Azizova O A, Panasenko O M, Vol'nova T V, Vladimirov Y A
Research Institute of Physico-Chemical Medicine, Moscow, U.S.S.R.
Free Radic Biol Med. 1989;7(3):251-7. doi: 10.1016/0891-5849(89)90132-9.
Human erythrocytes were incubated for 5 h at 37 degrees C with lipoproteins (LP), preliminary oxidized to different extent, as assessed by thiobarbituric acid (TBA) test. Cholesterol content in the cells was increased by 12-14% after incubation with low-density lipoproteins (LDL) along with augmentation of order parameter and rotational correlation time of spin-labeled stearic acids incorporated into membranes. If erythrocytes were incubated with oxidized LDL, containing 2.5-4 times more TBA-reactive material than native ones, cellular content of cholesterol was increased by 24-28%. In contrast, high-density lipoproteins (HDL2 and HDL3) removed cholesterol from cell membranes, when incubated with erythrocytes. This was followed by increased fluidity of membrane lipid phase as detected by the spin probe method. Oxidation of HDL2 and HDL3 decreased their ability to accept cholesterol from cell membranes. No detectable accumulation of TBA-reactive material was observed in the samples during the incubation. The antioxidant, butylated hydroxytoluene (BHT), in the concentration of 10(-5) M did not influence the cholesterol transfer between LP and erythrocytes. Hence, the effects of lipid peroxidation (LPO) on the cholesterol transfer seem to result from LP alterations by oxidation rather than from free radical reactions occurring during the incubation. By increasing cholesterol-donating ability of LDL and inhibition of cholesterol-accepting capacity of HDL lipid peroxidation in LP may activate cholesterol accumulation in blood vessel cells and thus contribute to atherosclerosis.
将人红细胞与脂蛋白（LP）在37℃下孵育5小时，脂蛋白预先氧化至不同程度，通过硫代巴比妥酸（TBA）试验评估。与低密度脂蛋白（LDL）孵育后，细胞内胆固醇含量增加了12 - 14%，同时掺入膜中的自旋标记硬脂酸的有序参数和旋转相关时间也增加。如果红细胞与氧化型LDL孵育，其TBA反应性物质比天然LDL多2.5 - 4倍，细胞内胆固醇含量会增加24 - 28%。相反，当与红细胞孵育时，高密度脂蛋白（HDL2和HDL3）会从细胞膜中去除胆固醇。通过自旋探针法检测发现，这随后伴随着膜脂相流动性的增加。HDL2和HDL3的氧化降低了它们从细胞膜接受胆固醇的能力。孵育过程中样品未观察到可检测到的TBA反应性物质积累。浓度为10(-5) M的抗氧化剂丁基羟基甲苯（BHT）不影响LP与红细胞之间的胆固醇转移。因此，脂质过氧化（LPO）对胆固醇转移的影响似乎是由LP氧化改变引起的，而非孵育过程中发生的自由基反应。通过增加LDL的胆固醇捐赠能力和抑制HDL的胆固醇接受能力，LP中的脂质过氧化可能会激活血管细胞中的胆固醇积累，从而促进动脉粥样硬化。
