Lipid peroxidation in cancer

A su ested mode of action for the inhibitory effects of CLA on the initiation of cancer forms the interference of CLA with DNA adduct formation. Effects of CLA on 2-amino-3-methylimidazo [4,5] quinoline (IQ, heterocyclic amine carcinogen) induced DNA adduct formation in different organs in rats and mice have been reported, although CLA was not successful in inhibiting adduct formation in all organs (49, 50). The inhibition of tumor growth by CLA has been attributed to the induction of lipid peroxidation in cancer cells (but not in neutral, lipid-rich tissues) (38), although work by Banni has shown that CLA does not behave differently than other polyunsaturated fatty acids (51). 

Two studies in mice (52) and rats (62) reported an increase in lipid peroxidation products, whereas studies in rabbits (54) and rats (16) reported no change. One study in rabbits and one in rats even reported a decrease in lipid peroxidation products (25, 63). The effects of CIA on lipid peroxidation seem conflicting, but may be tissue-specific. In fact, CLA has been claimed to inhibit tumorigenesis by inducing lipid peroxidation in cancer cells, producing a cytotoxic effect on tumor cells and concomitantly attenuating lipid peroxidation in neutral, hpid rich tissues (38). In humans, Basu et al. and Riserus et al. found a 3-7-fold increase in urinary prostaglandin F2a in subjects supplemented with CIA compared to olive oil supplemented controls (35, 64). 

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See also in sourсe #XX -- [ ]

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