A fish oil-rich diet reduces vascular oxidative stress in apoE^–/–mice

Abstract

Oxidative stress contributes to lipid peroxidation and decreases nitric oxide (NO) bioavailability in atherosclerosis. While long-chain (n-3) polyunsaturated fatty acids (PUFA) are easily oxidized in vitro, they improve endothelial function. Hence, this study postulates that long-chain (n-3) PUFA decrease atherogenic oxidative stress in vivo. To test this, apoE(-/-) mice were fed a corn oil- or a fish oil (FO)-rich diet for 8, 14 or 20 weeks and parameters related to NO and superoxide (O(2)(.-)) plus markers of lipid peroxidation and protein oxidative damage in the aortic root were evaluated. The FO-rich diet increased NO production and endothelial NO synthase (NOS) expression and lowered inducible NOS, p22(phox) expression and O(2)(.-)production after 14 and 20 weeks of diet. Protein lipoxidative damage (including 4-hydroxynonenal) was decreased after a long-term FO-diet. This supports the hypothesis that a FO-rich diet could counteract atherogenic oxidative stress, showing beneficial effects of long-chain (n-3) PUFA.

Docosahexaenoic Acid Supplemented Diet Influences the Orchidectomy-Induced Vascular Dysfunction in Rat Mesenteric Arteries

“…The influence of the DHA-supplemented diet, showed a restoration in NO release levels, closely to the ones from the control group, as previously found in aorta [24]. However, DHA has been reported not to modify the release of NO in aged [36] and hypertensive [37] rats, indicating that the choice of the experimental model is crucial.…”

“…These actions seem to be specific on EFS-induced contraction since the contraction induced by 75 mM of KCl was not modified by the orchidectomy or DHA-diet. In this regard, the contractile response induced by potassium depolarization was not altered by a DHA diet in hypertensive rats [37]. Although, we have previously reported that the orchidectomy did not modify the release of neuronal NO [13] and NA [18], it would have been desirable to determine the neurogenic release of NA and NO.…”

Treatment with n-3 polyunsaturated fatty acids reverses endothelial dysfunction and oxidative stress in experimental menopause

“…In observational studies, the relative risk of cardiac events is inversely correlated with baseline blood and tissue levels of eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids [9,10]. Potential mechanisms underlying beneficial effects of n-3 PUFA on endothelial dysfunction and atherosclerosis include enhanced vasodilation by correction of the imbalance between vasoconstrictor and vasodilator endothelium-derived factors [11], inhibition of nuclear factor kappa B (NF-kB) activation and of cyclooxygenase-2 (COX-2) expression [11], reduction of endothelial expression of adhesion molecules [12,13], suppression of leukocyte adhesion to endothelial cells [14] and modulation of oxidative stress [15][16][17]. Several studies suggest a link between n-3 PUFA-mediated cardioprotective effects and the involvement of caveolae [18], a subset of membrane lipid rafts which plays a key role in endothelial function [19].…”

4-Hydroxy Hexenal Derived from Docosahexaenoic Acid Protects Endothelial Cells via Nrf2 Activation

“…More recent large-scale interventions and cross-sectional studies have shown that n-3 PUFAs reduce cardiovascular events independently of the classical risk factors for atherosclerosis [3]–[6], which suggests direct anti-atherogenic effects of n-3 PUFAs on vascular tissues. Many studies have already demonstrated that n-3 PUFAs display a variety of bioactive actions such as anti-inflammatory [7], [8] and antioxidant effects [9], [10], improvement of endothelial function [11], [12] and a suppressive effect on monocyte adhesion in vascular tissue [8], [13], [14] explaining the anti-atherogenic effects of n-3 PUFA. In a recent study, enzymatic metabolites from n-3 PUFAs, including resolvins and protectins, were reported to exert potent anti-inflammatory effects in aortic endothelial cells, leading to atheroprotective effects [15].…”