Department of Physiology, INSA, RETICS, University of Barcelona, Spain.
Free Radic Res. 2010 Jul;44(7):821-9. doi: 10.3109/10715762.2010.485992.
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.
氧化应激导致动脉粥样硬化中的脂质过氧化和一氧化氮(NO)生物利用度降低。虽然长链(n-3)多不饱和脂肪酸(PUFA)在体外很容易氧化,但它们可以改善内皮功能。因此,本研究假设长链(n-3)PUFA 可降低体内动脉粥样硬化性氧化应激。为了验证这一点,apoE(-/-)小鼠分别用玉米油或富含鱼油(FO)的饮食喂养 8、14 或 20 周,并评估与 NO 和超氧阴离子(O(2)(.-))相关的参数以及主动脉根部的脂质过氧化和蛋白质氧化损伤的标志物。FO 丰富的饮食增加了 NO 的产生和内皮型一氧化氮合酶(NOS)的表达,并降低了诱导型 NOS、p22(phox)表达和 O(2)(.-)的产生,在饮食 14 和 20 周后。蛋白质脂质过氧化损伤(包括 4-羟基壬烯醛)在长期 FO 饮食后减少。这支持了富含 FO 的饮食可以对抗动脉粥样硬化性氧化应激的假说,显示了长链(n-3)PUFA 的有益作用。