Zheng Qianqian, Yang Lu, Xin Jianpan, Zhao Chu, Li Yan, Tian Runan
College of Architecture Landscape, Nanjing Forestry University, Nanjing, 210037, Jiangsu, China.
College of Architecture Landscape, Nanjing Forestry University, Nanjing, 210037, Jiangsu, China.
Plant Physiol Biochem. 2025 Jul;224:109940. doi: 10.1016/j.plaphy.2025.109940. Epub 2025 Apr 22.
Exogenous salicylic acid (SA) enhances plant tolerance to cadmium (Cd) stress by preserving chlorophyll, stabilizing osmoprotectants, and upregulating antioxidant activity alongside the ASA-GSH system. However, the role of endogenous SA in plant tolerance to Cd stress remains poorly understood. Therefore, we cultivated Monochoria korsakowii hydroponically and sprayed the SA biosynthesis inhibitors (2-aminoindane-2-phosphonic acid and 1-aminobenzotriazole) in an attempt to explore the correlation between endogenous SA and other Cd tolerance mechanisms. Compared with control, 0.3 mM Cd treatment induced reductions of net photosynthetic rate (Pn), total chlorophyll (T Chl), catalase (CAT), and soluble protein (SP), while malondialdehyde increased. To mitigate Cd toxicity, M. korsakowii upregulated peroxidase (POD), superoxide dismutase (SOD), glutathione reductase (GR), ascorbic acid (ASA), nonprotein thiols (NPT), phytochelatin (PC), and proline. High concentrations of SA inhibitors exacerbated Cd-induced oxidative damage and suppressed these tolerance mechanisms. Compared with T4, T6 plants exhibited marked reductions in Pn, T Chl, CAT, POD, SOD, GSH, GR, ASA, ascorbate peroxidase, NPT, PCs, SP, and translocation factors. Concurrently, T6 plants sprayed with SA inhibitors exhibited suppressed SA, methyl salicylate, and zeatin accumulation, contrasting with heightened jasmonic acid and abscisic acid concentrations. We propose that endogenous SA is crucial for preserving the photosynthetic apparatus, activating the antioxidant system, and promoting the accumulation of chelators and SP in M. korsakowii under Cd stress. Furthermore, endogenous SA may function synergistically with methyl salicylate and zeatin to regulate plant physiological responses to Cd. This study provides valuable insights into the Cd tolerance mechanisms in M. korsakowii.
外源水杨酸（SA）通过保护叶绿素、稳定渗透保护剂以及上调抗氧化活性和抗坏血酸-谷胱甘肽（ASA-GSH）系统来增强植物对镉（Cd）胁迫的耐受性。然而，内源SA在植物对Cd胁迫耐受性中的作用仍知之甚少。因此，我们水培了雨久花，并喷施了SA生物合成抑制剂（2-氨基茚-2-膦酸和1-氨基苯并三唑），以探索内源SA与其他Cd耐受机制之间的相关性。与对照相比，0.3 mM Cd处理导致净光合速率（Pn）、总叶绿素（T Chl）、过氧化氢酶（CAT）和可溶性蛋白（SP）降低，而丙二醛增加。为减轻Cd毒性，雨久花上调了过氧化物酶（POD）、超氧化物歧化酶（SOD）、谷胱甘肽还原酶（GR）、抗坏血酸（ASA）、非蛋白硫醇（NPT）、植物螯合肽（PC）和脯氨酸。高浓度的SA抑制剂加剧了Cd诱导的氧化损伤并抑制了这些耐受机制。与T4相比，T6植株的Pn、T Chl、CAT、POD、SOD、GSH、GR、ASA、抗坏血酸过氧化物酶、NPT、PCs、SP和转运因子显著降低。同时，喷施SA抑制剂的T6植株的SA、水杨酸甲酯和玉米素积累受到抑制，而茉莉酸和脱落酸浓度升高。我们认为，内源SA对于在Cd胁迫下保护雨久花的光合机构、激活抗氧化系统以及促进螯合剂和SP的积累至关重要。此外，内源SA可能与水杨酸甲酯和玉米素协同作用，调节植物对Cd的生理反应。本研究为雨久花的Cd耐受机制提供了有价值的见解。
