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Hydrogen Sulfide Alleviates Cadmium-Induced Cell Death through Restraining ROS Accumulation in Roots of Brassica rapa L. ssp. pekinensis

Hydrogen sulfide (H(2)S) is a cell signal molecule produced endogenously and involved in regulation of tolerance to biotic and abiotic stress in plants. In this work, we used molecular biology, physiology, and histochemical methods to investigate the effects of H(2)S on cadmium- (Cd-) induced cell d...

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Detalles Bibliográficos
Autores principales: Zhang, Liping, Pei, Yanxi, Wang, Hongjiao, Jin, Zhuping, Liu, Zhiqiang, Qiao, Zengjie, Fang, Huihui, Zhang, Yanjie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4442412/
https://www.ncbi.nlm.nih.gov/pubmed/26078819
http://dx.doi.org/10.1155/2015/804603
Descripción
Sumario:Hydrogen sulfide (H(2)S) is a cell signal molecule produced endogenously and involved in regulation of tolerance to biotic and abiotic stress in plants. In this work, we used molecular biology, physiology, and histochemical methods to investigate the effects of H(2)S on cadmium- (Cd-) induced cell death in Chinese cabbage roots. Cd stress stimulated a rapid increase of endogenous H(2)S in roots. Additionally, root length was closely related to the cell death rate. Pretreatment with sodium hydrosulfide (NaHS), a H(2)S donor, alleviated the growth inhibition caused by Cd in roots—this effect was more pronounced at 5 μM NaHS. Cd-induced cell death in roots was significantly reduced by 5 μM NaHS treatment. Under Cd stress, activities of the antioxidant enzymes were significantly enhanced in roots. NaHS + Cd treatment made their activities increase further compared with Cd exposure alone. Enhanced antioxidant enzyme activity led to a decline in reactive oxygen species accumulation and lipid peroxidation. In contrast, these effects were reversed by hydroxylamine, a H(2)S inhibitor. These results suggested that H(2)S alleviated the cell death caused by Cd via upregulation of antioxidant enzyme activities to remove excessive reactive oxygen species and reduce cell oxidative damage.