文献类型： 外文期刊

作者： Wei, Aili ¹ ; Fu, Baocun ² ; Wang, Yunshan ² ; Zhai, Xiaoyan ¹ ; Xin, Xiaojing ³ ; Zhang, Chao ² ; Cao, Dongmei ² ; Zhang ¹ ;

作者机构： 1.Taiyuan Normal Univ, Dept Biol, Taiyuan 030031, Peoples R China

2.Shanxi Acad Agr Sci, Inst Hort, Taiyuan 030031, Peoples R China

3.Nankai Univ, Coll Life Sci, Dept Plant Biol & Ecol, Tianjin 300071, Peoples R China

关键词： SO2;NO;ROS;Tagetes erecta;Guard cell apoptosis

期刊名称：ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY （ 影响因子：6.291； 五年影响因子：6.393 ）

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收录情况： SCI

摘要： Both nitric oxide (NO) and reactive oxygen species (ROS) are very important signal molecules, but the roles they play in signal transduction of sulfur dioxide (SO2) induced toxicities on ornamental plants is not clear. In this study, the functions of NO and ROS in SO2-induced death of lower epidermal guard cells in ornamental plant Tagetes erecta were investigated. The results showed that SO2 derivatives (0.4-4.0 mmol L-1 of final concentrations) could reduce the guard cells' viability and increase their death rates in a dose-dependent manner. Meanwhile, the significant increase of cellular NO, ROS, and Ca2+ levels (P < 0.05) and typical apoptosis features including nucleus condensation, nucleus break and nucleus fragmentation were observed. However, exposure to 2.0 mmol L-1 of SO2 derivatives combined with either NO antagonists (NO scavenger c-PTIO; nitrate reductase inhibitor NaN3; NO synthase inhibitor L-NAME), ROS scavenger (AsA or CAT) or Ca2+ antagonists (Ca2+ scavenger EGTA or plasma membrane Ca2+ channel blocker Lads) can effectively block SO2-induced guard cells death and corresponding increase of NO, ROS and Ca2+ levels. In addition, addition of L-NAME or AsA in 2.0 mmol L-1 of SO2 derivatives led to significant decrease in the levels of NO, ROS and Ca2+, whereas addition of LaCI3 in them just resulted in the decrease of Ca2+ levels, hardly making effects on NO and ROS levels. It was concluded that NO and ROS were involved in the apoptosis induced by SO2 in T. erecta, which regulated the cell apoptosis at the upstream of Ca2+. (C) 2015 Elsevier Inc. All rights reserved.