Volf I, Roth A, Cooper J, Moeslinger T, Koller E
Institute of Physiology, Schwarzspanierstr. 17, A-1090 Vienna, Austria.
FEBS Lett. 2000 Oct 20;483(2-3):155-9. doi: 10.1016/s0014-5793(00)02104-9.
Experimental low density lipoprotein (LDL) oxidation is usually performed using trace copper, although the in vivo relevance of this method has been called into question. Such LDL augment adenosine 5'-diphosphate (ADP) induced platelet aggregation, presumably by the action of lipid derived compounds. In striking contrast, we find that LDL oxidized to a comparable extent by hypochlorite, an in vivo occurring oxidant, reveal themselves to be potent promoters of platelet aggregation. Interestingly, hypochlorite modified LDL seem to mediate their influence on human platelets by means of the modified apolipoprotein B-100 (apoB) moiety. Also, the finding that hypochlorite modified albumin is able to trigger platelet aggregation suggests an essential role for hypochlorite modified protein(s) in the process of platelet activation.
实验性低密度脂蛋白（LDL）氧化通常使用痕量铜来进行，尽管这种方法在体内的相关性受到了质疑。这种LDL会增强腺苷5'-二磷酸（ADP）诱导的血小板聚集，推测是通过脂质衍生化合物的作用。与之形成鲜明对比的是，我们发现，被次氯酸盐（一种体内存在的氧化剂）氧化到相当程度的LDL，显示出自身是血小板聚集的强效促进剂。有趣的是，次氯酸盐修饰的LDL似乎通过修饰的载脂蛋白B-100（apoB）部分来介导它们对人血小板的影响。此外，次氯酸盐修饰的白蛋白能够触发血小板聚集这一发现表明，次氯酸盐修饰的蛋白质在血小板激活过程中起着至关重要的作用。
