Salicylic acid-induced nitric oxide enhances arsenic toxicity tolerance in maize plants by upregulating the ascorbate-glutathione cycle and glyoxalase system.

The role of nitric oxide (NO) in salicylic acid (SA)-induced tolerance to arsenic (As) stress in maize plants is not reported in the literature. Before starting As stress (AsS) treatments, SA (0.5 mM) was sprayed to the foliage of maize plants. Thereafter, AsV (0.1 mM as sodium hydrogen arsenate heptahydrate) stress (AsS) was initiated and during the stress period, sodium nitroprusside (SNP 0.1 mM), a NO donor, was sprayed individually or in combination with SA. Furthermore, cPTIO (0.1 mM) was also applied as a NO scavenger during the stress period. Arsenic stress led to significant reductions in plant growth, photosynthesis, water relation parameters and endogenous NO content, but it increased hydrogen peroxide, malondialdehyde, electrolyte leakage, methylglyoxal, proline, the activities of major antioxidant enzymes, and leaf and root As content. The combined treatment of SA+SNP was more effective to reverse oxidative stress related parameters and reduce the As content in both leaves and roots, with a concomitant increase in antioxidant defense system, the ascorbate-glutathione (AsA-GSH) cycle-related enzymes, glyoxalase system enzymes, plant growth, and photosynthetic traits. The beneficial effects of SA were completely abolished with cPTIO supply by blocking the NO synthesis in AsS-maize plants, indicating that NO effectively participated in SA-improved tolerance to AsS in maize plants.