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Cadmium Disrupts the Balance between Hydrogen Peroxide and Superoxide Radical by Regulating Endogenous Hydrogen Sulfide in the Root Tip of Brassica rapa

Cd (cadmium) stress always alters the homeostasis of ROS (reactive oxygen species) including H(2)O(2) (hydrogen sulfide) and [Formula: see text] (superoxide radical), leading to the oxidative injury and growth inhibition in plants. In addition to triggering oxidative injury, ROS has been suggested a...

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Detalles Bibliográficos
Autores principales: Lv, Wenjing, Yang, Lifei, Xu, Cunfa, Shi, Zhiqi, Shao, Jinsong, Xian, Ming, Chen, Jian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5318417/
https://www.ncbi.nlm.nih.gov/pubmed/28270829
http://dx.doi.org/10.3389/fpls.2017.00232
Descripción
Sumario:Cd (cadmium) stress always alters the homeostasis of ROS (reactive oxygen species) including H(2)O(2) (hydrogen sulfide) and [Formula: see text] (superoxide radical), leading to the oxidative injury and growth inhibition in plants. In addition to triggering oxidative injury, ROS has been suggested as important regulators modulating root elongation. However, whether and how Cd stress induces the inhibition of root elongation by differentially regulating endogenous H(2)O(2) and [Formula: see text] , rather than by inducing oxidative injury, remains elusive. To address these gaps, histochemical, physiological, and biochemical approaches were applied to investigate the mechanism for Cd to fine-tune the balance between H(2)O(2) and [Formula: see text] in the root tip of Brassica rapa. Treatment with Cd at 4 and 16 μM significantly inhibited root elongation, while only 16 μM but not 4 μM of Cd induced oxidative injury and cell death in root tip. Fluorescent and pharmaceutical tests suggested that H(2)O(2) and [Formula: see text] played negative and positive roles, respectively, in the regulation of root elongation in the presence of Cd (4 μM) or not. Treatment with Cd at 4 μM led to the increase in H(2)O(2) and the decrease in [Formula: see text] in root tip, which may be attributed to the up-regulation of Br_UPB1s and the down-regulation of their predicted targets (four peroxidase genes). Cd at 4 μM resulted in the increase in endogenous H(2)S in root tip by inducing the up-regulation of LCDs and DCDs. Treatment with H(2)S biosynthesis inhibitor or H(2)S scavenger significantly blocked Cd (4 μM)-induced increase in endogenous H(2)S level, coinciding with the recovery of root elongation, the altered balance between H(2)O(2) and [Formula: see text] , and the expression of Br_UPB1s and two peroxidase genes. Taken together, it can be proposed that endogenous H(2)S mediated the phytotoxicity of Cd at low concentration by regulating Br_UPB1s-modulated balance between H(2)O(2) and [Formula: see text] in root tip. Such findings shed new light on the regulatory role of endogenous H(2)S in plant adaptions to Cd stress.