钙离子在登革病毒诱导的细胞毒素细胞毒性活性中的必要作用。
Obligatory role of Ca2+ in the cytotoxic activity of dengue virus-induced cytotoxin.
作者信息
Dhawan R, Chaturvedi U C, Khanna M, Mathur A, Tekwani B L, Pandey V C, Rai R N
机构信息
Postgraduate Department of Microbiology, K.G. Medical College, Lucknow, India.
出版信息
Int J Exp Pathol. 1991 Feb;72(1):31-9.
The role of calcium ions (Ca2+) in the cytotoxic activity of the dengue type 2 virus (DV)-induced macrophage (M phi) cytotoxin (CF2) was investigated in the present study. The findings show that CF2 prepared in Ca(2+)-free medium had no cytotoxic activity on normal mouse spleen cells suspended in Ca(2+)-free medium but killed the cells suspended in the medium with Ca2+. Substitution with calcium chloride restored the cytotoxic activity of CF2 the optimal dose being 10(-4) M concentration. CF2 induced an influx of Ca2+, as assayed by uptake of radiolabelled calcium chloride (45Ca), in the susceptible target cells, viz. M phi and T lymphocytes. The cytotoxic activity of CF2 as well as the CF2-induced influx of 45Ca was inhibited by treatment of the target cell with the calcium channel blocking drugs verapamil and nifedipine. Thus, the presence of Ca2+ is obligatory for the cytotoxic activity of CF2 and cell death is associated with increased intracellular Ca2+.
本研究调查了钙离子（Ca2+）在登革2型病毒（DV）诱导的巨噬细胞（M phi）细胞毒素（CF2）细胞毒性活性中的作用。研究结果表明，在无钙培养基中制备的CF2对悬浮于无钙培养基中的正常小鼠脾细胞没有细胞毒性活性，但能杀死悬浮于含Ca2+培养基中的细胞。用氯化钙替代可恢复CF2的细胞毒性活性，最佳剂量为10（-4）M浓度。CF2可诱导易感靶细胞（即M phi和T淋巴细胞）摄入放射性标记的氯化钙（45Ca），从而导致Ca2+内流。用钙通道阻滞剂维拉帕米和硝苯地平处理靶细胞可抑制CF2的细胞毒性活性以及CF2诱导的45Ca内流。因此，Ca2+的存在是CF2细胞毒性活性所必需的，细胞死亡与细胞内Ca2+增加有关。
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