活性氧介导砷诱导的蚕豆保卫细胞死亡  

Involvement of ROS in Arsenic-Induced Guard Cell Death in Detached Epidermis of Vicia faba Leaves

作　　者：薛美昭[1] 仪慧兰[1] 

机构地区：[1]山西大学生命科学学院,太原030006

出　　处：《生态毒理学报》2013年第2期257-261,共5页Asian Journal of Ecotoxicology

基　　金：国家自然科学基金(30870454;30470318);教育部高等学校博士学科点基金(20070108007;20121401110007);山西省回国留学人员科研资助项目(2012013)

摘　　要：采用蚕豆(Vicia fabaL.)表皮条生物法,研究砷的细胞毒性作用机制。结果发现,一定浓度的NaAsO2可使气孔保卫细胞活性降低,部分细胞死亡,细胞死亡率呈浓度依赖性增高;砷处理组保卫细胞内活性氧(reactive oxygen species,ROS)水平升高。抗氧化剂抗坏血酸和过氧化氢酶及Ca2+特异性螯合剂EGTA、Ca2+通道抑制剂LaC13与NaAsO2共同作用时,砷诱发的细胞死亡被显著抑制;MAPK激酶抑制剂PD98059亦能有效阻止NaAsO2诱发的细胞死亡。研究结果表明,砷胁迫引起的胞内ROS合成增加可能通过Ca2+信号途径介导了保卫细胞的死亡过程,MAPK途径参与了砷诱导的细胞死亡。The stomatal guard cells from Vicia faba L. was selected to study the toxic mechanism of arsenic exposure. The results of cell viability analysis showed that NaAsO2 treatment significantly decreased cell viability in the concentration range of 0.3 to 10 mg·L-1. A synchronous increase in cell death rate and intracellular levels of ROS occurred in V. faba guard cells exposed to arsenic. Application of antioxidants ascorbic acid and catalase significantly inhibited As-induced cell death. Both Ca2+ chelating agent ethylene glycol bis-(2-aminoethyl)-tetraacetic acid and Ca2+ channel blocker LaCl3 decreased the cell death rate caused by NaAsO2. PD98059, a specific inhibitor of mitogen-activated protein kinase also significantly inhibited As-induced cell death, suggesting the involvement of MAPK in As-induced cell death. Results suggest that As-induced cell death of V. faba guard cells could be mediated by ROS generation through the activation of cytosolic Ca2+ signaling.

关 键 词：NaAsO2 细胞毒性 蚕豆保卫细胞 ROS CA2+ MAPK 

分 类 号：X171.5[环境科学与工程—环境科学]