Exogenous glutathione enhances cadmium accumulation and alleviates its toxicity in Populus × canescens

Glutathione (GSH) plays an important role in cadmium (Cd) tolerance in woody plants, but the underlying mechanisms remain largely unknown. To elucidate the physiological and transcriptional regulation mechanisms of GSH-mediated Cd tolerance in woody plants, we exposed Populus × canescens (Ait.) Smith saplings to either 0 or 75 μM Cd together with one of three external GSH levels. Glutathione treatments include buthionine sulfoximine (BSO, an inhibitor of GSH biosynthesis), no external GSH and exogenous GSH. External GSH resulted in higher Cd2+ uptake rate in the roots, greater Cd amount in poplars, lower Cd-induced H2O2 levels in the roots, and higher contents of endogenous GSH in Cd-treated roots and leaves. Furthermore, external GSH led to upregulated transcript levels of several genes including zinc/iron regulated transporter related protein 6.2 (ZIP6.2) and natural resistance-associated macrophage protein 1.3 (NRAMP1.3), which probably take part in Cd uptake, glutathione synthetase 2 (GS2) implicated in Cd detoxification, metal tolerance protein 1 (MTP1) and ATP-binding cassette transporter C3 (ABCC3) involved in Cd vacuolar accumulation in the roots, γ-glutamylcysteine synthetase (ECS) and phytochelatin synthetase family protein 1 (PCS1) involved in Cd detoxification, and oligopeptide transporter 7 (OPT7) probably implicated in Cd detoxification in the leaves of Cd-exposed P. × canescens. In contrast, BSO often displayed the opposite effects on Cd-triggered physiological and transcriptional regulation responses in poplars. These results suggest that exogenous GSH can enhance Cd accumulation and alleviate its toxicity in poplars. This is probably attributed to external-GSH-induced higher net Cd2+ influx in the roots, greater Cd accumulation in aerial parts, stronger scavenging of reactive oxygen species, and transcriptional overexpression of several genes involved in Cd uptake, detoxification and accumulation.