Abstract:In this experiment, tobacco suspension cell BY2 was used as the material, and 0.05, 0.10, 0.15, 0.20 mmol·L-1 AlCl3 was added to the tobacco suspension cells, and the suspension cell solution treatment with equal volume of deionization water was used as a control. And, according to the above experimental results, 0.15 mmol·L-1 AlCl3 was selected, 5 mmol·L-1 DMTU (H2O2 inhibitor), 20 μmol·L-1 CaCl2, 15 μmol·L-1 LaCl3 (Ca2+ channel inhibitor) and 50 μmol·L-1 ATP was used to analyze the effects of extracellular ATP (eATP) on plant cell death and intracellular H2O2 and Ca2+ induced by aluminum ion (Al3+) stress and to reveal plant the possible mechanism of eATP in regulating cell death under Al3+ stress, and further extend the perception of eATP function. The results showed that: (1) with the increase of AlCl3 concentration, the levels of cell death and intracellular H2O2 were increased, while the levels of intracellular Ca2+and eATP were decreased; (2) Application of DMTU (dimethylthiourea, a scavenger of H2O2) and exogenous Ca2+ effectively attenuated the AlCl3induced cell death, while barium trichloride (LaCl3, the Ca2+ channel inhibitor) aggravated the AlCl3induced cell death, indicating that AlCl3induced cell death is regulated by H2O2 and Ca2+; (3) The addition of exogenous ATP effectively impeded the increase of intracellular H2O2 production and decrease of intracellular Ca2+ under AlCl3 stress, and the cell death induced by AlCl3 were also alleviated by exogenous ATP. It can be seen that aluminuminduced cell death is regulated by changes in H2O2 and Ca2+ levels, and extracellular ATP affects the aluminuminduced cell death by regulating H2O2 and Ca2+ levels.Theses observations indicated that the level of cell death and intracellular H2O2 were increased, while the level of intracellular Ca2+ and eATP were decreased in a dosedependent manner under Al3+ stress. It can be seen that aluminuminduced cell death is regulated by changes in H2O2 and Ca2+ levels, and extracellular ATP affects the aluminuminduced cell death by regulating H2O2 and Ca2+ levels. We predicated that Al3+ stress may destroy the synergistic relationship between H2O2 and Ca2+ in cells by inhibiting calcium channel, and the alleviation effect of exogenous ATP on Al3+ induced H2O2 elevation may be due to its enhanced antioxidant capacity.