Elferink J G
Biochem Med Metab Biol. 1986 Aug;36(1):25-35. doi: 10.1016/0885-4505(86)90103-9.
Microcrystals of hydroxyapatite cause severe membrane damage in human erythrocytes, as is evident from the strong hemolysis that is caused by these crystals. Hemolysis by hydroxyapatite crystals is time and concentration dependent, and is preceded by aggregation of erythrocytes. Polyvinylpyridine-N-oxide, a strong hydrogen acceptor, has no inhibiting effect on hydroxyapatite-induced hemolysis. This suggest that the mechanism of action of these crystals is different from that of urate crystals and silica particles, where hydrogen bonding interaction is supposed to be important. Negatively charged macromolecules, such as dextran sulfate, heparin, and polyglutamic acid, inhibit hydroxyapatite crystal-induced hemolysis, suggesting that positive charges, probably located on the crystals, play an important role in the membrane-damaging effect of these crystals. The structures with which these positive charges interact remain to be determined because removal of negative charges from the erythrocytes by treatment with neuraminidase does not affect crystal-induced hemolysis.
羟基磷灰石微晶会对人类红细胞造成严重的膜损伤,这从这些晶体引起的强烈溶血现象中可以明显看出。羟基磷灰石晶体引起的溶血具有时间和浓度依赖性,并且在红细胞聚集之前发生。聚乙烯吡啶-N-氧化物是一种强氢受体,对羟基磷灰石诱导的溶血没有抑制作用。这表明这些晶体的作用机制与尿酸盐晶体和二氧化硅颗粒不同,在尿酸盐晶体和二氧化硅颗粒中,氢键相互作用被认为是重要的。带负电荷的大分子,如硫酸葡聚糖、肝素和聚谷氨酸,可抑制羟基磷灰石晶体诱导的溶血,这表明可能位于晶体上的正电荷在这些晶体的膜损伤作用中起重要作用。由于用神经氨酸酶处理红细胞以去除负电荷并不影响晶体诱导的溶血,因此这些正电荷与之相互作用的结构仍有待确定。