Changes in the antioxidant systems as part of the signaling pathway responsible for the programmed cell death activated by nitric oxide and reactive oxygen species in tobacco Bright-Yellow 2 cells
Changes in the antioxidant systems as part of the signaling pathway responsible for the programmed cell death activated by nitric oxide and reactive oxygen species in tobacco Bright-Yellow 2 cells
复制标题
DOI：
10.1104/pp.005629
复制
发表时间：
2002-10-01
期刊：
影响因子：
7.4
通讯作者：
De Gara, L
中科院分区：
文献类型：
--
作者：
de Pinto, MC;Tommasi, F;De Gara, L
一氧化氮（NO）与活性氧（ROS）一起被认为是激活植物过敏反应所必需的，过敏反应是在不相容的植物-病原体相互作用中诱导的一种防御反应。然而，其参与激活植物细胞中的程序性细胞死亡（PCD）受到质疑。在本文中，参与的细胞抗氧化代谢的信号转导所触发的这些生物活性分子进行了研究。通过向培养基中加入NO和/或ROS发生器，烟草（Nicotiana tabacum cv N-Yellow 2）细胞中的NO和ROS水平单独或同时增加。NO或ROS的单独增加对所研究的参数有不同的影响，而不是同时增加两种活性物质。NO的产生并没有引起苯丙氨酸解氨酶（PAL）活性的增加或诱导细胞死亡。它只引起抗坏血酸（ASC）和谷胱甘肽（GSH）代谢的微小变化。ROS的增加诱导细胞中的氧化应激，导致ASC和GSH氧化还原对的氧化;然而，它对PAL活性没有影响，并且当它在低浓度下产生时不会诱导细胞死亡。与此相反，同时增加NO和ROS激活的死亡过程与典型的细胞学和生化特征的超敏感的PCD和PAL活性显着上升。在同时产生NO和ROS的情况下，细胞的抗氧化能力也受到抑制。ASC和GSH作为导致PCD的转导途径的一部分的参与进行了讨论。
Nitric oxide (NO) has been postulated to be required, together with reactive oxygen species (ROS), for the activation of the hypersensitive reaction, a defense response induced in the noncompatible plant-pathogen interaction. However, its involvement in activating programmed cell death (PCD) in plant cells has been questioned. In this paper, the involvement of the cellular antioxidant metabolism in the signal transduction triggered by these bioactive molecules has been investigated. NO and ROS levels were singularly or simultaneously increased in tobacco (Nicotiana tabacum cv Bright-Yellow 2) cells by the addition to the culture medium of NO and/or ROS generators. The individual increase in NO or ROS had different effects on the studied parameters than the simultaneous increase in the two reactive species. NO generation did not cause an increase in phenylalanine ammonia-lyase (PAL) activity or induction of cellular death. It only induced minor changes in ascorbate (ASC) and glutathione (GSH) metabolisms. An increase in ROS induced oxidative stress in the cells, causing an oxidation of the ASC and GSH redox pairs; however, it had no effect on PAL activity and did not induce cell death when it was generated at low concentrations. In contrast, the simultaneous increase of NO and ROS activated a process of death with the typical cytological and biochemical features of hypersensitive PCD and a remarkable rise in PAL activity. Under the simultaneous generation of NO and ROS, the cellular antioxidant capabilities were also suppressed. The involvement of ASC and GSH as part of the transduction pathway leading to PCD is discussed.