Kruman I I, Matylevich N P, Rochev Iu A, Beletskiĭ I P, Afanas'ev V N, Umanskiĭ S R
Tsitologiia. 1992;34(2):43-53.
By flow cytometry, imitation modelling and biochemical analysis, the mode and kinetics of dexamethasone-treated T-lymphoma cell death were studied. The hormone was shown to induce delays in pre- and postsynthetic phases of the cell cycle and the death of part of cells. A short exposure to dexamethasone reveals its cytostatic rather than cytolytic effect. Following G2/M delay and cytokinesis, part of cells dies. A reduced serum concentration (2%) causes shorter delays in the cell cycle and a more rapid cell death. Dexamethasone stimulates apoptosis which is indicated by internucleosomal DNA fragmentation, and by a coincidence in time of the processes of DNA degradation and increase in the other membrane permeability. These results are discussed in relation to the cell death and proliferation.
通过流式细胞术、模拟建模和生化分析，研究了地塞米松处理的T淋巴瘤细胞死亡的方式和动力学。结果显示，该激素可诱导细胞周期合成前期和后期延迟，并导致部分细胞死亡。短期暴露于地塞米松显示其具有细胞抑制而非细胞溶解作用。在G2/M期延迟和胞质分裂后，部分细胞死亡。血清浓度降低（2%）会导致细胞周期延迟缩短和细胞死亡加快。地塞米松刺激细胞凋亡，这可通过核小体间DNA片段化以及DNA降解过程与其他膜通透性增加在时间上的巧合来表明。结合细胞死亡和增殖对这些结果进行了讨论。
