Hydrogen sulfide alleviates aluminum toxicity in barley seedlings |
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Authors: | Juan Chen Wen-Hua Wang Fei-Hua Wu Chun-Yan You Ting-Wu Liu Xue-Jun Dong Jun-Xian He Hai-Lei Zheng |
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Institution: | 1. Key Laboratory for Subtropical Wetland Ecosystem Research of MOE, College of the Environment and Ecology, Xiamen University, Xiamen, Fujian, 361005, People’s Republic of China 2. Central Grasslands Research Extension Center, North Dakota State University, Streeter, ND, 58483, USA 3. State Key Laboratory of Agobiotechnology and School of Life Sciences, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
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Abstract: | Aims Aluminum (Al) toxicity is one of the major factors that limit plant growth. Low concentration of hydrogen sulfide (H2S) has been proven to function in physiological responses to various stresses. The objective of this study is to investigate the possible role of H2S in Al toxicity in barley (Hordeum vulgare L) seedlings. Methods Barley seedlings pre-treated with sodium hydrosulfide (NaHS), a H2S donor, and subsequently exposed to Al treatment were studied for their effects on root elongation, Al accumulation in seedlings, Al-induced citrate secretion and oxidative stress, and plasma membrane (PM) H+-ATPase expression. Results Our results showed that H2S had significant rescue effects on Al-induced inhibition of root elongation which was correlated well with the decrease of Al accumulation in seedlings. Meanwhile, Al-induced citrate secretion was also significantly enhanced by NaHS pretreatment. Al-induced oxidative stress as indicated by lipid peroxidation and reactive oxygen species burst was alleviated by H2S through the activation of the antioxidant system. Moreover, Al-induced reduction in PM H+-ATPase expression was reversed by exogenous NaHS. Conclusions Altogether, our results suggest H2S plays an ameliorative role in protecting plants against Al toxicity by inducing the activities of antioxidant enzymes, increasing citrate secretion and citrate transporter gene expression, and enhancing the expression of PM H+-ATPase. |
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