Magnesium hydride confers copper tolerance in alfalfa via regulating nitric oxide signaling.

ABSTRACT

Magnesium hydride (MgH2) as a solid-state hydrogen source might be potentially applied in industry and medicine. However, its biological function in plants has not yet been fully discovered. In this report, it was observed that MgH2 administration could relieve copper (Cu) toxicity in alfalfa that was confirmed by a reduction in root growth inhibition. By using old MgH2 as a negative control, it was concluded that above MgH2 function was primarily derived from the releasing of molecular hydrogen (H2), but not caused by either magnesium metabolites or pH alteration. Further results revealed that Cu-triggered nitric oxide (NO) production was intensified by MgH2. Subsequent pharmacological and biochemical experiments suggested that nitrate reductase might be mainly responsible for NO production during above processes. Cu accumulation in the root tissues was also obviously reduced in the presence of MgH2. Meanwhile, increased non-protein thiols (NPTs) content and the deposition of Cu in cell wall of seedling roots could be used to explain the mechanism underlying MgH2-alleviated Cu toxicity via NO signaling. Further, the plant redox balance was reestablished since the Cu stress-modulated antioxidant enzymes activities, reactive oxygen species (ROS) accumulation, and oxidative injury detected by in vivo histochemical and biochemical analyses, were differentially abolished by MgH2. The above responses could be blocked by the removal of endogenous NO after the addition of its scavenger. Taken together, these results clearly suggested that MgH2 control of plant tolerance against Cu toxicity might be mediated by NO signaling, which might open a new window for the application of solid-state hydrogen materials in agriculture.