Dietary fat is known to promote certain types of cancer. One of the ways certain fats may facilitate cancer is through a class of reactive chemicals derived from the fat, for example, arachidonic...

Dietary fat is known to promote certain types of cancer. One of the ways certain fats may facilitate cancer is through a class of reactive chemicals derived from the fat, for example, arachidonic acid, an n-6 fatty acid. Another class of fats, the so-called n-3 fatty acids that are found in high quantities in fish oil, may be less active in promoting tumors. Because n3 acids can replace n-6 acids in cell membrane phospholipids, it may be possible to modify tumorigenesis by modifying the type of fat in the diet. In order to compare the relative tumorigenicity of the n-6 fatty acid, arachidonic acid (AA), to that of the n-3 fatty acid, eicosapentanoic acid (EPA), Belury and coworkers* used a well-known tumor induction model in which the chemical 12-O-tetradecanoylphorbol-13-acetate (TPA) is added to a cell culture to promote the carcinogenic activity of a suspected carcinogen. If either AA or EPA is carcinogenic, they would be expected to increase the DNA synthesis in skin cells grown in cell culture in the presence of TPA. These investigators measured the specific activity of DNA synthesis under four conditions, AA, EPA, AA with TPA, and EPA with TPA (the data are in Table D-21, Appendix D). Is there any evidence that AA and EPA have different carcinogenic potential?

Table D-21