Salt stress-induced H2O2and Ca2+mediate K+/Na+homeostasis inPyropia haitanensis

Maintaining K+/Na(+)homeostasis and redox homeostasis is crucial for the tolerance ofP. haitanensisto hypersalinity. However, the precise link between the signaling role of reactive oxygen species (ROS) and K+/Na(+)homeostasis remains poorly characterized. In this study, we analyze hydrogen peroxide (H2O2) production and flux as well as H(2)O(2)effects on K+, Na+, and Ca(2+)transport inP. haitanensisunder hypersaline condition. An exposure to hypersaline stress (110 parts per thousand, 15 min) rapidly increased the H(2)O(2)content and efflux inP. haitanensiscells, which was counteracted by the rapid increase in superoxide dismutase activity and activation of defense responses. The enhanced Na(+)efflux and Ca(2+)influx induced by salt stress were substantially suppressed by an NADPH oxidase inhibitor (DPI) or an ROS scavenger (DMTU). Additionally, Na(+)efflux decreased in response to a plasma membrane Ca2+-permeable channel inhibitor (verapamil). This suggested that NADPH oxidase-mediated H(2)O(2)production may promote Na(+)efflux via the Ca2+-dependent Na+/H(+)antiporter system in salt-stressedP. haitanensisthalli. Moreover, salt-induced H(2)O(2)accumulation also enhanced K(+)efflux, which was alleviated by exogenous Ca2+. H(2)O(2)and Ca(2+)may independently mediate K(+)homeostasis inP. haitanensis. H2O2-induced K(+)leakage may induce cells to switch from normal metabolic activities to those associated with adaptation and repair. The present results provide new insight for clarifying the relationship between salt-induced ROS signaling and ion homeostasis in intertidal seaweed species.