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In vitro studies, using low FFA concentrations and experimental conditions nonconducive to lipid peroxidation, support the contention that cancer cell growth is enhanced by AA-derived eicosanoids and that their effects are counteracted by long-chain n-3 PUFAs. (19,32,33) It has also been shown that tumor cells produce a potent mitogenic compound from LA (13-hydroxyoctadecadienoic acid) via a lipoxygenase pathway, and that n-3 PUFAs inhibit cellular gout uptake of LA, thereby reducing the rate of cell proliferation. gout (34) Additionally, incorporation of EPA, DHA, and GLA into cancer cell membranes may alter cancer growth and metastasis by mechanisms independent of their effects on gout eicosanoid synthesis. Such mechanisms include alteration of surface receptors or signaling proteins of the cell membrane, initiating cell cycle arrest of apoptosis; (15) alteration of cancer cell adhesion; and enhancement of tight junction function. (35) Thus, suppressing the synthesis of AA-derived eicosanoids or alteration of cell membrane function by EPA, DHA, or GLA can alter the growth of cancer cells and potentially lead to misinterpretation of the impact of PUFAs on the effects of cytotoxic anticancer agents and radiation.
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