González-Flores D, Rodríguez A B, Pariente J A
Department of Physiology, Neuroimmunophysiology and Chrononutrition Research Group, Faculty of Science, University of Extremadura, 06006, Badajoz, Spain,
Mol Cell Biochem. 2014 May;390(1-2):281-7. doi: 10.1007/s11010-014-1979-5. Epub 2014 Feb 2.
The present study determines the role of reactive oxygen species (ROS) production and calcium signaling evoked by the tumor necrosis factor-alpha (TNFα) on apoptosis in the human leukemia HL-60 and K562 cell lines. The results show that treatment of both cell lines cells with 10 ng/mL TNFα resulted in a rise in the percentage of apoptotic cells after 6 h of treatment. It was also observed that the administration of 10 ng/mL TNFα increased intracellular ROS production, as well as a time-dependent increase in caspase-8, -3, and -9 activities. The present results also show that the pretreatment with well-known antioxidants such as trolox and N-acetyl cysteine partially reduced the caspase activation caused by the administration of TNFα. The findings suggest that TNFα-induced apoptosis is dependent on alterations in intracellular ROS generation in human leukemia HL-60 and K562 cells.
本研究确定了肿瘤坏死因子-α（TNFα）引发的活性氧（ROS）生成和钙信号传导在人白血病HL-60和K562细胞系凋亡中的作用。结果显示，用10 ng/mL TNFα处理这两种细胞系的细胞6小时后，凋亡细胞百分比上升。还观察到，给予10 ng/mL TNFα会增加细胞内ROS生成，以及半胱天冬酶-8、-3和-9活性的时间依赖性增加。本研究结果还表明，用知名抗氧化剂如曲洛司坦和N-乙酰半胱氨酸预处理可部分降低因给予TNFα而导致的半胱天冬酶激活。这些发现表明，TNFα诱导的凋亡依赖于人类白血病HL-60和K562细胞内ROS生成的改变。
