylase activity was observed, but the activity in the adjacent liver tissue was essentially normal. For the first 4 weeks the lowered decarboxylase activity in the liver of animals fed 3'-Me-DAB was not due to dietary restriction, nor was it reversed by pyridoxine supplementation of the diet. Removal of 3'-Me-DAB from the diets restored activity to normal levels in 7 days.

Serotonin deaminase activity was essentially absent in four transplanted rat hepatomas but was readily demonstrated in the Morris 5123. Activity was observed in mouse Hepatoma 134, but activity was absent in Hepatoma 129. No alteration of serotonin deaminase activity was observed during the 12 weeks on diets containing 3'-Me-DAB; however, activity was absent in primary lesions and was significantly lowered in liver tissue adjacent to primary lesions.

^* Present address: University of Wisconsin, Department of Physiological Chemistry, Madison 6, Wisconsin.

Received 8/22/60.