CuCl2胁迫对烟草BY-2悬浮细胞死亡的诱导

本文以不含叶绿体的烟草BY-2悬浮细胞系为实验材料,研究了CuCl2胁迫对BY-2细胞呼吸速率、呼吸途径以及细胞内H2O2和ATP含量的影响。结果表明：0.5mmol·L-1CuCl2胁迫明显导致了烟草BY-2细胞的死亡,引起了胞内H2O2爆发和ATP含量下降,严重抑制了BY-2细胞的总呼吸和交替氧化酶途径（alternative oxidase pathway,AOX）。此外,CuCl2对BY-2细胞的线粒体电子传递具有即时的抑制作用。加入外源腺苷（ATP合成的底物）显著抑制了CuCl2胁迫引起的ATP损耗,并阻止了细胞死亡。上述结果表明CuCl2胁迫导致的ATP损耗在CuCl2诱导烟草BY-2细胞死亡过程中起重要的作用。

Cell Death Induced by CuCl2 Stress in Tobacco BY-2 Cells

The tobacco BY-2 cells without chloroplast were used in this study to explore the mechanism of the cell death induced by CuCl2. The effects of CuCl2 stress on the respiration rate and alternative oxidase pathway were studied in tobacco BY-2 cells treated with 0.5 mmol·L^1 CuCl2. The results showed that 0.5 mmol·L^-1 CuCl2 led to remarkable cell death, overproduction of reactive oxygen species, a rapid depletion of ATP, significant declines in respiration and in alternative oxidase pathway （AOX） in tobacco BY-2 cells. Moreover, the addition of exogenous adenosine with CuCl2 significantly inhibited ATP depletion and prevented cell death. The data presented here demonstrated that the ATP depletion played an important role in CuCl2-induced cell death in the tobacco BY-2 cells.