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一氧化氮提高 S 同化和 GSH 产生,以防止镉胁迫对芥菜(芸薹属植物)光合作用的抑制作用。

Nitric oxide improves S-assimilation and GSH production to prevent inhibitory effects of cadmium stress on photosynthesis in mustard (Brassica juncea L.).

机构信息

Plant Physiology and Biochemistry Laboratory, Department of Botany, Aligarh Muslim University, Aligarh, 202002, U.P, India.

Plant Physiology and Biochemistry Laboratory, Department of Botany, Aligarh Muslim University, Aligarh, 202002, U.P, India.

出版信息

Nitric Oxide. 2017 Aug 1;68:111-124. doi: 10.1016/j.niox.2016.12.012. Epub 2016 Dec 25.

Abstract

Nitric oxide (NO) is an important gaseous signalling molecule that participates in many developmental and physiological processes, including defense responses against toxic metals in plants. The role of NO in cadmium (Cd)-induced toxic effects on photosynthesis was examined in mustard (Brassica juncea L.) plants. Exposure of plants to 50 μM Cd significantly enhanced oxidative stress (HO content and lipid peroxidation) and impaired plant growth and photosynthesis, chlorophyll fluorescence and reduced chlorophyll content and stomatal conductance. However, the exogenous application of 100 μM sodium nitroprusside (SNP, a donor of NO) reversed the effects of Cd through its stimulation of ROS-scavenging compounds (superoxide dismutase, ascorbate peroxidase, glutathione reductase and reduced glutathione). Exogenous SNP significantly increased plant growth, photosynthesis and chlorophyll content and diminished the accumulation of reactive oxygen species (HO) and TBARS content. It also reduced the effects of Cd on thylakoid membrane of the chloroplasts. Application of SNP together with 1.0 mM SO showed better responses than SNP alone. The protective effect of NO was achieved through enhanced production of reduced glutathione (GSH). GSH biosynthesis in plants treated with buthionine sulfoximine (BSO), a GSH biosynthetic inhibitor, was not completely inhibited in presence of NO and S, suggesting that NO stimulated S-assimilation and GSH production of Cd exposed plants. This study concludes that NO counteracts Cd toxicity in B. juncea strongly by regulating S-assimilation and GSH production.

摘要

一氧化氮(NO)是一种重要的气态信号分子,参与许多发育和生理过程,包括植物对有毒金属的防御反应。本研究探讨了一氧化氮在镉(Cd)诱导的光合作用毒性中的作用。将植物暴露于 50 μM Cd 可显著增强氧化应激(HO 含量和脂质过氧化),损害植物生长和光合作用、叶绿素荧光和降低叶绿素含量以及气孔导度。然而,100 μM 硝普钠(SNP,NO 的供体)的外源应用通过刺激 ROS 清除化合物(超氧化物歧化酶、抗坏血酸过氧化物酶、谷胱甘肽还原酶和还原型谷胱甘肽)逆转了 Cd 的作用。外源 SNP 显著增加了植物生长、光合作用和叶绿素含量,减少了活性氧(HO)和 TBARS 含量的积累。它还减轻了 Cd 对叶绿体类囊体膜的影响。与 SNP 单独应用相比,SNP 与 1.0 mM SO 一起应用具有更好的效果。NO 的保护作用是通过增强还原型谷胱甘肽(GSH)的产生来实现的。在存在 NO 和 S 的情况下,用谷胱甘肽生物合成抑制剂丁硫氨酸亚砜(BSO)处理的植物中的 GSH 生物合成并未完全被抑制,这表明 NO 刺激了 Cd 暴露植物的 S 同化和 GSH 产生。本研究得出结论,NO 通过调节 S 同化和 GSH 产生强烈拮抗 B. juncea 中的 Cd 毒性。

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