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

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), increa...

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Bibliographic Details
Published in:Plant growth regulation 2005-07, Vol.46 (3), p.261-266
Main Authors: Chang, H.B, Lin, C.W, Huang, H.J
Format: Article
Language:English
Subjects:
Apoptosis
Cells
enzyme activity
enzyme inhibitors
Inhibitors
mitogen-activated protein kinase
Mortality
Oryza sativa
phenylarsine oxide
phosphatidylinositol 3-kinase
phosphorylation
phytotoxicity
protein kinases
Proteins
reactive oxygen species
rice
Roots
Rotenone
signal transduction
Sodium
sodium benzoate
sodium orthovanadate
Zinc
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Summary: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 (Na^sub 3^VO^sub 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.[PUBLICATION ABSTRACT]
ISSN:0167-6903
1573-5087
DOI:10.1007/s10725-005-0162-0