An experimentation was carried out to appraise whether or not nitric oxide (NO) contributes to salicylic acid (SA)-induced salinity tolerance particularly by regulating ascorbate-glutathione (AsA-GSH) cycle. Before starting salinity stress (SS), SA (0.5 mM) was sprayed to the foliage of plants once every other day for a week and then seedlings were grown under control or SS (100 mM NaCl), for five weeks. Salinity stress enhanced the AsA-GSH cycle-related enzymes, glutathione reductase (GR), ascorbate peroxidase (APX), and dehydroascorbate reductase (DHAR), and monodehydroascorbate reductase (MDHAR). Furthermore, SS caused substantial decreases in plant physiological-related traits such as leaf potassium (K) contents, K+/Na+ ratio, the ratios of reduced ascorbate/dehydroascorbic acid (AsA/DHA) and reduced glutathione/oxidized glutathione (GSH/GSSG), but in contrast, significant increases occurred in leaf hydrogen peroxide, malondialdehyde, electron leakage, proline, the premier antioxidant enzymes' activities, Na+ and NO. SA reduced leaf Na+ content and oxidative stress-related traits, but improved all earlier-mentioned traits compared with those in plants treated with SS alone. All positive effects of SA were eliminated by NO scavenger, 0.1 mM 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1- oxyl-3-oxide (c-PTIO) by reducing NO, suggesting that NO produced by SA up-regulated the activities of AsA-GSH cycle and antioxidant enzymes, so it could play a central function as a signal molecule in salt tolerance of pepper plants.

中文翻译：

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内源性一氧化氮在水杨酸诱导的抗坏血酸-谷胱甘肽循环上调中的作用与辣椒植物的耐盐性有关。

进行了一项实验，以评估一氧化氮（NO）是否有助于水杨酸（SA）诱导的盐度耐受性，特别是通过调节抗坏血酸-谷胱甘肽（AsA-GSH）循环来进行。在开始盐分胁迫（SS）之前，每隔一天将SA（0.5 mM）喷洒到植物的叶子上，持续一周，然后在对照或SS（100 mM NaCl）下使幼苗生长五周。盐分胁迫增强了AsA-GSH循环相关的酶，谷胱甘肽还原酶（GR），抗坏血酸过氧化物酶（APX）和脱氢抗坏血酸还原酶（DHAR）和单脱氢抗坏血酸还原酶（MDHAR）。此外，SS引起植物生理相关性状的显着降低，例如叶钾（K）含量，K + / Na +比，抗坏血酸/脱氢抗坏血酸（AsA / DHA）减少比例以及谷胱甘肽/氧化型谷胱甘肽（GSH / GSSG）减少比例，但是相比之下，叶片中的过氧化氢，丙二醛，电子泄漏，脯氨酸，主要的抗氧化酶活性，Na +和NO显着增加。与单独使用SS处理的植物相比，SA减少了叶片Na +含量和与氧化胁迫相关的性状，但改善了所有较早提及的性状。NO清除剂，0.1 mM 2-（4-羧基苯基）-4,4,5,5-四甲基咪唑啉-1-氧基-3-氧化物（c-PTIO）通过还原NO消除了SA的所有积极作用，表明NO SA产生的上调了AsA-GSH循环和抗氧化酶的活性，因此它在辣椒植物的耐盐性中起着信号分子的核心作用。活动，Na +和NO。与单独使用SS处理的植物相比，SA减少了叶片Na +含量和与氧化胁迫相关的性状，但改善了所有较早提及的性状。NO清除剂，0.1 mM 2-（4-羧基苯基）-4,4,5,5-四甲基咪唑啉-1-氧基-3-氧化物（c-PTIO）通过还原NO消除了SA的所有积极作用，表明NO SA产生的上调了AsA-GSH循环和抗氧化酶的活性，因此它在辣椒植物的耐盐性中起着信号分子的核心作用。活动，Na +和NO。与单独使用SS处理的植物相比，SA减少了叶片Na +含量和与氧化胁迫相关的性状，但改善了所有较早提及的性状。NO清除剂，0.1 mM 2-（4-羧基苯基）-4,4,5,5-四甲基咪唑啉-1-氧基-3-氧化物（c-PTIO）通过还原NO消除了SA的所有积极作用，表明NO SA产生的上调了AsA-GSH循环和抗氧化酶的活性，因此它在辣椒植物的耐盐性中起着信号分子的核心作用。