The Regulatory Mechanism Of Antioxidant Defense Signal Induced By Salt Stress In Cells Of Populus Euphratica

Dirersifolious Poplar is a valuable tree species for afforestation on saline and alkaline desert sites, and plays key roles in stabilizing sand dunes and in agriculture shelter belt construction in north-west China. Dirersifolious Poplar received much attention recently and there is considerable progress in physiological, biochemical and molecular mechanism of salt resistance. However, the signaling mechanisms of salt-induced antioxidant defense at cellular level and the relevane to the ionic homeostaisis control is still unclear. In this dissertation, the callus cells of Populus euphratica Olive and salt-sensitive Populus pupularis 35-44', P. popularis were adopted as material. We compared the difference of K+/Na+ homeostais control and antioxidant enzymes in salinized poplar cells. In addition, we also compared the difference of signaling responses of H2O2 and NO. The contrubiton of H2O2 and NO signaling to the salinity tolerance in two poplar cells were discussed and we further porposed a signaling model for the signaling regulation of antioxidant homeostasis. The detail resusts are as follows:(1) Compared with control cells, treatment of 150 mM NaCl for 6,12 and 24 hours caused the decrease of cell viability, K+ level and K+/Na+ ratio in two poplar species. However, the amplitude of the decrease was higher in P. popularis than P. euphratica. Similarly, the electrolyte leakge and Na+ accumulation were more evident in P. popularis cells. Salt stress upregulated the antioxidant enzymes in P. euphratica cells, including SOD, CAT, APX and GR, but significantly decreased the antioxidant enzymes in P. popularis cells. The results indicating that the salt tolerance of P. euphratica callus cells is evidently higher than P. popularis callus cells.(2) Salt shock with 150 mM NaCl induced a rapid burst of H2O2 in P. euphratica cells. The salt-induced H2O2 was time-dependent and usually reached its maximum after 20 min of NaCl treatment. NaCl-induced H2O2 production in P. euphratica was maintained significantly higher in salinised cells than in the controls, although it was lower than the peaking level at 20 min. However, there were no corresponding changes in salt stressed P. popularis cells. The NO level in P. euphratica cells gradually increased upon NaCl shock and reached its peaking level at 60 min, then remained constant throughout the experiment. However, the NaCl-induced NO was absent in P. popularis cells regardless of treatment time.(3) Pharmacological experiments proved that the salt-induced NO and H2O2 contributed to the K+/Na+ homeostasis and antioxidant defenses in P. euphratica cells. (4) Pretreated cells with EGTA, amiloride and vanadate significantly dereased the salt-upregulated antioxidant enzymes in P. euphratica cells, indicating that cytosolic Ca2+ signal, plasma membrane Na+/H+ antiporter and H+-ATPase involved in the mediating of antioxidant banlance in P. euphratica cells. Accordingly, based on the results in this dissertation and our previous reports, we suggested a signaling mechanism contributes to the salt-induced increase of antioxidant defense in P. euphratica cells.