通过大鼠心肌缺血/再灌及高脂血症的模型证实,两者均有明显的生物膜损伤,主要表现为膜磷脂的降低、胆固醇及胆固醇/磷脂比增高、膜脂流动性及膜酶(Ca2+, Mg2+-ATPase)活性降低,这些异常变化与氧自由基引发的脂质过氧化增强或脂质交换有关.
Through the experiment model of the myocardial ischemia/reperfusion and lipoidaemia in rat, both of them obviously induce membrane injury: a drop of membrane phospholipids, an increase in content of free fatty acids, cholesterol and cholesterol/phospholipid ratio, a decrease in membrane lipids fluidity and activity of membrane enzymes (Ca2+, Mg2+-ATPase). These aterations perhaps related to the increase of lipids hyperoxidation induced by free radical and exchange of lipids.
董传仁,喻学刚,汪学军.大鼠心肌缺血/再灌及高脂血症的心肌膜损伤[J].生物化学与生物物理进展,1994,21(4):347-350
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