中文摘要：

以烟草悬浮细胞BY-2（Nicotiana tabacum L.cv.Bright Yellow-2）为材料,探讨了在铜离子胁迫下植物细胞死亡发生过程中胞外H2O2及NADPH氧化酶所扮演的角色。实验结果表明,随着外源Cu Cl2浓度的上升（从0～700μmol·L-1）,细胞死亡水平不断上升,且胞外H2O2的水平也不断增加。在300μmol·L-1的Cu Cl2诱导细胞死亡的过程中,加入H2O2清除剂N-N-二甲基硫脲（DMTU）降低了胞外Cu Cl2胁迫下H2O2含量增加的同时也降低了细胞死亡水平的上升,这一观察表明了铜离子胁迫所导致的细胞死亡的发生和胞外H2O2的增加有关。进一步的研究表明,300μmol·L-1Cu Cl2的胁迫导致了NADPH氧化酶活性的显著性上升,而加入NADPH氧化酶的抑制剂（二亚苯基碘,DPI,）则降低了Cu Cl2胁迫所导致的细胞死亡和胞外H2O2含量的上升。上述结果表明,胞外H2O2和NADPH氧化酶参与了Cu Cl2对植物细胞死亡的诱导作用。

英文摘要：

By using the tobacco （Nicotiana tabacum cv. Bright Yellow-2） cell suspension culture, we studied the roles of extracellular H2O2 and NADPH oxidase in the copper-induced cell death. With the increase of exogenous CuCl2 from 0 to 700 μmol · L-1, the level of cell death were increased followed by the increase of extracellular H2O2. In the cell subjected to 300 μmol · L-1 CuCl2, the addition of exogenous dimethyl thiourea （DMTU, a scavenger of H2O2 ） alleviated the increases of both the cell death level and the production of extracellular H2O2, which were induced by CuCl2 （300 μmol · L-1）. The copper-induced increase in the cell death was associated with the increase of extracellular H2O2. The CuCl2（ 300 μmol · L-1） stress induced an increase of the activity of NADPH oxidase. The addition of diphenylene iodonium （ DPI, an inhibitor of NADPH oxidase） alleviated the increases of both the cell death level and the production of extracellular H2O2, which were induced by CuCl2 （300 μmol · L- 1 ）. Our results indicate that extracellular H2O2 and NADPH oxidase are involved in the copper-induced cell death.