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Lanthanum Prevents Salt Stress-induced Programmed Cell Death in Rice Root Tip Cells by Controlling Early Induction Events

Lanthanum Prevents Salt Stress-induced Programmed Cell Death in Rice Root Tip Cells by Controlling Early Induction Events

作     者:Jian-You Li Ai-Liang Jiang Hai-Yan Chen Ying Wang Wei Zhang 

作者机构:Department of Biochemistry and Molecular Biology College of Life Science Nanjing Agricultural University Nanjing 210095 China 

出 版 物:《Journal of Integrative Plant Biology》 (植物学报(英文版))

年 卷 期:2007年第49卷第7期

页      面:1024-1031页

核心收录:

学科分类:09[农学] 0901[农学-作物学] 

基  金:Supported by the National Natural Science Foundation of China (30400030.) and the Grant to Innovative Young Scholars of Jiangsu Province (BK 2004416.) 

主  题:Ca^2+ Oryza sativa programmed cell death reactive oxygen species salt stress. 

摘      要:In a previous study, a salt stress-induced programmed cell death (PCD) model was established in rice root tip cells. Here, by using Wuyunjing 8th rice seedlings, the effects of lanthanum on salt stress-induced PCD early events were studied. The results indicated that low concentrations (10 μmol/L), but not high concentrations (100 μmol/L) of LaCl3 could effectively prevent salt stress-induced PCD. Further study demonstrated that in the early stages of salt-induced PCD process, 10 μmol/L of La^3+ could prevent the increase of cytoplasmic calcium levels, inhibit reactive oxygen species (ROS) production, and enhance the ROS-scavenging enzyme activities such as superoxide dismutases (SOD) and ascorbate peroxidase (APX). Imidazole (20 mmol/L), the inhibitor of nicotinamide adenine dinucleotide phosphate-oxidase (NADPH oxidase), could alleviate the occurrence of PCD obviously, and such alleviation could be enhanced by the addition of La^3+, indicating the involvement of NADPH oxidase in the salt stress-induced PCD process. Taken together, lanthanum could prevent salt stress-induced PCD occurrence in the rice root tip cells by blocking the calcium influx under stress, which was followed by inhibiting calcium-dependent NADPH oxidase activity to prevent O2^·- production and, enhancing the cytosolic antioxidative enzyme activities to scavenge the reactive oxygen species.

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