Aviram M, Eias K
Lipid Research Laboratory, Rambam Medical Center, Rappaport Family Institute for Research in the Medical Sciences, Technion Faculty of Medicine, Haifa, Israel.
Ann Nutr Metab. 1993;37(2):75-84. doi: 10.1159/000177753.
Low-density lipoprotein (LDL) oxidation and macrophage cholesterol accumulation are both involved in atherogenesis. Recently it was shown that feeding rabbits or humans with an oleic-acid-rich diet reduced the susceptibility of their LDL to in vitro oxidation. Since olive oil is highly enriched with oleic acid, we tested the effect of olive oil supplementation (50 g/day) to the diet of 10 healthy male subjects, during a 2-week period, on macrophage uptake of their LDL and on the propensity of their LDL to oxidation (with copper ions). Olive oil supplementation to the diet resulted in LDL enrichment with oleic acid (C18:1) and sitosterol. No effect on plasma cholesterol levels was found, but the LDL cholesteryl ester content was reduced (16%) whereas its unesterified cholesterol was increased (41%). Even after 1 week of the olive oil diet, the LDL susceptibility to in vitro oxidation was significantly reduced (p < 0.01). Macrophage uptake of LDL was studied by analysis of cellular cholesterol content and by analysis of the macrophage cholesterol esterification rates. LDL obtained after 1 and 2 weeks of the olive oil diet demonstrated reduced cellular uptake in comparison with LDL obtained before the supplementation of olive oil, by 50 and 61%, respectively. The LDL resistance to oxidation was shown by a reduction in its peroxide, malondialdehyde and conjugated diene content by 73, 28 and 32%, respectively. LDL incubation with oleic acid for the period of its oxidation with copper ions demonstrated a dose-dependent inhibition of lipoprotein oxidation by up to 72% as opposed to linoleic and arachidonic acids (50 microM) which increased LDL oxidation by 22 and 72%, respectively. Sitosterol, in a similar incubation system, inhibited LDL oxidation by up to 26%. We conclude that olive oil supplementation to the diet modifies LDL lipid composition and enriches the lipoprotein with oleic acid and sitosterol. The antiatherogenic properties of this modified lipoprotein may be related to its resistance to in vitro peroxidation and its reduced uptake by macrophages.
低密度脂蛋白(LDL)氧化和巨噬细胞胆固醇蓄积均参与动脉粥样硬化的发生。最近有研究表明,用富含油酸的饮食喂养兔子或人类可降低其LDL在体外的氧化敏感性。由于橄榄油富含油酸,我们测试了在为期2周的时间里,向10名健康男性受试者的饮食中补充橄榄油(50克/天)对其巨噬细胞摄取LDL以及LDL氧化倾向(用铜离子)的影响。向饮食中补充橄榄油导致LDL富含油酸(C18:1)和植物甾醇。未发现对血浆胆固醇水平有影响,但LDL胆固醇酯含量降低(16%),而其未酯化胆固醇增加(41%)。即使在食用橄榄油饮食1周后,LDL在体外的氧化敏感性也显著降低(p < 0.01)。通过分析细胞胆固醇含量和巨噬细胞胆固醇酯化率来研究巨噬细胞对LDL的摄取。与补充橄榄油之前获得的LDL相比,食用橄榄油1周和2周后获得的LDL的细胞摄取分别减少了50%和61%。LDL的抗氧化性表现为其过氧化物、丙二醛和共轭二烯含量分别降低了73%、28%和32%。在LDL与铜离子氧化期间,用油酸孵育显示出对脂蛋白氧化的剂量依赖性抑制,最高可达72%,而亚油酸和花生四烯酸(50微摩尔)分别使LDL氧化增加22%和72%。在类似的孵育系统中,植物甾醇对LDL氧化的抑制作用高达26%。我们得出结论,向饮食中补充橄榄油可改变LDL的脂质组成,使脂蛋白富含油酸和植物甾醇。这种修饰后的脂蛋白的抗动脉粥样硬化特性可能与其对体外过氧化的抗性及其被巨噬细胞摄取减少有关。