Glutathione is involved in selenium detoxification and suppresses the selenate-induced SULTR1;1 gene expression in plants

Abstract

Selenium (Se) as a sulfur (S) analog is beneficial to plants. However, excessive Se is toxic. Glutathione (GSH) can protect plant cells from metal toxicity. In this study, we investigated the role of GSH in resistance to Se toxicity and in regulating sulfate/selenate transporter gene expression. We also examined the effects of Se and S treatments on GSH production and growth of Arabidopsis thaliana (a non-Se-accumulator) and broccoli (Brassica oleracea var. italica, a secondary-Se-accumulator). By treating the Arabidopsis wild-type and the glutathione-deficient mutant pad2–1 plants with and without selenate, reduced glutathione, or GSH synthesis inhibitor L-buthionine sulfoximine, we demonstrated that GSH is involved in Se detoxification. The pad2–1 mutant exhibited lower selenate tolerance, and GSH supply alleviated the toxicity. However, selenate treatment reduced GSH levels in a dose-dependent manner, which was further augmented in low sulfur (S) conditions as shown in broccoli plants. Interestingly, the selenate-induced SULTR1;1 gene expression was negatively associated with GSH levels in plants. The pad2–1 mutant showed a much higher AtSULTR1;1 expression than WT under excess Se supply, and GSH supply partially inhibited its expression. Moreover, selenate conferred higher toxicity than selenite under a low S supply in broccoli plants. In contrast, S alleviated selenate toxicity, which was associated with GSH levels. These findings demonstrate the critical role of GSH in resistance to Se toxicity and provide insights into processes related to Se toxicity resistance in plants, which enhances our understanding of metal tolerance for Se biofortification in crops.