• 关键词：胡杨  细胞死亡  H₂O₂  NO

• 基金项目：国家自然科学基金（No.31500504,31371868）

• 韩彦莎
• 山西大学生命科学学院, 太原 030006

• 李琳
• 山西大学生命科学学院, 太原 030006

• 王朝阳
• 山西大学生命科学学院, 太原 030006

• 涂建
• 山西大学生命科学学院, 太原 030006

• 仪慧兰
• 山西大学生命科学学院, 太原 030006

• 摘要：二氧化硫（SO₂）是一种常见的大气污染物，目前关于SO₂对木本植物的毒害作用及相关机制并不清楚.本文以木本植物胡杨的愈伤细胞为材料，研究SO₂衍生物对胡杨细胞的致死效应，以及过氧化氢（H₂O₂）与一氧化氮（NO）在SO₂诱导胡杨细胞死亡中的信号调节作用.研究发现：SO₂衍生物处理（1～5 mmol·L^-1）可诱发胡杨细胞死亡，且SO₂衍生物浓度越大、处理时间越长，细胞死亡率越高.2 mmol·L^-1 SO₂衍生物处理胡杨细胞后，胞内H₂O₂和NO水平显著升高，且H₂O₂水平的升高先于NO.一定浓度的外源H₂O₂或NO供体SNP能够提高SO₂胁迫下胡杨细胞的死亡率；而使用H₂O₂清除剂CAT和ASA、NO清除剂cPTIO、NO合成抑制剂钨酸钠后，SO₂诱导的细胞死亡率明显降低.进一步实验发现，外源H₂O₂可以提高SO₂胁迫下胡杨细胞的硝酸还原酶（NR）活性，促进胞内NO产生；而利用CAT和ASA清除H₂O₂后，细胞NR活性和NO产生均受到明显抑制.此外，SO₂胁迫下，外源SNP能够抑制抗氧化酶（CAT和APX）活性，增加胡杨细胞内的H₂O₂水平，而一定浓度的cPTIO和钨酸钠均可提高CAT和APX活性，降低胞内H₂O₂水平.结果表明：SO₂胁迫下，胡杨细胞快速产生的H₂O₂能够激活硝酸还原酶活性，促进NO生成，同时NO能够通过抑制抗氧化酶活性而提高H₂O₂水平.H₂O₂与NO互作调控SO₂诱导的胡杨细胞死亡.

• Abstract：Sulfur dioxide (SO₂) is a common air pollutant. In woody plants, the toxic effects of SO₂ on cells and the relevant mechanisms remain largely unknown. In this study, callus cells of a woody species Populus euphratica were applied to investigate the lethal effects of SO₂ and the roles of H₂O₂ and NO in the regulation of SO₂-induced cell death. The results showed that 1~5 mmol·L^-1 SO₂ derivatives caused a dose- and time-dependent increase of cell death rate. Upon 2 mmol·L^-1 SO₂ treatment, the intercellular H₂O₂ and NO levels increased, and the rise of H₂O₂ level was prior to NO. Exogenous H₂O₂ or NO donor elevated SO₂-induced cell death rate, while application of H₂O₂ scavenger (catalase (CAT) or ascorbic acid (ASA)), NO scavenger (cPTIO), or NO synthase inhibitor (sodium tungstate) markedly reduced the cell death rate induced by SO₂. Further studies showed that exogenous H₂O₂ enhanced nitrate reductase (NR) activity and promoted NO production in P. euphratica cells exposure to SO₂ stress. When CAT or ASA was applied, the NR activity and SO₂-induced NO generation was significantly repressed. Meanwhile, exogenous SNP reduced the antioxidant enzymes activities (CAT and APX), and thus enhanced intercellular H₂O₂ level; whereas cPTIO and sodium tungstate led to increased CAT and APX activities and decreased H₂O₂ accumulation within cells. These results suggested that in SO₂-stressed P. euphratica cells, H₂O₂ could activate nitrate reductase activity and thus promote NO generation. NO could improve H₂O₂ accumulation by inhibiting antioxidant enzymes activities. Crosstalk between H₂O₂ and NO regulated the SO₂-induced cell death of P. euphratica.

• Key words：Populus euphratica  cell death  H₂O₂  NO

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