中文摘要：

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-1SO2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c PTIO、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c PTIO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.

英文摘要：

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-1SO2 derivatives caused a dose-and time-dependent increase of cell death rate.Upon 2 mmol·L-1SO2 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 H2O2scavenger（catalase（CAT） or ascorbic acid（ASA））,NO scavenger（c PTIO）,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 H2O2level;whereas c PTIO 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.