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中文摘要：
以蚕豆为材料,研究一氧化氮合酶（NOS）途径在SO2诱发气孔运动中的作用.研究发现：浓度7.5~200μmol·L-1的SO2衍生物处理后,蚕豆叶面气孔开度减小,气孔开度与SO2衍生物浓度呈负相关;SO2衍生物处理组叶组织中NOS活性增强;加入NO清除剂c-PTIO或NOS抑制剂L-NAME可抑制SO2衍生物诱发的气孔关闭;SO2衍生物处理组保卫细胞内NO和Ca2＋水平升高,用c-PTIO降低胞内NO水平后Ca2＋水平随之下降.结果表明,SO2衍生物胁迫可诱发保卫细胞内NO合成增加,NO通过调节胞内Ca2＋水平升高,激活下游信号转导途径,调节气孔运动;NOS途径介导的NO合成参与了SO2胁迫下蚕豆气孔运动的调节.
英文摘要：
The potential role of nitric oxide synthase（ NOS） in stomatal movement regulation in the response of plants to sulfur dioxide（ SO2） was investigated in Vicia faba L. The results showed that SO2 hydrates significantly decreased stomatal aperture in the concentration range of 7. 5 to 200μmol·L-1. SO2 hydrates induced stomatal closure in a concentration-dependent manner. SO2hydrates-evoked stomatal closure was correlated with increasing activities of NOS in the whole leaves from four-week-old V. faba plants. Both NO scavenger c-PTIO and NOS inhibitor L-NAME can block SO2hydrates-evoked stomatal closure. Moreover,exposure to SO2 hydrates enhanced the intracellular levels of NO and Ca2＋in guard cell. Application of exogenous NO scavenger c-PTIO blocked the increases of intracellular NO and Ca2＋levels in SO2-treated guard cells. These results indicated that SO2hydrates-triggered NO production mediated stomatal movement regulation via Ca2＋signaling,and that nitric oxide synthase-dependent NO production played a crucial role in SO2hydrates-evoked stomatal movement in V. faba.
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