Exogenous nitric oxide limits salt-induced oxidative damage in maize by altering superoxide dismutase activity

Salinity stress causes accumulation of reactive oxygen species (ROS) to levels that are toxic to plants. Inefficient scavenging of ROS by antioxidant enzymes like superoxide dismutase (SOD; EC 1.15.1.1) results in cell death and inhibition of growth, which ultimately 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 salinity stress tolerance is only partially understood. This study thus evaluated the effect of exogenously applied NO on maize leaf superoxide accumulation and SOD enzymatic activity in the presence and absence of salinity stress to delineate SOD isoforms that contribute to NO-mediated salinity tolerance. Salinity stress caused elevation of superoxide generation and lipid peroxidation in maize leaves, along with elevated activity of a number of SOD isoforms. 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 lipid peroxidation in maize leaves and corresponded with an amplification of the increase in the activity of some SOD isoforms. Based on this analysis, the study suggests that exogenously applied NO reduces salinity-induced oxidative stress by up-regulating the enzymatic activity of some SOD isoforms, thus increasing the scavenging of excessive superoxide radicals to limit oxidative stress.