Prevention of Adaptive Formation of Tryptophan Peroxidase by a Carcinogenic Azo Dye

Abstract

THE carcinogenic azodye 3′-methyl,4-dimethyl aminoazobenzene induces gross tumours in livers of rats fed a basal diet poor in riboflavin¹. The whole process, in Sprague–Dawley rats, takes approximately 200 days. Structural damage to liver tissue may be detected histologically during the first weeks of carcinogen feeding². Intracellular changes, manifested by the gradual depletion of mitochondria and ergastoplasm, which result in respiratory damage to the cell, can be detected by differential centrifugation weeks and even months before onset of malignancy³; yet all these changes are long-range effects. Even though the continual administration of this carcinogen brings about respiratory damage to the cell, the carcinogen is not a respiratory inhibitor^4,5. It can be shown that the specific respiratory activity (activity per mgm. protein nitrogen) with sodium pyruvate as substrate remains normal for mitochondria during feeding with this carcinogen although the tissue is full of protein-bound azodye⁵. In short, the immediate chemical effect of this carcinogen, apart from its binding to one or more proteins not yet functionally characterized⁶, is still obscure.