SO_2诱导的萱草保卫细胞凋亡及其信号调节

SO_2-induced guard cells apoptosis and its signal regulation in Hemerocallis fulva

SO2是一种常见的大气污染物，急性和慢性暴露都会对植物造成伤害.因此，本文以景观绿化植物萱草叶片下表皮为材料，研究了SO2对气孔保卫细胞的致死效应及其可能的信号调节途径.结果表明，利用SO2体内衍生物-亚硫酸钠和亚硫酸氢钠混合液处理萱草表皮3 h后，随着处理浓度（1.0-5.0 mmol L-1）的增加，萱草保卫细胞生理活性下降，甚至死亡；浓度超过2.0 mmol L-1时，细胞死亡率显著增高（p〈0.05），死细胞出现核固缩、核拉长、核碎片等典型凋亡特征，保卫细胞内的活性氧种（ROS）、一氧化氮（NO）和Ca2＋水平显著升高.采用不同浓度的抗氧化剂过氧化氢酶（CAT）、抗坏血酸（AsA），Ca2＋螯合剂乙二醇双四乙酸（EGTA） 和Ca2＋通道抑制剂氯化镧（LaCl3）及NO清除剂羧基-2苯-4，4，5，5-四甲基咪唑-1-氧-3氧化物（C-PTIO）和合成抑制剂叠氮钠（NaN3）处理后，均可使SO2衍生物诱发的细胞死亡率降低，以200 U mL-1 CAT、0.05 mmol L-1的AsA、EGTA、LaCl3及0.20 mmol L-1的C-PTIO、NaN3的效果最佳，同时胞内ROS、NO和Ca2＋水平下降.以上结果表明，一定浓度的SO2可诱导萱草保卫细胞死亡，可能通过诱导ROS和NO爆发，激活细胞质膜钙通道，进而引起胞内Ca2＋增加，通过ROS-NO-Ca2＋信号途径介导细胞死亡.SO2诱导的萱草细胞死亡可能存在细胞凋亡过程.

Chronic and acute exposure to SO2 is associated with increased risk of various damages of plants. In this study, SO2-induced guard cells apoptosis and its signal regulation in Hemerocallis fulva were studied using epidermal strip experiment treated with different mixtures of sodium sulfite and sodium bisulfite （3：1, mmol L-1/mmol L-1）. The results showed that with the increase of treatment concentration, the physiological activity of the guard cells declined and cell death occurred. While the concentration of SO2 derivatives exceeded 2.0 mmol L-1, the percentage of cell death increased significantly （p〈0.05）. Typical features of apoptosis including nuclear condensation, nuclear elongation, fragmentation and apoptotic bodies were founded. Meanwhile, ROS, NO and Ca2＋ level increased. However, the percentage of the cell death decreased when the strips exposed to SO2 derivatives combined with different concentrations of antioxidant ascorbic acid （AsA） or catalase （CAT）, C-PTIO （NO scavenger） or NaN3 （nitrite reductase inhibitor）, EGTA （Ca2＋ chelating agent） or LaCl3 （plasma membrane Ca2＋ channel blocker）, especially the concentration of 200 U mL-1 CAT, 0.05 mmol L-1 AsA, EGTA, LaCl3 and 0.20 mmol L-1 C-PTIO, NaN3. ROS, NO and Ca2＋ level decreased as well. All results showed that the apoptosis induced by SO2 in H. fulva might occur via ROS-NO-Ca2＋ signal pathway.