Nitrate-induced AHb1 expression aggravates Cd toxicity in plants.

ABSTRACT

Cadmium (Cd) causes severe toxicity in plants. However, the molecular mechanisms underlying plant resistance to Cd in relation to nitrogen (N) supply remain unclear. The non-symbiotic hemoglobin gene Hb1 plays an important role in scavenging nitric oxide (NO) in plants. In this study, there was no differential effect of Cd on the biomass of wild-type (WT) and AHb1-overexpressing (H7) plants when NH4+-N was used as a nitrogen source. However, under NO3--N conditions, Cd exerted less biomass stress on AHb1-silenced (L3) plants and more stress on H7 plants than on WT plants. The Cd tolerance index followed the order L3 > WT > H7. However, there was no difference in Cd concentrations in the roots or shoots of the WT, L3, and H7 plants, indicating that differences in AHb1 expression were unrelated to Cd uptake. Further investigation showed that Cd exposure enhanced H2O2 accumulation and aggravated oxidative damage in H7 plants. The application of an NO donor effectively reversed growth inhibition, H2O2 burst, and oxidative stress induced by Cd in H7 plants. Thus, we suggest that NO3--induced AHb1 expression suppresses Cd-induced NO production in plants, increasing the ROS burst and exacerbating Cd toxicity.