Di Pietro R, Robuffo I, Pucci A M, Bosco D, Santavenere E
Istituto di Morfologia Umana Normale, Via. dei Vestini 6, 66100 Chieti, Italy.
Cytokine. 1999 Feb;11(2):144-50. doi: 10.1006/cyto.1998.0406.
Tumour necrosis factor alpha (TNF-alpha) kills Daudi cells (Human Burkitt Lymphoma), inducing either necrosis or apoptosis without DNA fragmentation. Therefore, we were interested in studying the molecular and ultrastructural events occurring when the nucleus is more accessible and cells are blocked in mitosis, following colchicine treatment. In fact, as early as after 1 h treatment a typical ladder pattern was shown by means of DNA gel electrophoresis. In parallel the quantitative analysis of the different morphological patterns observed gave evidence of an increased percentage of primary necrosis after 6 h treatment, and a higher incidence of cells in late apoptosis as well as in secondary necrosis after 24 h treatment. Our findings show that Daudi cells respond to the combined treatment with an increased formation of micronuclei and nuclear alterations which follow a number of early mitochondrial changes and result in enhanced cell death. These data imply that TNF-alpha-induced apoptosis of Daudi cells can be triggered by mitochondrial changes and is somehow related to microtubule organization.
肿瘤坏死因子α（TNF-α）可杀死Daudi细胞（人伯基特淋巴瘤细胞），诱导细胞发生坏死或凋亡，且不会出现DNA片段化。因此，我们感兴趣的是研究在秋水仙碱处理后，细胞核更容易接近且细胞被阻滞在有丝分裂期时所发生的分子和超微结构事件。事实上，早在处理1小时后，通过DNA凝胶电泳就显示出典型的梯状条带模式。同时，对所观察到的不同形态模式的定量分析表明，处理6小时后原发性坏死的百分比增加，处理24小时后晚期凋亡细胞以及继发性坏死细胞的发生率更高。我们的研究结果表明，Daudi细胞对联合处理的反应是微核形成增加和核改变，这些改变伴随着一些早期线粒体变化，并导致细胞死亡增加。这些数据表明，TNF-α诱导的Daudi细胞凋亡可由线粒体变化触发，并且在某种程度上与微管组织有关。
