Cadmium-induced nitric oxide burst enhances Cd tolerance at early stage in roots of a hyperaccumulator Sedum alfredii partially by altering glutathione metabolism.

Understanding cadmium (Cd) tolerance and accumulation strategies of hyperaccumulators is crucial for promoting phytoremediation of polluted soils. Root resistance to Cd regulated by nitric oxide (NO) was investigated for the Cd hyperaccumulating ecotype (HE) of Sedum alfredii. Differed from that of its non-hyperaccumulating ecotype, Cd stress in HE roots triggered a strong NO burst mediated through both nitrate reductase and nitric oxide synthase. Elimination of endogenous NO did not affect Cd levels in roots, but greatly aggravated the metal toxicity, including increased reactive oxygen species (ROS) accumulation, oxidative damage and cell ultrastructure injury. Cadmium stress in HE triggered up-regulated SOD activities but down-regulated POD, CAT, and APX activities, which were significantly inverted by NO scavenger. The NO burst also expanded the glutathione (GSH) pool in HE roots by activation of GR, GSNOR, and γ-ECS, but had no effects on the ascorbate acid (AsA) recycle. Similar to that of NO, preferential localizations of ROS and GSH to meristem and cylinder were observed in root tips of HE. Cadmium uptake and translocation were not affected by the NO levels. These results suggest that NO burst activated a GSH-involved strategy, instead of altering Cd accumulation, to protect root tips of HE S. alfredii against Cd toxicity at early stage.