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A Prooxidant Based Anticancer Mechanism Of Plant Derived Polyphenolic Nutraceuticals

Plant polyphenols are recognized as antioxidants but also act as prooxidants in the presence of transition metal ions, such as copper. Using a cellular system of lymphocytes isolated from human blood and Comet assay we have shown that polyphenols cause oxidative DNA breakage in cells. We have also shown that polyphenols generate oxidative stress in lymphocytes which is inhibited by scavengers of reactive oxygen species. Incubation of lymphocytes with neocuproine (cell membrane permeable Cu(I) chelator) inhibited DNA degradation, confirming that Cu(I) is an intermediate in the DNA cleavage reaction. Bathocuproine, a cell impermeable analogue of neocuproine, did not cause such inhibition. Polyphenols are able to degrade DNA in cell nuclei and that such DNA degradation is inhibited by neocuproine as well as bathocuproine (both permeate the nuclear pore complex) but not by compounds that specifically bind iron and zinc. Similarly, the polyphenol genistein induced apoptosis in breast cancer cells is also inhibited by the copper chelator neocuproine. The results support our hypothesis that anticancer mechanism of polyphenols involves mobilization of endogenous copper, possibly chromatin bound, and the consequent prooxidant action. Such a common mechanism would better explain the anticancer effects of polyphenols with diverse chemical structures as also the preferential cytotoxicity towards cancer cells.