Elferink J G, Deierkauf M
Department of Medical Biochemistry, Sylvius Laboratories, University of Leiden, The Netherlands.
Inflammation. 1989 Jun;13(3):285-94. doi: 10.1007/BF00914395.
In the absence of extracellular Ca2+, poly-L-arginine induces little lysozyme release from rabbit polymorphonuclear leukocytes (PMNs). The polycation causes plasma membrane damage, which is evident from the release of the cytoplasmic enzyme lactate dehydrogenase (LDH). In the presence of Ca2+ concentrations higher than 0.2 mM, poly-L-arginine induces a strong lysozyme release that is superimposed on the membrane-damaging effect. The results suggest that poly-L-arginine permeabilizes the plasma membrane, enabling Ca2+ to enter the cell, which results in the exocytotic release of granule constituents. The GTP analog GTP gamma S shifts the Ca2+ requirement of exocytosis to slightly higher concentrations, whereas it completely inhibits poly-L-arginine-induced LDH release. Pertussis toxin gives a moderate inhibition, and La3+ completely inhibits poly-L-arginine-induced enzyme release. Whereas poly-L-arginine alone induces little superoxide generation in rabbit PMNs, there is a synergistic enhancement of superoxide production when GTP gamma S and poly-L-arginine are present together. Guanine nucleotides apparently have a modulating effect on the actions of poly-L-arginine on the PMN, but the nature of this effect remains to be determined.
在没有细胞外钙离子的情况下，聚-L-精氨酸从兔多形核白细胞（PMN）诱导出很少的溶菌酶释放。这种聚阳离子导致质膜损伤，这从细胞质酶乳酸脱氢酶（LDH）的释放中可以明显看出。在钙离子浓度高于0.2 mM时，聚-L-精氨酸诱导强烈的溶菌酶释放，这种释放叠加在膜损伤效应之上。结果表明，聚-L-精氨酸使质膜通透性增加，使钙离子能够进入细胞，从而导致颗粒成分的胞吐释放。GTP类似物GTPγS将胞吐作用的钙离子需求转移到略高的浓度，而它完全抑制聚-L-精氨酸诱导的LDH释放。百日咳毒素有中度抑制作用，而La3+完全抑制聚-L-精氨酸诱导的酶释放。虽然单独的聚-L-精氨酸在兔PMN中诱导很少的超氧化物生成，但当GTPγS和聚-L-精氨酸同时存在时，超氧化物产生有协同增强作用。鸟嘌呤核苷酸显然对聚-L-精氨酸对PMN的作用有调节作用，但这种作用的性质仍有待确定。
