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Integrated analysis of the detoxification responses of two Euramerican poplar genotypes exposed to ozone and water deficit: Focus on the ascorbate-glutathione cycle

机译:综合分析臭氧和水赤字暴露于臭氧和水赤字的两种欧洲人杨树基因型的排毒响应:专注于抗坏血酸 - 谷胱甘肽循环

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摘要

Ozone (O-3) and drought increase tree oxidative stress. To protect forest health, we need to improve risk assessment, using metric model such as the phytotoxic O-3 dose above a threshold of y nmol.m(-2).s(-1) (PODy), while taking into account detoxification mechanisms and interacting stresses. The impact of drought events on the effect of O-3 pollution deserves special attention. Water deficit may decrease O-3 entrance into the leaves by reducing stomatal opening; however, water deficit also induces changes in cell redox homeostasis. Besides, the behaviour of the cell antioxidative charge in case of stress combination (water deficit and O-3) still remains poorly investigated. To decipher the response of detoxification mechanisms relatively to the Halliwell-Asada-Foyer cycle (HAF), we exposed poplar saplings (Populus nigra x deltoides) composed of two genotypes (Carpaccio and Robusta), to various treatments for 17 days, i.e. i) mild water deficit, ii) 120 ppb O-3, and iii) a combination of these two treatments. Ozone similarly impacted the growth of the two genotypes, with an important leaf loss. Water deficit decreased growth by almost one third as compared to the control plants. As for the combined treatment, water deficit protected the saplings from leaf ozone injury, but with an inhibitory effect on growth. The pool of total ascorbate was not modified by the different treatments, while the pool of total glutathione increased with POD0. We noticed a few differences between the two genotypes, particularly concerning the activity of monodehydroascorbate reductase and glutathione reductase relatively to POD0. The expression profiles of genes coding for the dehydroascorbate reductase and glutathione reductase isoforms differed, probably in link with the putative localisation of ROS production in response to water deficit and ozone, respectively. Our result would argue for a major role of MDHAR, GR and glutathione in the preservation of the redox status. (C) 2018 Elsevier B.V. All rights reserved.
机译:臭氧(O-3)和干旱增加树氧化应激。为了保护森林健康,我们需要使用诸如植物毒性O-3剂量之类的度量模型来改善风险评估,例如在Y Nmol.m(-2)的阈值上方。(-1)(Pody),同时考虑解毒机制和相互作用的应力。干旱事件对O-3污染效果的影响值得特别关注。通过减少气孔开口,水赤字可以将O-3进入叶子进入叶子;然而,水缺陷也诱导细胞氧化还原稳态的变化。此外,在应力组合(水赤字和O-3)的情况下,细胞抗氧化充电的行为仍然仍然仍然很差。要解读排毒机制的响应相对哈里韦尔 - 亚拉达 - 门厅(HAF),我们暴露于由两种基因型(Carpaccio和Robusta)组成的杨树树苗(Populus nigra x Deltoides),对各种治疗组成17天,即i)温和的水缺陷,II)120 ppb O-3和III)这两种治疗的组合。臭氧同样影响了两种基因型的生长,具有重要的叶片损失。与对照植物相比,水赤字减少了近三分之一的增长。至于组合治疗,水分不足保护叶片损伤的树苗,但对生长抑制作用。抗坏血酸池池未被不同的治疗修饰,而总谷胱甘肽的池池与POD0增加。我们注意到两种基因型之间的几个差异,特别是关于莫达脱石血酸盐还原酶和谷胱甘肽还原酶相对的活性差异。编码用于脱氢血冰酸盐还原酶和谷胱甘肽还原酶同种型的基因的表达谱不同,可能与ROS产生的推定定位分别响应水缺陷和臭氧。我们的结果将争论Mdhar,GR和谷胱甘肽在保存氧化还原状态的主要作用。 (c)2018年elestvier b.v.保留所有权利。

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