Salt induced modulations in antioxidative defense system of Desmostachya bipinnata.

This study addressed the interactions between salt stress and the antioxidant responses of a halophytic grass, Desmostachya bipinnata. Plants were grown in a semi-hydroponic system and treated with different NaCl concentrations (0 mM, 100 mM, 400 mM) for a month. ROS degradation enzyme activities were stimulated by addition of NaCl. Synthesis of antioxidant compounds, such as phenols, was enhanced in the presence of NaCl leading to accumulation of these compounds under moderate salinity. However, when the ROS production rate exceeded the capacity of enzyme-controlled degradation, antioxidant compounds were consumed and oxidative damage was indicated by significant levels of hydrogen peroxide at high salinity. The cellular concentration of salicylic acid increased upon salt stress, but since no direct interaction with ROS was detected, a messenger function may be postulated. High salinity treatment caused a significant decrease of plant growth parameters, whereas treatment with moderate salinity resulted in optimal growth. The activity and abundance of superoxide dismutase (SOD) increased with salinity, but the abundance of SOD isoforms was differentially affected, depending on the NaCl concentration applied. Detoxification of hydrogen peroxide (H2O2) was executed by catalase and guaiacol peroxidase at moderate salinity, whereas the enzymes detoxifying H2O2 through the ascorbate/glutathione cycle dominated at high salinity. The redox status of glutathione was impaired at moderate salinity, whereas the levels of both ascorbate and glutathione significantly decreased only at high salinity. Apparently, the maximal activation of enzyme-controlled ROS degradation was insufficient in comparison to the ROS production at high salinity. As a result, ROS-induced damage could not be prevented, if the applied stress exceeded a critical value in D. bipinnata plants.