Hydrogen sulfide alleviates cadmium toxicity through regulations of cadmium transport across the plasma and vacuolar membranes in Populus euphratica cells

Hydrogen sulfide (H2S) is emerging as a novel signalling molecule involved in plant growth and responses against abiotic stresses. However, little information is known about its role in cadmium (Cd) detoxification. In the present study, the effects of H2S on Cd toxicity were investigated in Populus euphratica cells using fluorescence imaging technique and a non-invasive vibrating ion-selective microelectrode. Pretreatment with a H2S donor, sodium hydrosulfide (NaHS), significantly mitigated the Cd-induced programmed cell death in P. euphratica cells. The alleviation effect of NaHS was more pronounced at 50–100 μM as compared to low (25 μM) and high doses (200 μM). Under Cd stress, total activities of antioxidant enzymes, such as ascorbate peroxidase, catalase and glutathione reductase, were significantly enhanced in NaHS-treated cells, leading to a decline of H2O2 accumulation and lipid peroxidation. Moreover, NaHS reduced Cd accumulation in the cytoplasm but increased the fraction of Cd in the vacuole. Cd flux profiles revealed that H2S inhibited the Cd influx through the plasma membrane (PM) calcium channels that activated by H2O2. NaHS enhanced Cd influx into the vacuole, and the Cd influx was dependent on the pH gradients across the tonoplast. Taken together, these results suggest that H2S alleviates Cd toxicity via the improvement of antioxidant system and cellular Cd homeostasis. The up-regulation of antioxidant enzymes by H2S reduced the accumulation of H2O2, and thus decreased Cd influx through the H2O2-activated PM calcium channels. The H2S-simulated vacuolar Cd sequestration was presumably due to the activation of tonoplast Cd2+/H+ antiporters.

► We examined H2S alleviation on Cd toxicity in Cd-susceptible Populus euphratica.
► H2S alleviates Cd toxicity via mediations of antioxidant system and Cd homeostasis.
► H2S reduced H2O2 accumulation in Cd-treated poplar cells.
► H2S decreased Cd influx through the PM calcium channels that activated by H2O2.
► H2S stimulated vacuolar Cd sequestration through the tonoplast Cd2+/H+ antiporters.