Cadmium-induced hydrogen sulfide synthesis is involved in cadmium tolerance in Medicago sativa by reestablishment of reduced (homo)glutathione and reactive oxygen species homeostases.
Until now, physiological mechanisms and downstream targets responsible for the cadmium (Cd) tolerance mediated by endogenous hydrogen sulfide (H2S) have been elusive. To address this gap, a combination of pharmacological, histochemical, biochemical and molecular approaches was applied. The perturbat...
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Public Library of Science (PLoS)
2014-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC4183592?pdf=render |
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| author | Weiti Cui Huiping Chen Kaikai Zhu Qijiang Jin Yanjie Xie Jin Cui Yan Xia Jing Zhang Wenbiao Shen |
| author_facet | Weiti Cui Huiping Chen Kaikai Zhu Qijiang Jin Yanjie Xie Jin Cui Yan Xia Jing Zhang Wenbiao Shen |
| author_sort | Weiti Cui |
| collection | DOAJ |
| description | Until now, physiological mechanisms and downstream targets responsible for the cadmium (Cd) tolerance mediated by endogenous hydrogen sulfide (H2S) have been elusive. To address this gap, a combination of pharmacological, histochemical, biochemical and molecular approaches was applied. The perturbation of reduced (homo)glutathione homeostasis and increased H2S production as well as the activation of two H2S-synthetic enzymes activities, including L-cysteine desulfhydrase (LCD) and D-cysteine desulfhydrase (DCD), in alfalfa seedling roots were early responses to the exposure of Cd. The application of H2S donor sodium hydrosulfide (NaHS), not only mimicked intracellular H2S production triggered by Cd, but also alleviated Cd toxicity in a H2S-dependent fashion. By contrast, the inhibition of H2S production caused by the application of its synthetic inhibitor blocked NaHS-induced Cd tolerance, and destroyed reduced (homo)glutathione and reactive oxygen species (ROS) homeostases. Above mentioned inhibitory responses were further rescued by exogenously applied glutathione (GSH). Meanwhile, NaHS responses were sensitive to a (homo)glutathione synthetic inhibitor, but reversed by the cotreatment with GSH. The possible involvement of cyclic AMP (cAMP) signaling in NaHS responses was also suggested. In summary, LCD/DCD-mediated H2S might be an important signaling molecule in the enhancement of Cd toxicity in alfalfa seedlings mainly by governing reduced (homo)glutathione and ROS homeostases. |
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| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-11T21:08:03Z |
| publishDate | 2014-01-01 |
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| spelling | doaj.art-c9aad54f7e53493983328d03c82f7fce2022-12-22T00:50:48ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-01910e10966910.1371/journal.pone.0109669Cadmium-induced hydrogen sulfide synthesis is involved in cadmium tolerance in Medicago sativa by reestablishment of reduced (homo)glutathione and reactive oxygen species homeostases.Weiti CuiHuiping ChenKaikai ZhuQijiang JinYanjie XieJin CuiYan XiaJing ZhangWenbiao ShenUntil now, physiological mechanisms and downstream targets responsible for the cadmium (Cd) tolerance mediated by endogenous hydrogen sulfide (H2S) have been elusive. To address this gap, a combination of pharmacological, histochemical, biochemical and molecular approaches was applied. The perturbation of reduced (homo)glutathione homeostasis and increased H2S production as well as the activation of two H2S-synthetic enzymes activities, including L-cysteine desulfhydrase (LCD) and D-cysteine desulfhydrase (DCD), in alfalfa seedling roots were early responses to the exposure of Cd. The application of H2S donor sodium hydrosulfide (NaHS), not only mimicked intracellular H2S production triggered by Cd, but also alleviated Cd toxicity in a H2S-dependent fashion. By contrast, the inhibition of H2S production caused by the application of its synthetic inhibitor blocked NaHS-induced Cd tolerance, and destroyed reduced (homo)glutathione and reactive oxygen species (ROS) homeostases. Above mentioned inhibitory responses were further rescued by exogenously applied glutathione (GSH). Meanwhile, NaHS responses were sensitive to a (homo)glutathione synthetic inhibitor, but reversed by the cotreatment with GSH. The possible involvement of cyclic AMP (cAMP) signaling in NaHS responses was also suggested. In summary, LCD/DCD-mediated H2S might be an important signaling molecule in the enhancement of Cd toxicity in alfalfa seedlings mainly by governing reduced (homo)glutathione and ROS homeostases.http://europepmc.org/articles/PMC4183592?pdf=render |
| spellingShingle | Weiti Cui Huiping Chen Kaikai Zhu Qijiang Jin Yanjie Xie Jin Cui Yan Xia Jing Zhang Wenbiao Shen Cadmium-induced hydrogen sulfide synthesis is involved in cadmium tolerance in Medicago sativa by reestablishment of reduced (homo)glutathione and reactive oxygen species homeostases. PLoS ONE |
| title | Cadmium-induced hydrogen sulfide synthesis is involved in cadmium tolerance in Medicago sativa by reestablishment of reduced (homo)glutathione and reactive oxygen species homeostases. |
| title_full | Cadmium-induced hydrogen sulfide synthesis is involved in cadmium tolerance in Medicago sativa by reestablishment of reduced (homo)glutathione and reactive oxygen species homeostases. |
| title_fullStr | Cadmium-induced hydrogen sulfide synthesis is involved in cadmium tolerance in Medicago sativa by reestablishment of reduced (homo)glutathione and reactive oxygen species homeostases. |
| title_full_unstemmed | Cadmium-induced hydrogen sulfide synthesis is involved in cadmium tolerance in Medicago sativa by reestablishment of reduced (homo)glutathione and reactive oxygen species homeostases. |
| title_short | Cadmium-induced hydrogen sulfide synthesis is involved in cadmium tolerance in Medicago sativa by reestablishment of reduced (homo)glutathione and reactive oxygen species homeostases. |
| title_sort | cadmium induced hydrogen sulfide synthesis is involved in cadmium tolerance in medicago sativa by reestablishment of reduced homo glutathione and reactive oxygen species homeostases |
| url | http://europepmc.org/articles/PMC4183592?pdf=render |
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