Modulation of antioxidant enzyme activities and metabolites ratios by nitric oxide in short-term salt stressed soybean root nodules

Several abiotic factors cause molecular damage to plants either directly or through the accumulation of reactive oxygen species such as hydrogen peroxide (H2O2). We investigated if application of nitric oxide (NO) donor 2,2′- (hydroxynitrosohydrazono) bis-ethanimine (DETA/NO) could reduce the toxic effect resulting from short-term salt stress. Salt treatment (150 mM NaCl) alone and in combination with 10 μM DETA/NO or 10 μM DETA were given to matured soybean root nodules for 24 h. Salt stress resulted in high H2O2 level and lipid peroxidation while application of DETA/NO effectively reduced H2O2 level and prevented lipid peroxidation in the soybean root nodules. NO treatment increased the activities of ascorbate peroxidase and dehydroascorbate reductase under salt stress. Whereas short-term salt stress reduced AsA/DHAsA and GSH/GSSG ratios, application of the NO donor resulted in an increase of the reduced form of the antioxidant metabolites thus increasing the AsA/DHAsA and GSH/GSSG ratios. Our data suggests a protective role of NO against salt stress.Web of Scienc

Effect of exogenous application of nitric oxide on salt stress responses of soybean

AbstractSalinity stress is one of the major factors that reduce annual agricultural produce. This has led to numerous studies investigating means to improve tolerance to salt stress. Nitric oxide (NO) is a gaseous signaling molecule involved in the regulation of diverse processes in plants. Certain studies have demonstrated the role of exogenous application of NO in mediating responses to abiotic stress. We investigated the role of exogenously applied NO 2,2′(hydroxynitrosohydrazono) bis-ethanimine (DETA/NO) in ameliorating long term salinity stress on soybean. Long term salinity stress in the form of a final concentration of 80mM sodium chloride (NaCl) over a 16day period drastically affected the plants as indicated by decreased biomass of shoots, roots and nodules of soybean plants. In contrast, supplementation with 10μM DETA/NO improved growth of soybean plants under NaCl as evidenced by increased shoot, root and nodule weights and nodule number. Further analysis showed that long-term salinity stress led to increased cellular hydrogen peroxide (H2O2) content and high levels of cell death in the soybean. Treatments with NO, either as DETA/NO alone or in combination with NaCl, resulted in reversal of H2O2 to basal levels. This study showed that application of DETA/NO resulted in increased enzymatic activity of ascorbate peroxidase (APX). We propose that the role of NO in increasing tolerance to salinity stress in soybean may result from either its antioxidant capacity by direct scavenging of H2O2 or its role in activating APX activity that is crucial in scavenging H2O2

Nitric oxide increases the enzymatic activity of three ascorbate peroxidase isoforms in soybean root nodules

Ascorbate peroxidase is one of the major enzymes regulating the levels of H2O2 in plants and plays a crucial role in maintaining root nodule redox status. We used fully developed and mature nitrogen fixing root nodules from soybean plants to analyze the effect of exogenously applied nitric oxide, generated from the nitric oxide donor 2,2′-(hydroxynitrosohydrazono)bis-ethanimine, on the enzymatic activity of soybean root nodule ascorbate peroxidase. Nitric oxide caused an increase in the total enzymatic activity of ascorbate peroxidase. The nitric oxide-induced changes in ascorbate peroxidase enzymatic activity were coupled to altered nodule H2O2 content. Further analysis of ascorbate peroxidase enzymatic activity identified three ascorbate peroxidase isoforms for which augmented enzymatic activity occurred in response to nitric oxide. Our results demonstrate that nitric oxide regulates soybean root nodule ascorbate peroxidase activity. We propose a role of nitric oxide in regulating ascorbate-dependent redox status in soybean root nodule tissue. © 2011 Landes Bioscience.Articl