NO and H2O2 contribute to SO2 toxicity via Ca(2+) signaling in Vicia faba guard cells.

NO and H2O2 have been implicated as important signals in biotic and abiotic stress responses of plants to the environment. Previously, we have shown that SO2 exposure increased the levels of NO and H2O2 in plant cells. We hypothesize that, as signaling molecules, NO and H2O2 mediate SO2-caused toxicity. In this paper, we show that SO2 hydrates caused guard cell death in a concentration-dependent manner in the concentration range of 0.25 to 6 mmol L(-1), which was associated with elevation of intracellular NO, H2O2, and Ca(2+) levels in Vicia faba guard cells. NO donor SNP enhanced SO2 toxicity, while NO scavenger c-PTIO and NO synthesis inhibitors L-NAME and tungstate significantly prevented SO2 toxicity. ROS scavenger ascorbic acid (AsA) and catalase (CAT), Ca(2+) chelating agent EGTA, and Ca(2+) channel inhibitor LaCl3 also markedly blocked SO2 toxicity. In addition, both c-PTIO and AsA could completely block SO2-induced elevation of intracellular Ca(2+) level. Moreover, c-PTIO efficiently blocked SO2-induced H2O2 elevation, and AsA significantly blocked SO2-induced NO elevation. These results indicate that extra NO and H2O2 are produced and accumulated in SO2-treated guard cells, which further activate Ca(2+) signaling to mediate SO2 toxicity. Our findings suggest that both NO and H2O2 contribute to SO2 toxicity via Ca(2+) signaling.