Salinity stress causes accumulation of reactive oxygen species (ROS) to levels that are toxic to plants. Inefficientscavenging of ROS by antioxidant enzymes like superoxide dismutase (SOD; EC 1.15.1.1) results in cell death andinhibition of growth,whichultimately leads to reduced crop productivity.Recent studies suggest that nitric oxide(NO) can enhance plant tolerance to salinity stress but the molecular mechanism for the NO-mediated salinitystress tolerance is only partially understood. This study thus evaluated the effect of exogenously applied NO onmaize leaf superoxide accumulation and SOD enzymatic activity in the presence and absence of salinity stressto delineate SOD isoforms that contribute to NO-mediated salinity tolerance. Salinity stress caused elevation ofsuperoxide generation and lipid peroxidation in maize leaves, along with elevated activity of a number of SODisoforms. Exogenous application of 2,2′-(hydroxynitrosohydrazono)bis-ethanimine (DETA/NO) to salinity-treated maize reduced the salinity-induced superoxide accumulation and lowered the salinity-induced lipidperoxidation in maize leaves and corresponded with an amplification of the increase in the activity of someSOD isoforms. Based on this analysis, the study suggests that exogenously applied NO reduces salinity-inducedoxidative stress by up-regulating the enzymatic activity of some SOD isoforms, thus increasing the scavengingof excessive superoxide radicals to limit oxidative stress
Link: https://doi.org/10.1016/j.sajb.2017.12.010
DOI: https://doi.org/10.1016/j.sajb.2017.12.010
