细胞外ATP影响铜离子诱导烟草悬浮细胞的死亡和H2O2的产生

摘要 细胞外ATP是植物体中许多生理过程的调节信号.胞外ATP可以影响铜离子诱导的细胞死亡和H_{2}O_{2}的产生.100sim 700 textit{mu }molL CuCl_{2}导致烟草悬浮细胞的死亡量显著上升,而且胞内H_{2}O_{2}和胞外H_{2}O_{2}的含量也随之上升.选择了300 textit{mu }molLCuCl_{2}研究铜离子导致的细胞死亡量上升和H_{2}O_{2}产生的过程.结果表明, 此浓度的 CuCl_{2}提升了NADPH氧化酶的活性,而加入DPI(NADPH氧化酶抑制剂)缓解了CuCl_{2}引起的细胞死亡和H_{2}O_{2}的产生,这说明CuCl_{2}引起细胞死亡和H_{2}O_{2}产生与NADPH氧化酶活性的增加相关. 加入50textit{mu }molLATP进一步增加了CuCl_{2}引起的细胞死亡、H_{2}O_{2}的产生、NADPH氧化酶.而DPI预处理后，外源ATP并未引起变化. 这一实验表明,胞外ATP可以通过刺激NADPH氧化酶影响铜离子引起的细胞活性和H_{2}O_{2}产生的变化
Abstract：Extracellular ATP (eATP) has been considered as a mediating signal in several physiological processes of plants. In this article we showed that eATP can affect the copper-induced cell death and hydrogen peroxide (H_{2}O_{2}) production. CuCl_{2} at concentrations from 100 to 700 textit{mu }molL caused a significant increase of cell death in tobacco (textit{Nicotiana tabacum} L) suspension cultures, and this increase of cell death level was followed with increases of both intracellular and extracellular H_{2}O_{2} production. The cells exposed to 300 textit{mu }molL CuCl_{2} were chosen to investigate the mechanisms for the copper-induced increases of cell death and H_{2}O_{2} production and the effect on this process. The results showed that the treatment_{ }with CuCl_{2 } at this concentration increased the activity of NADPH oxidase, and addition of DPI (diphenylene iodonium, an inhibitor of NADPH oxidase)alleviated the CuCl_{2}-induced increases of cell death and H_{2}O_{2} production, indicating that the CuCl_{2}-induced increases of cell death and H_{2}O_{2} production were related to an increase of the activity of NADPH oxidase. Addition of exogenous ATP at 50 textit{mu }molL into the CuCl_{2}-stressed cells further enhanced the levels of cell death,H_{2}O_{2} production, and NADPH oxidase activity. However, in the presence of DPI, exogenous ATP failed to do so. These observations indicated that eATP can affect the copper-induced changes of cell viability and H_{2}O_{2} production bystimulating NADPH oxidase