Karelin A A
Shemyakin Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow.
Immunol Lett. 1994 Sep;42(1-2):13-7. doi: 10.1016/0165-2478(94)90028-0.
Tubocurarin was shown to mediate a wide spectrum of cytolytic processes in tumor cells while peritoneal murine macrophages were resistant to its action. Group I of these processes was due to rapid (within 1-3 h) and nonspecific lysis mediated by relatively high (> 10(-5) M) concentrations of tubocurarin. Membrane damage with subsequent osmotic lysis was associated with these events. Processes of groups II and III were highly specific, cytolysis of group II having developed within 4-5 h and characterized by saturation at 5 x 10(-7) M. It was proposed that two types of necrosis contributed to the processes of group II. These pathways were induced by different concentrations of tubocurarin and also differed in their sensitivity to lysosomal inhibitor NH4Cl. Cytolysis of group III was associated with apoptosis and developed within 8-24 h. The significant acceleration of DNA fragmentation and subsequent cell death was achieved by increase of tubocurarin concentration from 5 x 10(-8) to 10(-6) M.
筒箭毒碱被证明可介导肿瘤细胞中的多种细胞溶解过程,而小鼠腹腔巨噬细胞对其作用具有抗性。这些过程的第一组是由于相对高浓度(>10^(-5) M)的筒箭毒碱介导的快速(1-3小时内)非特异性裂解。膜损伤及随后的渗透性裂解与这些事件相关。第二组和第三组过程具有高度特异性,第二组细胞溶解在4-5小时内发生,其特征是在5×10^(-7) M时达到饱和。有人提出两种类型的坏死导致了第二组过程。这些途径由不同浓度的筒箭毒碱诱导,并且对溶酶体抑制剂NH4Cl的敏感性也不同。第三组细胞溶解与凋亡相关,并在8-24小时内发生。通过将筒箭毒碱浓度从5×10^(-8) M增加到10^(-6) M,可显著加速DNA片段化及随后的细胞死亡。