Zinc-induced cell death in rice (Oryza sativa L.) roots

TLDR: Results suggest that the ROS, protein phosphatase and PI-3K may function in the Zn-induced cellular toxicity in rice roots.

Abstract: 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 time-dependent 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 (Na3VO4) 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.