Mechanistic Insights of Carcinogenesis and Anti-carcinogenesis by Dietary Compounds

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Carcinogenesis by chemical carcinogens occurs in a stepwise manner that consists of at least three distinct steps: initiation, promotion, and progression. Evidence to date indicates that DNA damage is responsible for initiation by chemical carcinogens. Most carcinogens require metabolic activation by mammalian enzyme systems (e.g., CYPs) to more reactive forms before they could interact with DNA. The genetic damage might be mediated by the metabolically activated carcinogen itself, but might also result from by-products of metabolism, including reactive oxygen species. Damage to DNA at selective sites within the genome may either introduce or amplify a proliferative signal, diminish or eliminate response to a normally dominant inhibitory growth signal. Although initiation is dependent on DNA damage, chemically induced DNA damage alone is not mutagenic. Initiating mutations are permanent and depend on the unique properties (dose and metabolism) of the carcinogens, the identity of DNA damage, specific location of DNA damage, and saturation of endogenous protective systems. Newer evidence from laboratory animal studies suggests that certain dietary components have anti-carcinogenic effects. Their anti-carcinogenesis mechanisms include alteration of metabolic responses to carcinogenic initiators effectively decreasing activation and enhancing elimination of carcinogenic substances. Anti-carcinogens, including antioxidants, may also be chemopreventive by mechanisms such as minimizing DNA damage by reactive oxygen species or augmenting DNA repair following damage. This review focused some mechanistic effects of dietary anti-carcinogens, particularly how certain compounds act biochemically to reduce the interaction of chemical carcinogens with DNA.
金沢医科大学の論文

Mechanistic Insights of Carcinogenesis and Anti-carcinogenesis by Dietary Compounds

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