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PRIMARY carcinoma of the liver is a common disease amongst Africans (Berman, 1958), but the aetiology and mechanism still remain to be disclosed. Butter yellow (4-dimethylaminoazobenzene) produces liver cancer when fed to rats, and it was hoped that a better understanding of the action of butter yellow (BY) in rats would help to elucidate the mechanism of liver cancer in man. BY does not usually produce cancer in organs other than the liver, which suggests that at some stage in the chain of events initiated by BY a modification occurs in a metabolic pathway which is confined to the liver, and that the modification culminates in carci-noma. It seemed that one such pathway might be the degradation of cholesterol to bile acids, which is probably confined to the liver (Harold, Felts and Chaikoff, 1955). The cholesterol-bile acid pathway receives added importance in view of the conversion of bile acids and cholesterol into carcinogens. The carcinogen methyl-cholanthrene can be synthesized chemically from deoxycholic or cholic acids (reviewed by Greenstein, 1954, p. 49), and cholesterol can be oxidized to several carcinogenic compounds (Fieser, Greene, Bischoff, Lopez and Rupp, 1955). Even deoxycholic acid itself when injected under the skin of mice can lead to sarcomas (Cook, Kennaway and Kennaway, 1940). A particular disturbance in bile acid metabolism therefore might conceivably lead to the endogenous production of a carcinogen,a possibility that has often been suspected. A further indication for a link between cholesterol metabolism and hepato-carcinogenesis was supplied by Gillman, Gilbert and Spence (1954). These workers emphasized the frequent occurrence of bile duct hyperplasia in the livers of BY-fed rats, and they suggested an association between bile duct hyperplasia and a raised serum cholesterol, both of which were shown by these investigators to occur together after ligation of the bile duct, in hypothyroidism and (possibly) in avit-aminosis A. Since then Spain and Griffin (1957) have found an increased serum cholesterol after feeding the hepatocareinogen 3'-methyl-4-dimethylaminoazo-benzene for three weeks, at which stage bile duct hyperplasia also declares itself This rise in serum cholesterol might be linked to a faH in the rate of cholesterol degradation, which proceeds almost entirely by the pathway to bile acids (Siper-stein, Jayko, Chaikoff and Dauben, 1952). In this paper it is accordingly proposed to examine the bile acid metabolism of BY-fed rats and controls, as expressed by the amount and composition of the bile acids obtained after cannulation of the …

Bile Acid Composition and Bile Volume in Butter Yellow Fed Rats in Relation to Liver Cancer