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Salicylic acid negatively affects the response to salt stress in pea plants

2011; Wiley; Volume: 13; Issue: 6 Linguagem: Inglês

10.1111/j.1438-8677.2011.00461.x

1438-8677

Gregorio Barba‐Espín, María José Clemente‐Moreno, Sara Álvarez, Manuel Francisco García‐Legaz, José Antonio Hernández, Pedro Díaz‐Vivancos,

Plant Micronutrient Interactions and Effects

Abstract We studied the effect of salicylic acid (SA) treatment on the response of pea plants to salinity. Sodium chloride (NaCl)‐induced damage to leaves was increased by SA, which was correlated with a reduction in plant growth. The content of reduced ascorbate and glutathione in leaves of salt‐treated plants increased in response to SA, although accumulation of the respective oxidised forms occurred. An increase in hydrogen peroxide also occurred in leaves of salt‐exposed plants treated with SA. In the absence of NaCl, SA increased ascorbate peroxidase (APX; 100 μ m ) and glutathione‐S transferase (GST; 50 μ m ) activities and increased catalase (CAT) activity in a concentration‐dependent manner. Salinity decreased glutathione reductase (GR) activity, but increased GST and CAT activity. In salt‐stressed plants, SA also produced changes in antioxidative enzymes: 100 μ m SA decreased APX but increased GST. Finally, a concentration‐dependent increase in superoxide dismutase (SOD) activity was induced by SA treatment in salt‐stressed plants. Induction of PR‐1b was observed in NaCl‐stressed plants treated with SA. The treatment with SA, as well as the interaction between salinity and SA treatment, had a significant effect on PsMAPK3 expression. The expression of PsMAPK3 was not altered by 70 m m NaCl, but was statistically higher in the absence than in the presence of SA. Overall, the results show that SA treatment negatively affected the response of pea plants to NaCl, and this response correlated with an imbalance in antioxidant metabolism. The data also show that SA treatment could enhance the resistance of salt‐stressed plants to possible opportunistic pathogen attack, as suggested by increased PR‐1b gene expression.