Mise en évidence chez le rat d'un facteur génétique dans la cancérisation par le diméthylaminoazobenzène. Presence in the rat of a genetic control of dab‐carcinogenesis

Abstract

Abstract Two strains of white rats, one of which (Sprague‐Dawley) was sensitive, another (Wistar) not, to liver cancerization by DAB, were studied comparatively in an attempt to find biochemical characteristics which might explain this difference, that is changes in the activity of the enzyme, DAB‐reductase, and in the binding of azo metabolites to liver proteins. The animals were administered a whole diet, rich in proteins and in vitamins. When not fed DAB, the activity of DAB‐reductase was five‐fold higher in Wistar than in Sprague‐Dawley rats; the continuous administration of DAB causes a progressive decrease of the enzyme activity in the two strains. After 10 days of carcinogenic diet the amounts of azo proteins are maximal and at this time they are twice higher in Sprague‐Dawley than in the Wistar rats. Hepatomas appear in the Sprague‐Dawley strain without a lag phase, as early as the fifth week of treatment. The resistance to cancerization appears to depend principally on a genetic factor which would allow a more or less efficient detoxification, mediated by the enzyme, DAB‐reductase.