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Priming of tomato seedlings with 2-oxoglutarate induces arsenic toxicity alleviatory responses by involving endogenous nitric oxide
Physiologia Plantarum ( IF 6.4 ) Pub Date : 2020-07-12 , DOI: 10.1111/ppl.13168
Saud Alamri 1 , Qasi D Alsubaie 1 , Abdullah A Al-Amri 1 , Bandar Al-Munqedi 1 , Hayssam M Ali 1 , Bishwajit K Kushwaha 2 , Vijay P Singh 2 , Manzer H Siddiqui 1
Affiliation  

Metal toxicity in crop plants is a matter of scientific concern. Therefore, in recent years efforts have been made to minimize metal toxicity in crop plants. Out of various strategies, priming of seedlings with certain chemicals, like e.g. donors of signaling molecules, nutrients, metabolites or plant hormones has shown encouraging results. However, mechanisms related with the priming-induced mitigation of metal toxicity are still poorly known. Hence, we have tested the potential of 2-oxoglutarate (2-OG) priming in enhancing the arsenate (AsV) toxicity tolerance in tomato seedlings along with deciphering the probable role of nitric oxide (NO) in accomplishing this task. Arsenate decreased growth, endogenous NO and nitric oxide synthase-like activity but enhanced the accumulation of As, which collectively led to root cell death. Arsenate toxicity also decreased some photosynthetic characteristics (i.e. Fv/Fm, qP, Fv/F0 and Fm/F0, and total chlorophyll content) but enhanced NPQ. However, priming with 2-OG alleviated the toxic effect of AsV on growth, endogenous NO, cell death and photosynthesis. Moreover, arsenate inhibited the activities of enzymes of nitrogen metabolism (i.e. nitrate reductase, nitrite reductase, glutamine synthetase and glutamine 2-oxoglutarate aminotransferase) but increased the activity of glutamate dehydrogenase and NH4+ content. Superoxide radicals, hydrogen peroxide, lipid peroxidation, protein oxidation and membrane damage increased upon AsV exposure, but the antioxidant enzymes (i.e. superoxide dismutase, catalase and glutathione-S-transferase) showed differential responses. Overall, our results showed that 2-OG is capable of alleviating AsV toxicity in tomato seedlings but the involvement of endogenous NO is probably required.

中文翻译:

2-酮戊二酸引发番茄幼苗通过内源性一氧化氮诱导砷毒性缓解反应

作物植物中的金属毒性是科学关注的问题。因此,近年来已努力使作物植物中的金属毒性最小化。在各种策略中,用某些化学品(例如信号分子、营养物、代谢物或植物激素的供体)启动幼苗已显示出令人鼓舞的结果。然而,与引发引发的金属毒性减轻相关的机制仍知之甚少。因此,我们测试了 2-氧戊二酸 (2-OG) 引发在增强砷酸盐(As V) 番茄幼苗的毒性耐受性,同时破译一氧化氮 (NO) 在完成这项任务中的可能作用。砷酸盐会降低生长、内源性 NO 和一氧化氮合酶样活性,但会增加 As 的积累,从而共同导致根细胞死亡。砷酸盐毒性还降低了一些光合特性(即 F v /F m、 qP、F v /F 0和 F m /F 0以及总叶绿素含量)但提高了 NPQ。然而,用 2-OG 引发减轻了 As V的毒性作用生长、内源性 NO、细胞死亡和光合作用。此外,砷酸盐抑制氮代谢酶(即硝酸还原酶、亚硝酸还原酶、谷氨酰胺合成酶和谷氨酰胺2-酮戊二酸氨基转移酶)的活性,但增加谷氨酸脱氢酶的活性和NH 4 +含量。超氧自由基、过氧化氢、脂质过氧化、蛋白质氧化和膜损伤在 As V暴露后增加,但抗氧化酶(即超氧化物歧化酶、过氧化氢酶和谷胱甘肽-S-转移酶)表现出不同的反应。总体而言,我们的结果表明 2-OG 能够减轻番茄幼苗中的As V毒性,但可能需要内源性 NO 的参与。
更新日期:2020-07-12
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