Cell death in rice roots due to zinc (Zn) toxicity was investigated using inhibitors of signal molecules known to regulate programmed cell death in plants. Zn (5.0-25.0 mM) induced cell death in a dose-and timedependent manner. Sodium benzoate, a scavenger of reactive oxygen species (ROS), increased the cell viability under toxic Zn level (25.0 mM), suggesting a role of ROS in Zn-induced cell death. The protective role of rotenone in cell death indicated the involvement of mitochondrial electron transport chain in this Zn-induced ROS generation. Cantharidin and endothall, two serine/threonine phosphatase inhibitors, and sodium orthovanadate (Na 3 VO 4 ) and phenylarsine oxide (PAO), two protein tyrosine phosphatase inhibitors, blocked Zn-induced root cell death. Conversely, K252-a, a serine/threonine kinase inhibitor, increased Zn-induced cell death. Furthermore, the phosphatidylinositol 3-Kinase (PI-3K) inhibitors, LY 294002 and wortmannin inhibited Zn-induced root cell death. These results suggest that the ROS, protein phosphatase and PI-3K may function in the Zn-induced cellular toxicity in rice roots.Abbreviations: MAPK -mitogen-activated protein kinase; PAO -phenylarsine oxide; PI-3K -phosphatidylinositol 3-kinase; ROS -reactive oxygen species; SB -sodium benzoate; Na 3 VO 4 -sodium orthovanadate; Zinc -Zn
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