NO and HO contribute to SO toxicity via Ca signaling in Vicia faba guard cells.

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