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系统性 HO 信号介导表没食子儿茶素没食子酸酯诱导的番茄镉耐受性。

Systemic HO signaling mediates epigallocatechin-3-gallate-induced cadmium tolerance in tomato.

机构信息

State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-Products, Institute of Vegetables, Zhejiang Academy of Agricultural Sciences, Hangzhou 310021, PR China.

Key Laboratory of Tea Quality and Safety Control, Ministry of Agriculture and Rural Affairs, Tea Research Institute, Chinese Academy of Agricultural Sciences, Hangzhou 310008, PR China.

出版信息

J Hazard Mater. 2022 Sep 15;438:129511. doi: 10.1016/j.jhazmat.2022.129511. Epub 2022 Jul 2.

DOI:10.1016/j.jhazmat.2022.129511
PMID:35809367
Abstract

Toxic heavy metal cadmium (Cd) reduces crop yield and threatens human health via the food chain. The bioactive flavonoid 'Epigallocatechin-3-gallate' (EGCG) affects plant stress response; however, the function of EGCG in Cd tolerance and the molecular pathways remain largely unknown. Here, we revealed that root application of EGCG alleviated Cd stress in tomato plants. While Cd stress decreased Fv/Fm, Ф, photosynthetic rate, root growth, root vitality and biomass accumulation by increasing reactive oxygen species (ROS) accumulation and lipid peroxidation, exogenous EGCG minimized excessive ROS accumulation and oxidative stress by promoting the activity of antioxidant enzymes and redox poise in roots and leaves. Moreover, EGCG induced the transcript of RESPIRATORY BURST OXIDASE HOMOLOG1 (RBOH1) and decreased Cd content and photoinhibition in leaves. Interestingly, similar to EGCG, exogenous HO application also enhanced Cd tolerance; however, the application of an NADPH oxidase inhibitor, diphenyleneiodonium (DPI), aggravated Cd phytotoxicity and attenuated the beneficial effects of EGCG on plant tolerance to Cd stress, suggesting that root applied EGCG-induced expression of RBOH1 and associated HO signaling mediate the EGCG-induced enhanced Cd tolerance. This work elucidates a fundamental mechanism behind EGCG-mediated Cd tolerance and contributes to our existing knowledge of stress resistance properties of EGCG in plants.

摘要

有毒重金属镉(Cd)通过食物链降低作物产量并威胁人类健康。生物活性黄酮类化合物“表没食子儿茶素-3-没食子酸酯”(EGCG)影响植物的应激反应;然而,EGCG 在 Cd 耐受中的功能及其分子途径在很大程度上仍是未知的。在这里,我们揭示了根施 EGCG 可缓解番茄植株的 Cd 胁迫。虽然 Cd 胁迫通过增加活性氧(ROS)积累和脂质过氧化作用降低了 Fv/Fm、Ф、光合速率、根生长、根活力和生物量积累,但外施 EGCG 通过促进抗氧化酶和氧化还原平衡在根和叶中的活性,最大限度地减少了过量的 ROS 积累和氧化应激。此外,EGCG 诱导 RESPIRATORY BURST OXIDASE HOMOLOG1(RBOH1)的转录,并降低叶片中的 Cd 含量和光抑制。有趣的是,与 EGCG 相似,外源 HO 的应用也增强了 Cd 耐受性;然而,NADPH 氧化酶抑制剂二苯基碘(DPI)的应用加剧了 Cd 的植物毒性,并削弱了 EGCG 对植物耐受 Cd 胁迫的有益作用,表明根施 EGCG 诱导的 RBOH1 表达和相关的 HO 信号转导介导了 EGCG 诱导的增强的 Cd 耐受性。这项工作阐明了 EGCG 介导的 Cd 耐受的基本机制,并为我们现有的关于 EGCG 在植物中的应激抗性特性的知识做出了贡献。

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