Abstract

Lipid peroxidation of polyunsaturated fatty acids yields several electrophilic, reactive carbonyl metabolites. We hypothesized that an increased intake of omega‐3 fatty acids (n‐3) would lead to increased lipid peroxidation metabolites compared to a diet low in n‐3. As part of a randomized crossover dietary intervention trial, urinary markers of whole body lipid peroxidation were analyzed. Study subjects (n=15) included healthy, postmenopausal women who were fed a low‐fat diet (20% of energy from fat, LF) or low‐fat diet supplemented with 3% of energy from n‐3 fatty acids (LFn3) for 8 weeks. Urine was collected during two consecutive 24‐hour collections in the last two days of each diet. Whole body lipid peroxidation within each subject was measured via complementary methods. Analysis via urinary TBARS was followed by a sensitive HPLC separation and quantification of 2,4‐ dinitrophenylhydrazine‐reactive lipophilic aldehydes, including 4‐ hydroxynonenal, 4‐hydroxyhexenal, and other nonpolar aldehydes. The HPLC technique demonstrated that LFn3 resulted in increased levels of lipid peroxidation products by two‐fold relative to LF. These results show that increased n‐3 intake leads to increased production of in vivo secondary lipid peroxidation products. The impact of these results requires further investigation. This work was supported by the US DOD, NCI, NCRR, and Salmon of the Americas, Inc.Grant Funding Source: National Cancer Institute

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