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首页> 外文OA文献 >Hydrogen sulfide is involved in the regulation of ascorbate-glutathione cycle by exogenous ABA in wheat seedling leaves under osmotic stress
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Hydrogen sulfide is involved in the regulation of ascorbate-glutathione cycle by exogenous ABA in wheat seedling leaves under osmotic stress

机译：渗透胁迫下硫化氢参与小麦幼苗叶片中外源ABA对抗坏血酸-谷胱甘肽循环的调节

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This study investigated the role of hydrogen sulfide (HS) in the regulation of ascorbateglutathione (AsA-GSH) cycle by exogenous ABA in wheat leaves under osmotic stress. The results showed that osmotic stress significantly increased the activities of ascorbate peroxidase (APX), glutathione reductase (GR), monodehydroascorbate reductase (MDHAR) and dehydroascorbate reductase (DHAR), the ratio of reduced ascorbate to oxidized ascorbate (AsA/DHA) and reduced glutathione to oxidized glutathione (GSH/GSSG), the malondialdehyde content and electrolyte leakage, and the HS content, compared to control. Exogenous ABA significantly increased above indicators under osmotic stress, compared to osmotic stress alone. Above activity increases except MDHAR activity were suppressed by application of HS scavenger hypotaurine (HT) and synthesis inhibitor aminooxyacetic acid (AOA). Meanwhile, exogenous ABA significantly decreased malondialdehyde content and electrolyte leakage induced by osmotic stress. Application of HT and AOA reversed above effects of application of exogenous ABA. Application of NaHS can reversed above effects of HT and AOA. Our results suggested that HS induced by exogenous ABA is a signal that leads to the up-regulation of AsA-GSH cycle.
机译：本研究研究了渗透胁迫下小麦叶片中外源ABA对硫化氢（HS）在抗坏血酸谷胱甘肽（AsA-GSH）循环调控中的作用。结果表明，渗透胁迫显着提高了抗坏血酸过氧化物酶（APX），谷胱甘肽还原酶（GR），单脱氢抗坏血酸还原酶（MDHAR）和脱氢抗坏血酸还原酶（DHAR）的活性，降低了抗坏血酸与氧化型抗坏血酸的比例（AsA / DHA）与对照相比，谷胱甘肽转为氧化型谷胱甘肽（GSH / GSSG），丙二醛含量和电解质渗漏以及HS含量。与单独的渗透胁迫相比，在渗透胁迫下外源ABA明显高于指标。通过使用HS清道夫次牛磺酸（HT）和合成抑制剂氨氧基乙酸（AOA）抑制了上述活性的增加，除了MDHAR活性。同时，外源ABA显着降低了由渗透胁迫引起的丙二醛含量和电解质泄漏。 HT和AOA的应用逆转了外源ABA的应用效果。 NaHS的使用可以逆转HT和AOA的上述作用。我们的结果表明，外源ABA诱导的HS是导致AsA-GSH周期上调的信号。

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    Shan, C.; Zhang, S.; Zhou, Y.;

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