Nitric Oxide Alleviates Iron Toxicity by Reducing Oxidative Damage and Growth Inhibition in Wheat (Triticum aestivum L.) Seedlings

2019 ◽  
Vol 5 (01) ◽  
pp. 16-22
Author(s):  
Nalini Pandey ◽  
Laxmi Verma
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Oxidative Damage ◽  
Sodium Nitroprusside ◽  
Dry Weight ◽  
Triticum Aestivum L ◽  
Tolerance Index ◽  
Promoting Effect ◽  
Wheat Seedlings ◽  
Protein Thiols

Nitric oxide (NO) is an important bioactive signaling molecule in plants which modulates a variety of physiological processes and responses to abiotic and biotic stresses. In this study, the effects of exogenous NO supplied as sodium nitroprusside (SNP) in wheat seedlings under ironinduced oxidative damage was investigated. An appropriate concentration of NO was determined by conducting a preliminary experiment. In solution culture, wheat seeds were grown in the control (100 μM Fe), and toxic Fe (400 μM Fe) levels and the toxic Fe supply was treated with various levels of (50, 100, 200 and 500 μM) sodium nitroprusside (SNP). The results indicated that 400 μM Fe significantly decreased percentage germination, tolerance index, root lengths as well as fresh and dry weight compared to control. Exogenous SNP attenuated the inhibition of wheat seed germination. The promoting effect was most pronounced at 100 μM SNP. The accumulated concentration of iron and active Fe was significantly decreased by SNP treated Fe toxic seedlings. Toxicity of Fe caused oxidative stress by elevating hydrogen peroxide (H2O2), malondialdehyde (MDA) and proline contents in roots of wheat seedlings. One hundred μM SNP counteracted Fe toxicity by reducing the H2O2, MDA and proline contents of toxic Fe exposed seedlings. Meanwhile, application of SNP markedly reduced the activities of superoxide dismutases (SOD), catalases (CAT), peroxidase (POD), ascorbate peroxidases (APX), non protein thiols (NPT) and of glutathione reductase (GR) and increased ascorbate (ASc) compared with Fe toxic treatment alone, thereby indicating the modulation of the antioxidative capacity in the root under Fe stress by NO. The results indicated that the exogenous application of SNP, improved the antioxidant enzymes activity of wheat seedlings against Fe induced oxidative stress.

scholarly journals Seribiodiversity and their Role in Sustainable Development in India

2019 ◽  
Vol 5 (04) ◽  
pp. 243-246
Author(s):  
Debnirmalya Gangopadhyay ◽  
Ashmita Ghosh ◽  
Mrinal Ray
Keyword(s):  
Oxidative Stress ◽  
Sodium Nitroprusside ◽  
Dry Weight ◽  
Solution Culture ◽  
Tolerance Index ◽  
Promoting Effect ◽  
Wheat Seedlings ◽  
Biotic Stresses ◽  
Protein Thiols ◽  
Fe Toxicity

Nitric oxide (NO) is an important bioactive signaling molecule in plants which modulates a variety of physiological processes and responses to abiotic and biotic stresses. In this study, the effects of exogenous NO supplied as sodium nitroprusside (SNP) in wheat seedlings under ironinduced oxidative damage was investigated. An appropriate concentration of NO was determined by conducting a preliminary experiment. In solution culture, wheat seeds were grown in the control (100 μM Fe), and toxic Fe (400 μM Fe) levels and the toxic Fe supply was treated with various levels of (50, 100, 200 and 500 μM) sodium nitroprusside (SNP). The results indicated that 400 μM Fe significantly decreased percentage germination, tolerance index, root lengths as well as fresh and dry weight compared to control. Exogenous SNP attenuated the inhibition of wheat seed germination. The promoting effect was most pronounced at 100 μM SNP. The accumulated concentration of iron and active Fe was significantly decreased by SNP treated Fe toxic seedlings. Toxicity of Fe caused oxidative stress by elevating hydrogen peroxide (H2O2), malondialdehyde (MDA) and proline contents in roots of wheat seedlings. One hundred μM SNP counteracted Fe toxicity by reducing the H2O2, MDA and proline contents of toxic Fe exposed seedlings. Meanwhile, application of SNP markedly reduced the activities of superoxide dismutases (SOD), catalases (CAT), peroxidase (POD), ascorbate peroxidases (APX), non protein thiols (NPT) and of glutathione reductase (GR) and increased ascorbate (ASc) compared with Fe toxic treatment alone, thereby indicating the modulation of the antioxidative capacity in the root under Fe stress by NO. The results indicated that the exogenous application of SNP, improved the antioxidant enzymes activity of wheat seedlings against Fe induced oxidative stress.

scholarly journals Effect of Shuangdan Mingmu capsule, a Chinese herbal formula, on oxidative stress-induced apoptosis of pericytes through PARP/GAPDH pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Fujiao Nie ◽  
Jiazhao Yan ◽  
Yanjun Ling ◽  
Zhengrong Liu ◽  
Chaojun Fu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Oxidative Damage ◽  
Damage Model ◽  
B Cell Lymphoma ◽  
Cell Counting ◽  
Network Pharmacology ◽  
Diabetic Patients ◽  
Induced Apoptosis

Abstract Background Diabetic retinopathy (DR) has become a worldwide concern because of the rising prevalence rate of diabetes mellitus (DM). Despite much energy has been committed to DR research, it remains a difficulty for diabetic patients all over the world. Since apoptosis of retinal microvascular pericytes (RMPs) is the early characteristic of DR, this study aimed to reveal the mechanism of Shuangdan Mingmu (SDMM) capsule, a Chinese patent medicine, on oxidative stress-induced apoptosis of pericytes implicated with poly (ADP-ribose) polymerase (PARP) / glyceraldehyde 3-phosphate dehydrogenase (GAPDH) pathway. Methods Network pharmacology approach was performed to predict biofunction of components of SDMM capsule dissolved in plasma on DR. Both PARP1 and GAPDH were found involved in the hub network of protein-protein interaction (PPI) of potential targets and were found to take part in many bioprocesses, including responding to the regulation of reactive oxygen species (ROS) metabolic process, apoptotic signaling pathway, and response to oxygen levels through enrichment analysis. Therefore, in vitro research was carried out to validate the prediction. Human RMPs cultured with media containing 0.5 mM hydrogen oxide (H2O2) for 4 h was performed as an oxidative-damage model. Different concentrations of SDMM capsule, PARP1 inhibitor, PARP1 activation, and GAPDH inhibitor were used to intervene the oxidative-damage model with N-Acetyl-L-cysteine (NAC) as a contrast. Flow cytometry was performed to determine the apoptosis rate of cells and the expression of ROS. Cell counting kit 8 (CCK8) was used to determine the activity of pericytes. Moreover, nitric oxide (NO) concentration of cells supernatant and expression of endothelial nitric oxide synthase (eNOS), superoxide dismutase (SOD), B cell lymphoma 2 (BCL2), vascular endothelial growth factor (VEGF), endothelin 1 (ET1), PARP1, and GAPDH were tested through RT-qPCR, western blot (WB), or immunocytochemistry (ICC). Results Overproduction of ROS, high apoptotic rate, and attenuated activity of pericytes were observed after cells were incubated with media containing 0.5 mM H2O2. Moreover, downregulation of SOD, NO, BCL2, and GAPDH, and upregulation of VEGFA, ET1, and PARP1 were discovered after cells were exposed to 0.5 mM H2O2 in this study, which could be improved by PARP1 inhibitor and SDMM capsule in a dose-dependent way, whereas worsened by PARP1 activation and GAPDH inhibitor. Conclusions SDMM capsule may attenuate oxidative stress-induced apoptosis of pericytes through downregulating PARP expression and upregulating GAPDH expression.

scholarly journals Role of Oxidative and Nitro-Oxidative Damage in Silver Nanoparticles Cytotoxic Effect against Human Pancreatic Ductal Adenocarcinoma Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Ewelina Barcińska ◽  
Justyna Wierzbicka ◽  
Agata Zauszkiewicz-Pawlak ◽  
Dagmara Jacewicz ◽  
Aleksandra Dabrowska ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Pancreatic Cancer ◽  
Silver Nanoparticles ◽  
Oxidative Damage ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Cytotoxic Effect ◽  
Mrna Level ◽  
Ductal Adenocarcinoma ◽  
Adenocarcinoma Cells

Pancreatic ductal adenocarcinoma is one of the most aggressive human malignancies, where the 5-year survival rate is less than 4% worldwide. Successful treatment of pancreatic cancer is a challenge for today’s oncology. Several studies showed that increased levels of oxidative stress may cause cancer cells damage and death. Therefore, we hypothesized that oxidative as well as nitro-oxidative stress is one of the mechanisms inducing pancreatic cancer programmed cell death. We decided to use silver nanoparticles (AgNPs) (2.6 and 18 nm) as a key factor triggering the reactive oxygen species (ROS) and reactive nitrogen species (RNS) in pancreatic ductal adenocarcinoma cells (PANC-1). Previously, we have found that AgNPs induced PANC-1 cells death. Furthermore, it is known that AgNPs may induce an accumulation of ROS and alteration of antioxidant systems in different type of tumors, and they are indicated as promising agents for cancer therapy. Then, the aim of our study was to evaluate the implication of oxidative and nitro-oxidative stress in this cytotoxic effect of AgNPs against PANC-1 cells. We determined AgNP-induced increase of ROS level in PANC-1 cells and pancreatic noncancer cell (hTERT-HPNE) for comparison purposes. We found that the increase was lower in noncancer cells. Reduction of mitochondrial membrane potential and changes in the cell cycle were also observed. Additionally, we determined the increase in RNS level: nitric oxide (NO) and nitric dioxide (NO2) in PANC-1 cells, together with increase in family of nitric oxide synthases (iNOS, eNOS, and nNOS) at protein and mRNA level. Disturbance of antioxidant enzymes: superoxide dismutase (SOD1, SOD2, and SOD3), glutathione peroxidase (GPX-4) and catalase (CAT) were proved at protein and mRNA level. Moreover, we showed cells ultrastructural changes, characteristic for oxidative damage. Summarizing, oxidative and nitro-oxidative stress and mitochondrial disruption are implicated in AgNPs-mediated death in human pancreatic ductal adenocarcinoma cells.

Targeting Redox Overcomes Proteasome Inhibitor Resistance in Multiple Myeloma

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 1819-1819
Author(s):  
Nathan G. Dolloff ◽  
Leticia Reyes ◽  
Brittany Smith ◽  
John Fairbanks Langenheim ◽  
Yefim Manevich
Keyword(s):  
Oxidative Stress ◽  
Multiple Myeloma ◽  
Stress Response ◽  
Oxidative Damage ◽  
Small Molecules ◽  
Redox Balance ◽  
Oxidative Stress Response ◽  
Protein Thiols ◽  
Cellular Bioenergetics ◽  
Resistant Cells

Abstract Proteasome inhibitors (PIs) like bortezomib (Btz) and carfilzomib (Crflz) induce an oxidative stress response in Multiple Myeloma (MM) cells. Oxidative stress is a key effector pathway in PI-induced cell death, and altered redox signaling has been implicated in the acquisition of PI resistance. The potential of redox as a therapeutic target/pathway for PI resistant MM has not been realized due to the absence of a precise molecular targeted strategy that exploits redox signaling in a way that attacks PI resistant cells while sparing normal cells. Therefore, we set out in this study to characterize redox adaptations that contribute to PI resistance in MM, and to use drug screening platforms to identify specific redox-targeted small molecules that restore PI sensitivity. Using multiple isogenic pairs of PI sensitive and resistant MM cell lines, we found that resistant cells exist under high basal levels of reactive oxygen species (ROS) and oxidation of protein thiols (i.e., oxidative damage). Resistant cells induce significantly higher relative levels of ROS following PI treatment, but exhibit no further increase in oxidative damage. By comparison, their PI sensitive counterparts have relatively low levels of basal and PI-induced ROS levels, but undergo significantly higher levels of oxidative damage following PI treatment. These findings demonstrate that PI resistance is associated with alterations in redox balance; they further suggest that PI resistant cells have acquired adaptations that allow them to survive under high basal levels of oxidative stress, and that provide protection from PI-induced oxidative damage. We also identified significant changes in cellular bioenergetics that are typical of PI resistant cells. Generally, PI resistant cells appear to be more metabolically efficient, relying on mitochondrial respiration as their primary source of ATP production. Specifically, PI resistant cells have higher basal oxygen consumption rates (OCR), expanded respiratory capacity, increased NAD(P)H levels and pyruvate dehydrogenase (PDH) activity, and nearly absent activation of the AMP kinase energy stress signaling pathway. Thus, the acquisition of PI resistance is associated with significant changes in redox balance as well as in cellular bioenergetics. Given these findings, we next used a cell-based drug screening method to screen for redox-targeted small molecules capable of restoring PI sensitivity to resistant cells. We screened a compound collection of known pro- and anti-oxidant small molecules with wide-ranging mechanisms of action. From this screen we identified compound E61, which demonstrated strong synergy with multiple PIs, including Btz, Crflz, ixazomib, and oprozomib. E61 induced an oxidative stress response characterized by a burst of ROS generation and oxidation of protein thiols, and synergistically enhanced the PI-induced oxidative stress response in resistant cells. The synergistic cytotoxic response to E61 and PI co-treatment was dependent on ROS, and was evident across several models of PI resistance, representing cells of diverse genetic backgrounds. While E61 enhanced PI-induced cell death in resistant MM cells, its effects were protective in normal cell types, including peripheral blood mononuclear cells (PMBCs) and lymphocytes from normal human donors. These findings suggest that compound E61 will have a wide therapeutic index in combination with PI therapy in preclinical mouse models of MM, a hypothesis that we are currently testing. All together, our findings identify specific redox and bioenergetics changes that are acquired by PI resistant MM cells. Furthermore, our work offers a novel redox-targeted small molecule, E61, to be used in combination with PI-based therapeutic regimens in refractory MM. Disclosures No relevant conflicts of interest to declare.

scholarly journals Microbiological Insights into the Stress-Alleviating Property of an Endophytic Bacillus altitudinis WR10 in Wheat under Low-Phosphorus and High-Salinity Stresses

2019 ◽  
Vol 7 (11) ◽  
pp. 508 ◽  
Author(s):  
Yue ◽  
Shen ◽  
Chen ◽  
Liang ◽  
Chu ◽  
...  
Keyword(s):  
Abiotic Stresses ◽  
Germination Rate ◽  
Acc Deaminase ◽  
Dry Weight ◽  
Triticum Aestivum L ◽  
Culture Conditions ◽  
Wheat Seedlings ◽  
Bacillus Altitudinis ◽  
Phosphorus Stress ◽  
Low Phosphorus

An indole–3–acetic acid producing Bacillus altitudinis WR10 was previously isolated from the root of wheat (Triticum aestivum L.). In this study, the strain WR10 was used for relieving abiotic stresses in wheat under low phosphorus and high saline in hydroponic co-culture models. Significantly, strain WR10 improved wheat seed relative germination rate under salinity stress (200/400 mM NaCl) and the root dry weight in wheat seedlings under phosphorus stress (10 μM KH2PO3) when insoluble phosphates are available. To provide insights into its abiotic stress-alleviating properties, the strain was characterized further. WR10 grows well under different culture conditions. Particularly, WR10 resists salt (12% NaCl) and hydrolyzes both inorganic and organic insoluble phosphates. WR10 uses many plant-derived substrates as sole carbon and energy sources. It produces catalase, amylase, phosphatase, phytase, reductase, and 1–aminocyclopropane–1–carboxylate (ACC) deaminase. In addition, WR10 possesses long peritrichous flagella, and its biofilm formation, as well as phytase production, is induced by abiotic stresses. Overall, the salinity-alleviating property of WR10 in wheat can be attributed to its inherent tolerance to NaCl, formation of biofilm, and production of enzymes, like catalase, amylase, and ACC deaminase. Meanwhile, B. altitudinis WR10 reduces low-phosphorus stress in wheat by production of phosphatases and phytases in the presence of insoluble phosphates.

scholarly journals Partially Hydrolyzed Guar Gum Attenuates d-Galactose-Induced Oxidative Stress and Restores Gut Microbiota in Rats

2019 ◽  
Vol 20 (19) ◽  
pp. 4861 ◽  
Author(s):  
Xiaoyan Liu ◽  
Chenxuan Wu ◽  
Dong Han ◽  
Jun Liu ◽  
Haijie Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Oxidative Damage ◽  
Guar Gum ◽  
Telomerase Activity ◽  
Sirtuin 1 ◽  
Protective Effects ◽  
Rat Serum ◽  
Oxidative Damages ◽  
Partially Hydrolyzed Guar Gum

Partially hydrolyzed guar gum (PHGG) has received considerable attention for its various bioactive functions. The injection of d-galactose can cause aging-related injury which is usually resulted from oxidative stress on tissues and cells. In this study, d-galactose (200 mg/kg/day) was injected into rats, and the protective effects of PHGG (500, 1000, and 1500 mg/kg/day) against oxidative damages, as well as its probiotic functions, were analyzed. The results showed that PHGG treatment at a concentration of 1500 mg/kg/day greatly reduced the levels of lactic acid, nitric oxide, inducible nitric oxide synthase, advanced glycation end products, and increased the telomerase activity, by 7.60%, 9.25%, 12.28%, 14.58%, and 9.01%, respectively. Moreover, PHGG significantly elevated the activities of antioxidant enzymes and decreased the content of malondialdehyde in rat serum and brain. The oxidative damage was also significantly alleviated in the liver and hippocampus and the expressions of brain-derived neurotrophic factor and choline acetyltransferase also increased. Furthermore, PHGG treatment could significantly regulated the expression of sirtuin 1, forkhead box O1, and tumor protein p53 in the hippocampus. It also increased the levels of organic acids and improved the composition of intestinal microbiota. These findings demonstrated that PHGG treatment could effectively alleviate the oxidative damage and dysbacteriosis.

scholarly journals Electrolyte Leakage and the Protective Effect of Nitric Oxide on Leaves of Flooded Rice Exposed to Herbicides

2016 ◽  
Vol 34 (4) ◽  
pp. 777-786 ◽  
Author(s):  
K.S. SILVA ◽  
L.J. K. URBAN ◽  
A. BALBINOT ◽  
F.S. GNOCATO ◽  
N.D. KRUSE ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Protective Effect ◽  
Sodium Nitroprusside ◽  
Antioxidant System ◽  
Electrolyte Leakage ◽  
Rice Cultivar ◽  
Flooded Rice ◽  
Leaf Segments

ABSTRACT The nitric oxide acts on the antioxidant system of plants and can discontinue the damage of herbicides elicitors of oxidative stress that cause the disruption of membranes and leakage of cellular contents. In order to evaluate the protective effect of nitric oxide in electrolytes leakage, leaf segments of the Puita INTA CL rice cultivar were incubated with 0, 5, 50, 500 and 5,000 μM clomazone (360 g a.i. L-1), oxadiazon (250 g a.i. L-1), oxyfluorfen (240 g a.i. L-1) and the formulated mixture of paraquat (200 g a.i. L-1) + diuron (100 g a.i. L-1) to obtain the maximum potential conductivity of 50% (MPC50). Subsequently, leaf segments were pre-treated with 0, 200 and 2,000 μM of sodium nitroprusside (SNP) for four hours and further incubated for 48 hours with 0, 0.5, 1, 2 and 4 times the concentration of the herbicide that caused the CMP50, and the protective effect was reassessed in the presence of nitric oxide scavenger, cPTIO. The MPC50 was caused by exposure to 188.9, 273.4, 410.2 + 205.1 and 917.0 μM of Oxadiazon, Oxyfluorfen, Paraquat + Diuron and Clomazone. Pretreatment with 200 μM of SNP reduced electrolyte leakage in leaf segments exposed to 2 and 4 times the MPC50 to oxadiazon and paraquat + diuron, while 2,000 μM reduced the damage caused by oxyfluorfen, at the same concentrations. Also, 200 and 2,000 μM of SNP were efficient for clomazone, and the protection was confirmed by cPTIO in all cases.

scholarly journals Increased Blood Pressure Causes Lymphatic Endothelial Dysfunction via Oxidative Stress in Spontaneously Hypertensive Rats

Hypertension ◽  
2020 ◽  
Vol 76 (2) ◽  
pp. 598-606
Author(s):  
Masashi Mukohda ◽  
Risuke Mizuno ◽  
Hiroshi Ozaki
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Nadph Oxidase ◽  
Sodium Nitroprusside ◽  
P38 Mapk ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

The lymphatic system is involved in the pathogenesis of edema, inflammation, and cancer metastasis. Because lymph vessels control fluid electrolytes and volume balance, changes in lymphatic activity can be expected to alter systemic blood pressure. This study examined possible changes in lymphatic contractile properties in spontaneously hypertensive rats (SHR). Thoracic ducts isolated from 10- to 12-week-old SHR exhibited either decreased acetylcholine-induced endothelium-dependent relaxation or sodium nitroprusside-induced endothelium-independent relaxation compared with age-matched Wister-Kyoto rats. The impairment in acetylcholine responsiveness was more pronounced than sodium nitroprusside responsiveness. N-Nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor blunted acetylcholine-induced relaxation in Wister-Kyoto rats, indicating an involvement of endothelial nitric oxide production. Endothelial dysfunction in lymph vessels of SHR was attenuated by tempol (a superoxide dismutase mimetic), apocynin, or VAS-2870 (NADPH oxidase inhibitors). Consistent with these observations, nitrotyrosine levels were significantly elevated in SHR, indicative of increased oxidative stress. In addition, protein expression of NADPH oxidase 2 and phosphorylation of p47 phox (Ser345) were significantly increased in SHR. Further, SB203580 (a p38 MAPK inhibitor) restored the acetylcholine-induced relaxation in SHR. It is notable that 4-week-old SHR, which exhibited normal blood pressure, did not show any decreased activity of acetylcholine- or sodium nitroprusside-induced relaxation. Additionally, antihypertensive treatment of 4-week-old SHR with hydrochlorothiazide and reserpine or hydrochlorothiazide and hydralazine for 6 weeks completely restored lymphatic endothelial dysfunction. We conclude that contractile activity of lymphatic vessels is functionally impaired with the development of increasing blood pressure, which is mediated through increased oxidative stress via the p38 MAPK/NADPH oxidase 2 pathway.

scholarly journals Nitric Oxide Enhancing Resistance to PEG-Induced Water Deficiency is Associated with the Primary Photosynthesis Reaction in Triticum aestivum L.

2018 ◽  
Vol 19 (9) ◽  
pp. 2819 ◽  
Author(s):  
Ruixin Shao ◽  
Huifang Zheng ◽  
Shuangjie Jia ◽  
Yanping Jiang ◽  
Qinghua Yang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Triticum Aestivum L ◽  
Light Energy ◽  
Phosphorylation Sites ◽  
Water Deficiency ◽  
Primary Reaction ◽  
Wheat Seedlings ◽  
Chl A ◽  
Significant Difference ◽  
Phosphorylated Peptides

Photosynthesis is affected by water-deficiency (WD) stress, and nitric oxide (NO) is a free radical that participates in the photosynthesis process. Previous studies have suggested that NO regulates excitation-energy distribution of photosynthesis under WD stress. Here, quantitative phosphoproteomic profiling was conducted using iTRAQ. Differentially phosphorylated protein species (DEPs) were identified in leaves of NO- or polyethylene glycol (PEG)-treated wheat seedlings (D), and in control seedlings. From 1396 unique phosphoproteins, 2257 unique phosphorylated peptides and 2416 phosphorylation sites were identified. Of these, 96 DEPs displayed significant changes (≥1.50-fold, p < 0.01). These DEPs are involved in photosynthesis, signal transduction, etc. Furthermore, phosphorylation of several DEPs was upregulated by both D and NO treatments, but downregulated only in NO treatment. These differences affected the chlorophyll A–B binding protein, chloroplast post-illumination chlorophyll-fluorescence-increase protein, and SNT7, implying that NO indirectly regulated the absorption and transport of light energy in photosynthesis in response to WD stress. The significant difference of chlorophyll (Chl) content, Chl a fluorescence-transient, photosynthesis index, and trapping and transport of light energy further indicated that exogenous NO under D stress enhanced the primary photosynthesis reaction compared to D treatment. A putative pathway is proposed to elucidate NO regulation of the primary reaction of photosynthesis under WD.

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