Mechanisms by which docosahexaenoic acid and related fatty acids reduce colon cancer risk and inflammatory disorders of the intestine

We have previously demonstrated that butyrate induces colonocyte apoptosis via a non-mitochondrial, Fas-mediated, extrinsic pathway which is antagonized by activated Ras []. DHA and butyrate work coordinately in the colon to initiate a distinct intrinsic proapoptotic cycle involving the activation of store-operated channels (SOC), leading to rapid entry of Ca2+ through the plasma membrane and mitochondrial Ca2+ loading. This directly or indirectly increases mitochondrial phospholipid hydroperoxides (PLOOH) and triggers the opening of the permeability transition pore (PTP) and release of pro-apoptotic molecules like cytochrome C. These effects culminate in the induction of apoptosis.

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Mechanisms by which docosahexaenoic acid and related fatty acids reduce colon cancer risk and inflammatory disorders of the intestine. () Robert S. Chapkin, et al. Chem Phys Lipids. ;153(1):14-23. Figure: F2. All organisms Drosophila melanogaster Homo sapiens

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