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REVIEW ARTICLE |
1 From the Divisions of Nutritional Epidemiology (SCL and AW), Experimental Asthma and Allergy Research (MK), and Molecular Toxicology (MI-S), The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm.
Increasing evidence from animal and in vitro studies indicates that n–3 fatty acids, especially the long-chain polyunsaturated fatty acids eicosapentaenoic acid and docosahexaenoic acid, present in fatty fish and fish oils inhibit carcinogenesis. The epidemiologic data on the association between fish consumption, as a surrogate marker for n–3 fatty acid intake, and cancer risk are, however, somewhat less consistent. This review highlights current knowledge of the potential mechanisms of the anticarcinogenic actions of n–3 fatty acids. Moreover, a possible explanation of why some epidemiologic studies failed to find an association between n–3 fatty acid intake and cancer risk is provided. Several molecular mechanisms whereby n–3 fatty acids may modify the carcinogenic process have been proposed. These include suppression of arachidonic acid-derived eicosanoid biosynthesis; influences on transcription factor activity, gene expression, and signal transduction pathways; alteration of estrogen metabolism; increased or decreased production of free radicals and reactive oxygen species; and mechanisms involving insulin sensitivity and membrane fluidity. Further studies are needed to evaluate and verify these mechanisms in humans to gain more understanding of the effects of n–3 fatty acid intake on cancer risk.
Key Words: n–3 Fatty acids • eicosapentaenoic acid • docosahexaenoic acid • 
-linolenic acid • arachidonic acid • carcinogenesis • eicosanoids • gene expression • epidemiology
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