Effects of dietary fat on the uptake and clearance of 7,12-dimethylbenz(alpha)anthracene by rat mammary tissue.

The concentration of 7,12-dimethylbenz(a)anthracene ( D M B A ) i n mamm-Lry tissue was determined at different time intervals following its administration, in a single dose, to female Sprague-Dawley rats maintained on 3 different semisynthetic diets: low fat, high coconut oil, and high corn oil. In general, the rate of uptake and clearance of the carcinogen was similar in the 3 groups, with a peak concentration occurring 6 to 12 hours after its administration. At 6 hours the tissue level of DMBA in coconut oil fed rats was significantly lower than in the other 2 groups. IIowever, the data obtained could not fully explain the effects of dietary fat upon DMBA mammary carcinogenesis. Introduction. The influence of dietary fat upon 7,12-dimethylbenz (a) anthracene (DMBA)-induced mammary cancer in female rats was the subject of a recent study by the present authors (7). I t was demonstrated that the observed enhancement of tumor formation depended on the nature as well as the amount of fat in the diet. Thus, coconut oil ingested by one group of animals did not exert, the augmenting effect of an equally large amount of corn oil in another group. Moreover, parameters pertaining to tumor growth and development in the coconut oil-fed group were similar to those obtained in a group of rats fed a low fat diet. I t was shown also lhat, at the time of cancer induction, definite changes trod taken place in the fat ty acid eoml~ositioi1 of mammary tissue, reflecting lhe three different diet'try fat int~lkes. This pointed to a possible relationship between the nature of the fat in the immediate environment of the mammary gland and the carcinogenic process taking place in its epithelial cells. Tannenbaum had suggested earlier that the amount of fat in the breasts of mice on a fat-enriched diet was a factor in carcinogenesis (13). Following a study of the levels of 3methylehotanthrene (3-MC) in breast and fatty tissue after its administration to rats, Dao et al. (3) pointed to the role of mammary adipose tissue as a storage depot for this carcinogenic hydrocarbon. Later on, investigators using various methods of