Naringenin induces tolerance to salt/osmotic stress through the regulation of nitrogen metabolism, cellular redox and ROS scavenging capacity in bean plants.

The present study was conducted to uncover underlying possible effect mechanisms of flavonoid naringenin (Nar, 0.1-0.4 mM) in nitrogen assimilation, antioxidant response, redox status and the expression of NLP7 and DREB2A, on salt (100 mM NaCl) and osmotic-stressed (10% Polyethylene glycol, -0.54 MPa) Phaseolus vulgaris cv. Yunus 90). Nar ameliorated salt/osmotic stresses-induced growth inhibition and improved the accumulation of proline, glycine betaine and choline. In response to stress, Nar increased endogenous content of nitrate (NO) and nitrite (NO) by regulating of nitrate reductase and nitrite reductase. Stress-triggered NH was eliminated with Nar through increases in glutamine synthetase and glutamate synthase. After NaCl or NaCl + PEG exposure, Nar utilized the aminating activity of glutamate dehydrogenase in the conversion of NH. The stress-inducible expression levels of DREB2A were increased further by Nar, which might have affected stress tolerance of bean. Nar induced effectively the relative expression of NLP7 in the presence of the combination or alone of stress. Also, the impaired redox state by stress was modulated by Nar and hydrogen peroxide (HO) and TBARS decreased. Nar regulated the different pathways for scavenging of HO under NaCl and/or PEG treatments. When Nar + NaCl exposure, the damage was removed by superoxide dismutase (SOD), catalase (CAT), POX (only at 0.1 mM Nar + NaCl) and AsA-GSH cycle. Under osmotic stress plus Nar, the protection was manifested by activated CAT and, glutathione S-transferase and the regeneration of ascorbate. 0.1 mM Nar could protect bean plant against salt/osmotic stresses, likely by regulating nitrogen assimilation pathways, improving expression levels of genes associated with tolerance mechanisms and modulating the antioxidant capacity and AsA-GSH redox-based systems.