The effect of 2-acetylaminofluorene on growth and composition of the liver of the rat.

In the first study of the toxicity and carcino genic activity of 2-acetylaminofluorene (AAF), Wilson, DeEds, and Cox noted that the compound caused a profound inhibition of growth, when it was fed in a 10 per cent casein diet to albino rats (21). Inhibition of the growth of the rat has also been obtained with a number of carcinogenic aro matic hydrocarbons and with p-dimethylaminoazobenzene (11, 19, 20), and the growth-retarding ability of carcinogenic compounds has been con sidered a specific property of carcinogens inasmuch as structurally related noncarcinogenic compounds do not appear to possess this property (10). It is conceivable, therefore, that carcinogenic amines in producing growth inhibition cause the same or a similar metabolic disturbance as carcinogenic aro matic hydrocarbons and p-dimethylaminoazobenzene. Inasmuch as increasing the level of dietary pro tein has been shown to protect against growth in hibition by 1,2,5,6-dibenzanthracene (DBA) (7), there is some reason to believe that carcinogenic aromatic hydrocarbons cause a disturbance of pro tein metabolism. Whether the carcinogen inter feres with protein metabolism in general, or with the metabolism of specific amino acids only, is an unsettled problem. In the case of DBA, addition of cystine or methionine to a 5 per cent casein diet did not prevent the growth inhibition, indicating that DBA did not interfere with the metabolism of the sulfur amino acids (5). In contrast, either cystine or methionine was effective in relieving the growth inhibition induced by p-dimethylaminoazobenzene in rats maintained on a 6 per cent casein diet (19). In the case of 2-aminofluorene,