有核细胞中抗体和补体诱导的高能磷酸盐的预裂解还原。31日p-nmr研究。

R Tirosh, H Degani, G Berke
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引用次数: 9

摘要

利用31P-NMR波谱,我们研究了低水平的细胞表面抗原和补体抗体诱导有核细胞裂解的代谢过程的可能参与。在抗体加补体攻击的10分钟内,在明显裂解开始之前,我们观察到细胞内磷酸肌酸和三磷酸腺苷(ATP)含量的显著选择性减少。较长时间的攻击伴随着保留其他磷酸化合物的残余细胞中磷酸肌酸或ATP的完全耗尽。结果表明,在有核细胞中,假定的补体依赖性膜通道的形成诱导ATP的彻底水解。提示ATP剥夺可导致胶质渗透肿胀、膜破裂和细胞死亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Prelytic reduction of high-energy phosphates induced by antibody and complement in nucleated cells. 31P-NMR study.

Using 31P-NMR spectroscopy, we have investigated possible involvement of metabolic processes in the lysis of nucleated cells induced by low levels of antibody to cell surface antigens and complement. Within 10 min of antibody plus complement attack, before onset of overt lysis, we have observed a marked, selective reduction in the intracellular content of phosphocreatine and adenosine triphosphate (ATP). A longer attack is accompanied by total depletion of either phosphocreatine or ATP in residual cells which preserved other phosphate compounds. The results indicate that in nucleated cells formation of putative complement-dependent membrane channels induces exhaustive hydrolysis of ATP. It is suggested that ATP deprivation could in turn lead to colloid-osmotic swelling, membrane rupture, and cell death.

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