Hayek T, Oiknine J, Brook J G, Aviram M
Lipid Research Laboratory, Rambam Medical Center, Bruce Rappaport Faculty of Medicine, Technion, Israel.
Biochem Biophys Res Commun. 1994 Jun 30;201(3):1567-74. doi: 10.1006/bbrc.1994.1883.
Apo E-deficient mice which are highly atherogenic animals were used in order to study their plasma and lipoprotein lipid peroxidation in the absence or presence of oxidative stress. We have demonstrated that plasma from apo E knockout mice demonstrated increased lipid peroxidation both in the absence and in the presence of a free radical generating substance, 2,2-Azobis-(2-amidinopropane) hydrochloride (AAPH). Similarly, low and very low-density lipoprotein (LDL and VLDL) from apo E-deficient mice, but not their high-density lipoprotein (HDL), demonstrated increased lipid peroxidation. We suggest that in apo E-deficient mice, accelerated atherosclerosis is associated with increased lipid peroxidation of plasma, LDL and VLDL, as well as increased susceptibility of these lipoproteins to undergo lipid peroxidation under oxidative stress.
为了研究在有无氧化应激的情况下血浆和脂蛋白的脂质过氧化作用，我们使用了动脉粥样硬化高发的载脂蛋白E缺陷小鼠。我们已经证明，载脂蛋白E基因敲除小鼠的血浆在不存在和存在自由基生成物质2,2-偶氮二（2-脒基丙烷）盐酸盐（AAPH）的情况下均表现出脂质过氧化增加。同样，载脂蛋白E缺陷小鼠的低密度脂蛋白和极低密度脂蛋白（LDL和VLDL），而非其高密度脂蛋白（HDL），表现出脂质过氧化增加。我们认为，在载脂蛋白E缺陷小鼠中，动脉粥样硬化加速与血浆、LDL和VLDL的脂质过氧化增加以及这些脂蛋白在氧化应激下发生脂质过氧化的易感性增加有关。
