Tanaka Y, Inoue K, Nojima S
Biochim Biophys Acta. 1980 Jul 16;600(1):126-39. doi: 10.1016/0005-2736(80)90418-6.
The process of interaction of dilauroylglycerophosphocholine with erythrocytes that eventually results in hemolysis was examined. 1. The rate of uptake of dilauroylglycerophosphocholine by human erythrocytes was rather slow, but increased with increasing temperature. 2. The first observable change of human erythrocytes induced by dilauroylglycerophosphocholine was a morphological change from discocytes to spheroechinocytes. This change preceded K+ leakage. 3. Adsorption of dilauroylglycerophosphocholine to human erythrocytes caused K+ leakage. The rate of K+ leakage was also temperature-dependent. The temperature-dependence was due to the temperature-dependence of lipid uptake, because in order to cause K+ leakage a given amount of dilauroylglycerophosphocholine must be bound to the erythrocytes, irrespective of the temperature. 4. The temperature-dependence of hemolysis of human erythrocytes was different from that of pre-hemolytic events (morphological change, adsorption of lipids and K+ leakage). Hemolysis was rapid below 10 and above 37 degrees C, but slow at about 25 degrees C. The hemolysis observed below 10 degrees C seemed to be a 'colloid osmotic lysis', since it occurred immediately after K+ leakage, but the hemolysis above 37 degrees C may not be a colloid osmotic lysis. Above 37 degrees C, additional binding of dilauroylglycerophosphocholine to the erythrocyte membrane may cause hemolysis by a different mechanism from that working below 10 degrees C. 5. Above 25 degrees C, most human erythrocytes are resistant to colloid osmotic lysis induced by dilauroylglycerophosphocholine. It can be concluded that human erythrocytes are composed of two types of population, one resistant, and one sensitive to colloid osmotic lysis. The mechanism of the resistance was sensitive to temperature, pH and various sulfhydryl agents. 6. Pig erythrocytes were hemolysed immediately after K+ leakage even above 25 degrees C, indicating that they were sensitive to a colloid osmotic mechanism over the whole temperature range tested. Pig erythrocytes may lack the 'mechanism' giving resistance to colloid osmotic lysis. The process of hemolysis of erythrocytes by dilauroylglycerophosphocholine is shown schematically.
研究了二月桂酰甘油磷酸胆碱与红细胞相互作用最终导致溶血的过程。1. 人红细胞对二月桂酰甘油磷酸胆碱的摄取速率相当缓慢,但随温度升高而增加。2. 二月桂酰甘油磷酸胆碱诱导的人红细胞的第一个可观察到的变化是从双凹圆盘状细胞变为棘状球状细胞。这种变化先于钾离子泄漏。3. 二月桂酰甘油磷酸胆碱吸附到人红细胞上会导致钾离子泄漏。钾离子泄漏速率也与温度有关。温度依赖性是由于脂质摄取的温度依赖性,因为为了引起钾离子泄漏,一定量的二月桂酰甘油磷酸胆碱必须与红细胞结合,而与温度无关。4. 人红细胞溶血的温度依赖性与溶血前事件(形态变化、脂质吸附和钾离子泄漏)不同。在10℃以下和37℃以上溶血迅速,但在约25℃时缓慢。在10℃以下观察到的溶血似乎是一种“胶体渗透溶血”,因为它在钾离子泄漏后立即发生,但37℃以上的溶血可能不是胶体渗透溶血。在37℃以上,二月桂酰甘油磷酸胆碱与红细胞膜的额外结合可能通过与10℃以下不同的机制导致溶血。5. 在25℃以上,大多数人红细胞对二月桂酰甘油磷酸胆碱诱导的胶体渗透溶血具有抗性。可以得出结论,人红细胞由两种群体组成,一种具有抗性,一种对胶体渗透溶血敏感。抗性机制对温度、pH和各种巯基试剂敏感。6. 猪红细胞即使在25℃以上钾离子泄漏后也会立即溶血,表明它们在整个测试温度范围内对胶体渗透机制敏感。猪红细胞可能缺乏对胶体渗透溶血具有抗性的“机制”。示意性地展示了二月桂酰甘油磷酸胆碱使红细胞溶血的过程。