Nitric oxide modulates cadmium influx during cadmium-induced programmed cell death in tobacco BY-2 cells
Nitric oxide modulates cadmium influx during cadmium-induced programmed cell death in tobacco BY-2 cells
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一氧化氮在镉诱导的烟草 BY-2 细胞程序性细胞死亡过程中调节镉流入
DOI：
10.1007/s00425-010-1177-y
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发表时间：
2010-07-01
期刊：
影响因子：
4.3
通讯作者：
Ma, Mi
中科院分区：
文献类型：
--
作者：
Ma, Wenwen;Xu, Wenzhong;Ma, Mi
一氧化氮（NO）是一种生物活性气体，在植物受到包括镉（Cd（2+））在内的多种生物和非生物胁迫时起信号分子的作用。Cd（2+）是一种非必需的有毒重金属，可诱导植物细胞程序性死亡（PCD）。本文研究了NO在Cd（2+）诱导烟草BY-2细胞PCD中的作用。CV.亮黄色2）。在这项工作中，BY-2细胞暴露于150 μ M CdCl（2）后发生PCD，细胞核TUNEL阳性，染色质明显浓缩，PCD相关基因Hsr 203 J表达增加。随着PCD的发生，NO的产生明显增加。硝普钠（SNP）补充NO可促进PCD的发生，而NO合成酶抑制剂N ω-硝基-L-精氨酸甲酯盐酸盐（l-NAME）和NO特异性清除剂2-（4-羧基苯基）-4，4，5，5-四甲基咪唑啉-1-氧-3-氧化物（cPTIO）可减轻这种毒性。为了探讨NO发挥其作用的机制，随后测定了Cd（2+）浓度。SNP处理的Cd（2+）含量高于单独Cd（2+）处理。相反，用l-NAME抑制NO则可减少Cd（2+）的积累。采用扫描离子选择电极技术，分析了Cd（2+）的迁移模式和迁移速率。结果表明，SNP可促进Cd（2+）的内流，而l-NAME和cPTIO可降低Cd（2+）的吸收速率，甚至导致Cd（2+）的净流出。NO通过调节BY-2细胞对Cd（2+）的摄取，促进Cd（2+）的积累，在CdCl（2）诱导的PCD中发挥积极作用。
Nitric oxide (NO) is a bioactive gas and functions as a signaling molecule in plants exposed to diverse biotic and abiotic stresses including cadmium (Cd(2+)). Cd(2+) is a non-essential and toxic heavy metal, which has been reported to induce programmed cell death (PCD) in plants. Here, we investigated the role of NO in Cd(2+)-induced PCD in tobacco BY-2 cells (Nicotiana tabacum L. cv. Bright Yellow 2). In this work, BY-2 cells exposed to 150 mu M CdCl(2) underwent PCD with TUNEL-positive nuclei, significant chromatin condensation and the increasing expression of a PCD-related gene Hsr203J. Accompanied with the occurring of PCD, the production of NO increased significantly. The supplement of NO by sodium nitroprusside (SNP) had accelerated the PCD, whereas the NO synthase inhibitor N omega-nitro-l-arginine methyl ester hydrochloride (l-NAME) and NO-specific scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) alleviated this toxicity. To investigate the mechanism by which NO exerted its function, Cd(2+) concentration was measured subsequently. SNP led more Cd(2+) content than Cd(2+) treatment alone. By contrast, the prevention of NO by l-NAME decreased Cd(2+) accumulation. Using the scanning ion-selective electrode technique, we analyzed the pattern and rate of Cd(2+) fluxes. This analysis revealed the promotion of Cd(2+) influxes into cells by application of SNP, while l-NAME and cPTIO reduced the rate of Cd(2+) uptake or even resulted in net Cd(2+) efflux. Based on these founding, we concluded that NO played a positive role in CdCl(2)-induced PCD by modulating Cd(2+) uptake and thus promoting Cd(2+) accumulation in BY-2 cells.