Physiological role for zinc in prevention of apoptosis (gene-directed death).
Physiological role for zinc in prevention of apoptosis (gene-directed death).
复制标题
锌在预防细胞凋亡（基因定向死亡）中的生理作用。
DOI：
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发表时间：
1991
期刊：
影响因子：
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通讯作者：
C. Giannakis
中科院分区：
文献类型：
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作者：
Peter D. Zalewski;Ian J. Forbes;C. Giannakis
以慢性淋巴白血病（CLL）细胞为研究对象，研究了Zn ~（2+）对CLL细胞凋亡的调控作用。在培养18 h的过程中，部分细胞自发发生凋亡，秋水仙素处理的大多数细胞发生凋亡。自发和秋水仙素诱导的DNA断裂和细胞死亡的存在下，完全抑制生理浓度的Zn 2+与Zn 2+离子载体。螯合细胞内Zn ~（2+）诱导的DNA断裂和形态学变化的凋亡在大多数CLL细胞在5小时内，但不是在人口的CLL细胞耐其他凋亡刺激。佛波酯对秋水仙碱等刺激诱导的细胞凋亡有抑制作用，但对螯合细胞内Zn ~（2+）诱导的细胞凋亡无影响。我们建议，可螯合的锌2+细胞内池块凋亡，该池增加从介质中的摄取。
Chronic lymphatic leukaemia (CLL) cells were used to study regulation of apoptosis by Zn2+. Apoptosis occurred spontaneously in a proportion of the cells during culture for 18h and in most of the cells exposed to colchicine. Spontaneous and colchicine-induced DNA fragmentation and cell death were completely inhibited in the presence of physiological concentrations of Zn2+ with Zn2+ ionophores. Chelation of intracellular Zn2+ induced DNA fragmentation and morphological changes of apoptosis in most CLL cells within 5hr, but not in a population of CLL cells which were resistant to other apoptotic stimuli. Phorbol esters inhibited apoptosis induced by colchicine and other stimuli, but had no effect on apoptosis induced by chelation of intracellular Zn2+. We propose that an intracellular pool of chelatable Zn2+ blocks apoptosis and that this pool is increased by uptake from the medium.