Hydrogen Sulfide Mediates K(+) and Na(+) Homeostasis in the Roots of Salt-Resistant and Salt-Sensitive Poplar Species Subjected to NaCl Stress

Non-invasive micro-test techniques (NMT) were used to analyze NaCl-altered flux profiles of K(+), Na(+), and H(+) in roots and effects of NaHS (a H(2)S donor) on root ion fluxes in two contrasting poplar species, Populus euphratica (salt-resistant) and Populus popularis (salt-sensitive). Both poplar species displayed a net K(+) efflux after exposure to salt shock (100 mM NaCl), as well as after short-term (24 h), and long-term (LT) (5 days) saline treatment (50 mM NaCl, referred to as salt stress). NaHS (50 μM) restricted NaCl-induced K(+) efflux in roots irrespective of the duration of salt exposure, but K(+) efflux was not pronounced in data collected from the LT salt stress treatment of P. euphratica. The NaCl-induced K(+) efflux was inhibited by a K(+) channel blocker, tetraethylammonium chloride (TEA) in P. popularis root samples, but K(+) loss increased with a specific inhibitor of plasma membrane (PM) H(+)-ATPase, sodium orthovanadate, in both poplar species under LT salt stress and NaHS treatment. This indicates that NaCl-induced K(+) loss was through depolarization-activated K(+) channels. NaHS caused increased Na(+) efflux and a corresponding increase in H(+) influx for poplar roots subjected to both the short- and LT salt stress. The NaHS-enhanced H(+) influx was not significant in P. euphratica samples subjected to short term salt stress. Both sodium orthovanadate and amiloride (a Na(+)/H(+) antiporter inhibitor) effectively inhibited the NaHS-augmented Na(+) efflux, indicating that the H(2)S-enhanced Na(+) efflux was due to active Na(+) exclusion across the PM. We therefore conclude that the beneficial effects of H(2)S probably arise from upward regulation of the Na(+)/H(+) antiport system (H(+) pumps and Na(+)/H(+) antiporters), which promote exchange of Na(+) with H(+) across the PM and simultaneously restricted the channel-mediated K(+) loss that activated by membrane depolarization.