The carcinogenicity of p-dimethylaminoazobenzene in diets containing the fatty acids of hydrogenated coconut oil or of corn oil.

The striking retardation in the development of hepatomas in rats fed p-dimethylaminoazobenzene when hydrogenated coconut oil is included in the diet has been the subject of two communications from these laboratories (6, 7). When this fat was fed at a level of 5 per cent in a synthetic diet the incidence of liver tumors was found to be only 8 per cent or less at 6 months, in contrast to a usual incidence of 60 to 80 per cent at this time when the hydrogenated coconut oil was replaced by corn oil. Although great differences exist between the chemical and physical properties of these fats (3, 7), no conclusive basis has been found for the anticarcinogenic action of hydrogenated coconut oil. Thus the presence or absence of antioxidants in these fats did not affect the tumor incidence. The effect of hydrogenated coconut oil was maintained despite the presence of amounts of ethyl linolate sufficient for the growth and health of rats on a fat-free diet. Furthermore, the formation of hepatic tumors did not depend upon the development or prevention of the syndrome characteristic of a deficiency of essential fatty acids. Only slight protection against hepatoma formation was obtained wi th a diet containing trilaurin at a level equivalent to the laurie acid contributed by 5 per