Supplementation of postmenopausal women with fish oil does not increase overall oxidation of LDL ex vivo compared to dietary oils rich in oleate and linoleate

Although replacement of dietary saturated fat with monounsaturated and poly unsaturated fatty acids (MUFA and PUFA) has been advocated for the reductio n of cardiovascular disease risk, diets high in PUFA could increase low den sity lipoprotein (LDL) susceptibility to oxidation, potentially contributin g to the pathology of atherosclerosis. To investigate this possibility, 15 postmenopausal women in a blinded crossover trial consumed 15 g of sunflowe r oil (SU) providing 12.3 g/day of oleate, safflower oil (SA) providing 10. 5 g/day of linoleate, and fish oil (FO) providing 2.0 g/day of eicosapentae noate (EPA) and 1.4 g/day of docosahexaenoate (DHA). During CuSO4-mediated oxidation, LDL was depleted of alpha -tocopherol more rapidly after FO supp lementation than after supplementation with SU (P = 0.0001) and SA (P = 0.0 5). In LDL phospholipid and cholesteryl ester fractions, loss of n-3 PUFA w as greater and loss of n-6 PUFA less after FO supplementation than after SU and SA supplementation (P < 0.05 for all), but loss of total PUFA did not differ. The lag phase for phosphatidylcholine hydroperoxide (PCOOH) formati on was shorter after FO supplementation than after supplementation with SU (P = 0.0001) and SA (P = 0.006), whereas the lag phase for cholesteryl lino leate hydroperoxide (CE18:2OOH) formation was shorter after FO supplementat ion than after SU (P = 0.03) but not SA, In contrast, maximal rates of PCOO H and CE18:2OOH formation were lower after FO supplementation than after SA (P = 0.02 and 0.0001, respectively) and maximal concentrations of PCOOH an d CE18:2OOH were lower after FO supplementation than after SA (P = 0.03 and 0.0006, respectively). Taken together, our results suggest that FO supplem entation does not increase the overall oxidation of LDL ex vivo, especially when compared with SA supplementation, Consequently, health benefits relat ed to increased fish consumption may not be offset by increased LDL oxidati ve susceptibility.