Do We Go Rancid after Eating Fish?
By Rosemary C. Wander
ABSTRACT
Fish off-flavor and odor develops, in part, through oxidation of the long-chain, highly unsaturated fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), fish contain, a condition referred to as rancidity. This deterioration proceeds through a free-radical mediated, chain reaction. Even though numerous epidemiologic studies have shown that fish consumption decreases cardiovascular mortality, there is concern that its consumption could increase in vivo lipid oxidation, contributing to the development of such diseases as cardiovascular disease, cancer, and diabetes. In the past, a limitation to measuring in vivo oxidation was the lack of appropriate tools. Recently, more sensitive measures have been developed, e.g., the adduct formed by the reaction of malondialdehyde with thiobarbituric acid using high pressure liquid chromatography, F2-isoprostanes, malondialdehyde by gas chromatography/mass spectrometry, and protein oxidation. Using these techniques, we measured lipid oxidation in plasma of post menopausal women after they consumed a supplement of fish oil containing an amount of EPA/DHA equivalent to two servings of Chinook salmon. In vivo oxidation was either similar to or lower than that which occurred when the women were not consuming the fish oil. On the other hand, plasma concentrations of thiobarbituric acid reactive substances (TBARS), a much older method for measuring lipid oxidation, consistently increased. Using low-density lipoprotein (LDL)obtained from the same subjects, we determined that the ex vivo rate of oxidation of LDL enriched with EPA and DHA was slower than LDL not enriched. These data suggest that oxidative stress is not increased but may actually be lowered by fish consumption.
KEYWORDS: oxidation, cardiovascular disease, F2-isoprostanes, TBARS, malondialdehyde
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