The mouse is well known for its relative resistance to liver DAB carcinogenesis, when compared with the rat; the hamster is even more resistant (Miller and Miller, 1955; Homburger, 1968).Since the initial discovery of protein-bound azodyes in the liver of rats fed DAB (Miller and Miller, 1947), a large variety of azo compounds, either supplied in the diet or given by intraperitoneal injection, were shown to give rise to bound azo-dyes in rat liver (see review by Terayama, 1967;Lawson, 1968; Hughes, 1969/70;and Roberts, 1969). This binding was not specific to azo compounds and many other chemical carcinogens were found associated with proteins of target tissues (Hughes and Pilczyk, 1969;Sorof et al., 1969;Szafarz and Weisburger, 1969; Barry et al., 1969/70).In each case, soon after the beginning of carcinogen administration, the amount of bound dyes increased and reached a maximum; the decrease in binding which followed could possibly result in a gradual removal of the proteins able to combine with the dye.It is currently accepted that the molecule of DAB must be metabolized in order to express its carcinogenic effect and be bound to liver proteins (Terayama, 1958;Miller and Miller, 1969).