Abstract
An experimentation was carried out to appraise whether or not nitric oxide (NO) contributes to salicylic acid (SA)-induced salinity tolerance particularly by regulating ascorbate-glutathione (AsA-GSH) cycle. Before starting salinity stress (SS), SA (0.5 mM) was sprayed to the foliage of plants once every other day for a week and then seedlings were grown under control or SS (100 mM NaCl), for five weeks. Salinity stress enhanced the AsA-GSH cycle-related enzymes, glutathione reductase (GR), ascorbate peroxidase (APX), and dehydroascorbate reductase (DHAR), and monodehydroascorbate reductase (MDHAR). Furthermore, SS caused substantial decreases in plant physiological-related traits such as leaf potassium (K) contents, K+/Na+ ratio, the ratios of reduced ascorbate/ dehydroascorbic acid (AsA/DHA) and reduced glutathione/oxidized glutathione (GSH/GSSG), but in contrast, significant increases occurred in leaf hydrogen peroxide, malondialdehyde, electron leakage, proline, the premier antioxidant enzymes' activities, Na+ and NO. SA reduced leaf Na+ content and oxidative stress-related traits, but improved all earlier-mentioned traits compared with those in plants treated with SS alone. All positive effects of SA were eliminated by NO scavenger, 0.1 mM 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO) by reducing NO, suggesting that NO produced by SA up-regulated the activities of AsAGSH cycle and antioxidant enzymes, so it could play a central function as a signal molecule in salt tolerance of pepper plants.