Exogenous Abscisic Acid Alleviates Cadmium Toxicity by Restricting Cd2+ Influx in Populus euphratica Cells

Abscisic acid (ABA), a widely known phytohormone involved in the plant response to abiotic stress, plays a vital role in mitigating Cd2+ toxicity in herbaceous species. However, the role of ABA in ameliorating Cd2+ toxicity in woody species is largely unknown. In the present study, we investigated ABA restriction on Cd2+ uptake and the relevance to Cd2+ stress alleviation in Cd2+-hypersensitive Populus euphratica. ABA (5 μM) markedly improved cell viability and growth but reduced membrane permeability in CdCl2 (100 μM)-stressed P. euphratica cells. Moreover, ABA significantly increased the activity of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), and ascorbate peroxidase (APX), contributing to the scavenging of Cd2+-elicited H2O2 within P. euphratica cells during the period of CdCl2 exposure (100 μM, 24–72 h). ABA alleviation of Cd2+ toxicity was mainly the result of ABA restriction of Cd2+ uptake under Cd2+ stress. Steady-state and transient flux recordings showed that ABA inhibited Cd2+ entry into Cd2+-shocked (100 μM, 30 min) and short-term-stressed P. euphratica cells (100 μM, 24–72 h). Non-invasive micro-test technique data showed that H2O2 (3 mM) stimulated the Cd2+-elicited Cd2+ influx but that the plasma membrane (PM) Ca2+ channel inhibitor LaCl3 blocked it, suggesting that the Cd2+ influx was through PM Ca2+-permeable channels. These results suggested that ABA up-regulated antioxidant enzyme activity in Cd2+-stressed P. euphratica and that these enzymes scavenged the Cd2+-elicited H2O2 within cells. The entry of Cd2+ through the H2O2-mediated Ca2+-permeable channels was subsequently restricted; thus, Cd2+ buildup and toxicity were reduced in the Cd2+-hypersensitive species, P. euphratica.