Nitric oxide alleviates salt-induced stress damage by regulating the ascorbate-glutathione cycle and Na+/K+ homeostasis in Nitraria tangutorum Bobr.

Nitric oxide (NO) is an important signaling molecule involved in mediation of salt stress induced physiological responses in plants. In this study, we investigated the effect of NO on Nitraria tangutorum seedlings exposed to salt stress. Exogenous application of NO donor, sodium nitroprusside (SNP) increased fresh weight, shoot and root elongation and decreased electrolyte leakage and malondialdehyde (MDA) content in N. tangutorum seedlings under salt stress. Simultaneously, leaf senescence and root damage induced by salt stress were alleviated. SNP effectively increased NO content both in leaves and roots of plants under salt stress. Meanwhile, SNP activated the ascorbate-glutathione (AsA-GSH) cycle by increasing antioxidants contents, antioxidant enzymes activities, and related genes expression, thereby scavenging reactive oxygen species (ROS) and alleviating oxidative damage caused by salt stress. SNP alleviated salt stress induced ion toxicity by promoting Na+ efflux and ion transporter gene expression and reducing Na+ content and the Na+/K+ ratio. In addition, application of NO specific scavenger cPTIO and mammalian NO synthase inhibitor L-NAME sifnificantly aggravated stress damage in plant under salt stress. These results show the beneficial impacts of NO as a stress-signaling molecule that positively regulates defense response in N. tangutorum to salt stress.