Abstract
The participation of nitric oxide (NO) in wheat plant tolerance to salinity stress (SS) brought about by hydrogen sulphide (H2S) via modifying the ascorbate-glutathione (AsA-GSH) cycle was studied. The SS-plants received either 0.2 mM sodium hydrosulfide (NaHS; H2S donor), or NaHS plus 0.1 mM sodium nitroprusside (SNP; a NO donor) through the nutrient solution. Salinity stress decreased plant growth, leaf water status, leaf K+, and glyoxalase II (gly II), while it elevated proline content, leaf Na+ content, oxidative stress, methylglyoxal (MG), glyoxalase I (gly I), the superoxide dismutase, catalase and peroxidase activities, contents of endogenous NO and H2S. The NaHS supplementation elevated plant development, decreased leaf Na+ content and oxidative stress, and altered leaf water status, leaf K+ and involved enzymes in AsA-GSH, H2S and NO levels. The SNP supplementation boosted the positive impact of NaHS on these traits in the SS-plants. Moreover, 0.1 mM cPTIO, scavenger of NO, countered the beneficial effect of NaHS by lowering NO levels. SNP and NaHS + cPTIO together restored the beneficial effects of NaHS by increasing NO content, implying that NO may have been a major factor in SS tolerance in wheat plants induced by H2S via activating enzymes connected to the AsA-GSH cycle.
•Salinity stress (SS) led to a marked reduction in plant growth and enhanced oxidative stress in wheat.•NaHS markedly eliminated the SS-induced growth inhibition and oxidative stress.•NaHS increased the intrinsic level of H2S and NO as well as induced the antioxidant defence system.•The scavenger of NO, cPTIO, inverted the effect of NaHS by decreasing NO content.•H2S and NO work together to improve SS tolerance of wheat plants.