Song Kejin, Li Hongwei, Yang Kunjian, Ma Tengfei, Hu Yingying, Chen Ji, Zhu Shunqin, Liu Wanhong
School of Chemistry and Chemical Engineering, Chongqing University of Science and Technology, Chongqing, 401331, China.
School of Life Science, Southwest University, Chongqing, 400715, China.
Nitric Oxide. 2025 Feb;154:8-18. doi: 10.1016/j.niox.2024.11.002. Epub 2024 Nov 14.
As a donor of the gaseous signaling molecule nitric oxide (NO), sodium nitroprusside (SNP) has been shown to play a positive role in enhancing plant resistance to abiotic stress. However, its role in alleviating cadmium (Cd) toxicity in tobacco (Nicotiana tabacum L.) is not fully understood. This study found that Cd stress significantly inhibited tobacco growth. At the same time, 150 μM SNP was the most effective concentration in alleviating Cd toxicity in seedlings, restoring three stress tolerance indicators-MDA, HO, and proline-to control levels. Exogenous SNP mitigated Cd-induced oxidative stress by promoting the accumulation of non-enzymatic antioxidants (total phenolics and flavonoids) and activating key antioxidant enzymes (SOD, CAT, POD, APX, and GR) along with their gene expression. SNP also facilitated Cd accumulation in the root cell wall and prevented Cd translocation from roots to shoots. Additionally, SNP altered Cd's subcellular distribution, promoting its sequestration in vacuoles and cell walls, which may be related to the NO-mediated upregulation of the metallothionein gene NtMT2F and the phytochelatin gene NtPCS2. The addition of SNP significantly increased the proportion of Cd in less toxic chemical forms, with the residual Cd fraction in the Cd + SNP group reaching 7.30 %, higher than the 4.86 % in the Cd-only group. Furthermore, exogenous SNP counteracted Cd's inhibition of nitrate reductase (NR) activity, promoting endogenous NO production. This study systematically reveals the positive roles of exogenous SNP in mitigating Cd toxicity in tobacco, offering valuable insights for producing low-Cd tobacco.
作为气态信号分子一氧化氮(NO)的供体,硝普钠(SNP)已被证明在增强植物对非生物胁迫的抗性方面发挥积极作用。然而,其在缓解烟草(Nicotiana tabacum L.)镉(Cd)毒性方面的作用尚未完全明确。本研究发现,Cd胁迫显著抑制烟草生长。同时,150 μM SNP是缓解幼苗Cd毒性、将丙二醛(MDA)、过氧化氢(HO)和脯氨酸这三个胁迫耐受指标恢复到对照水平的最有效浓度。外源SNP通过促进非酶抗氧化剂(总酚和类黄酮)的积累以及激活关键抗氧化酶(超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、过氧化物酶(POD)、抗坏血酸过氧化物酶(APX)和谷胱甘肽还原酶(GR))及其基因表达,减轻了Cd诱导的氧化应激。SNP还促进了Cd在根细胞壁中的积累,并阻止了Cd从根向地上部的转运。此外,SNP改变了Cd的亚细胞分布,促进其在液泡和细胞壁中的螯合,这可能与NO介导的金属硫蛋白基因NtMT2F和植物螯合肽基因NtPCS2的上调有关。添加SNP显著增加了毒性较小的化学形态中Cd的比例,Cd + SNP组中残留Cd比例达到7.30%,高于仅Cd组的4.86%。此外,外源SNP抵消了Cd对硝酸还原酶(NR)活性的抑制,促进了内源性NO的产生。本研究系统地揭示了外源SNP在缓解烟草Cd毒性方面的积极作用,为生产低Cd烟草提供了有价值的见解。