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首页> 外文期刊>Journal of Plant Growth Regulation >Hydrogen Sulfide Protects Damage From Methyl Viologen-Mediated Oxidative Stress by Improving Gas Exchange, Fluorescence Kinetics of Photosystem II, and Antioxidant System in Arabidopsis thaliana
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Hydrogen Sulfide Protects Damage From Methyl Viologen-Mediated Oxidative Stress by Improving Gas Exchange, Fluorescence Kinetics of Photosystem II, and Antioxidant System in Arabidopsis thaliana

机译:硫化氢通过改善拟南芥的气体交换、光系统II的荧光动力学和抗氧化系统来保护甲基紫罗兰介导的氧化应激的损伤

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Considering the unfavorable impacts of methyl viologen-induced oxidative stress (MV1-2, 50 and 500 mu M) on growth, gas exchange (intercellular CO2 concentration, carbon assimilation rate, stomatal conductance, transpiration rate), the efficiency of PSII photochemistry and gene expressions of proteins related to photosystems, antioxidant capacity, and the content/histochemical staining of reactive oxygen species (ROS) markers, the experiment was conducted to evaluate the possible mechanisms of sodium hydrosulfide hydrate (a hydrogen sulfide donor, 500 mu M NaHS) and its scavenger/inhibitor (hypotaurine, 50 mu M and hydroxylamine, 100 mu M) in Arabidopsis thaliana for 24 h. NaHS alleviated stress-reduced growth (4.2-fold increase for MV2 + NaHS) and improved the gas exchange parameters. NaHS was capable of improving the photosynthetic ability under 50 mu M MV through sustaining photochemical activity in PSII and photochemical conversion efficiency as evident by transcript levels of psbA, psbD, psaA, and psaB. Stress-caused oxidative damage was scavenged by POX (a 90 increase). However, this action was not enough, suggested by increased ROS accumulation, lipid peroxidation (a 165 induction) and lipoxygenase activity (2.4-fold increase), and loss of membrane integrity. Meanwhile, NaHS successfully eliminated these responses against MV, evidenced by weak histochemical staining of ROS and lesser lipid peroxidation and membrane damage. The synchronized activities of both SOD and CAT triggered by NaHS were responsible for decreasing H2O2 content (by 57.4 decrease for MV2 + NaHS) in response to MV stress. After stress exposure, NaHS utilized the ascorbate-glutathione (AsA-GSH) cycle for removing H2O2. Arabidopsis subjected to MV1 plus NaHS exhibited the advanced levels of AsA regeneration (by 15.3 increase) and the redox state of GSH. Interestingly, NaHS under the high MV concentration did not maintain the re-establishment of GSH homeostasis and redox state of GSH in spite of the induced AsA/DHA (dehydroascorbate). NaHS could protect Arabidopsis from oxidative stress, likely by regulating growth, gas exchange, and photosynthetic performance, inducing expression levels of genes associated with photosystems and regulating antioxidant capacity, and redox balance for AsA and GSH.
机译:考虑甲基紫精诱导的氧化应激(MV1-2、50和500 μ M)对生长、气体交换(胞间CO2浓度、碳同化速率、气孔导度、蒸腾速率)、PSII光化学效率和光系统相关蛋白基因表达、抗氧化能力、活性氧(ROS)标记物含量/组织化学染色等的不利影响,研究了其可能的机制硫氢化钠水合物(硫化氢供体,500μM NaHS)及其清除剂/抑制剂(次牛磺酸,50μM和羟胺,100μM)在拟南芥中24小时。NaHS缓解了应力降低的生长(MV2 + NaHS增加了4.2倍)并改善了气体交换参数。NaHS通过维持PSII的光化学活性和光化学转化效率,提高了50 μ M MV下的光合能力,psbA、psbD、psaA和psaB的转录水平可见一斑。应激引起的氧化损伤被 POX 清除(增加 90%)。然而,这种作用还不够,ROS积累增加,脂质过氧化(诱导165%)和脂氧合酶活性(增加2.4倍)以及膜完整性丧失。同时,NaHS成功地消除了这些对MV的反应,ROS的组织化学染色较弱,脂质过氧化和膜损伤较小。NaHS触发的SOD和CAT的同步活性是MV胁迫下H2O2含量降低的原因(MV2 + NaHS降低57.4%)。在应激暴露后,NaHS利用抗坏血酸-谷胱甘肽(AsA-GSH)循环去除H2O2。MV1加NaHS的拟南芥表现出AsA再生的先进水平(增加15.3%)和GSH的氧化还原状态。有趣的是,尽管诱导了AsA/DHA(脱氢抗坏血酸),但在高MV浓度下的NaHS并没有维持GSH稳态的重建和GSH的氧化还原状态。NaHS可以通过调节生长、气体交换和光合性能、诱导与光系统相关的基因表达水平和调节抗氧化能力以及AsA和GSH的氧化还原平衡来保护拟南芥免受氧化应激。

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