Evaluation of mitochondrial toxicity of cadmium in clam Ruditapes philippinarum using iTRAQ-based proteomics
Ji, CL; Lu, Z; Xu, LL; Li, F; Cong, M; Shan, XJ; Wu, HF
Source PublicationENVIRONMENTAL POLLUTION
ISSN0269-7491
2019-08
Volume251Pages:802-810
KeywordCadmium iTRAQ Proteomics Mitochondrial toxicity Ruditapes philippinarum
MOST Discipline CatalogueEnvironmental Sciences
DOI10.1016/j.envpol.2019.05.046
Contribution Rank[Ji, Chenglong; Lu, Zhen; Xu, Lanlan; Li, Fei; Cong, Ming; Wu, Huifeng] Chinese Acad Sci, CAS Key Lab Coastal Environm Proc & Ecol Remediat, Yantai Inst Coastal Zone Res YIC, Shandong Key Lab Coastal Environm Proc,YICCAS, Yantai 264003, Peoples R China; [Ji, Chenglong; Shan, Xiujuan; Wu, Huifeng] Qingdao Natl Lab Marine Sci & Technol, Lab Marine Fisheries Sci & Food Prod Proc, Qingdao 266237, Shandong, Peoples R China; [Lu, Zhen; Xu, Lanlan] Univ Chinese Acad Sci, Beijing 100049, Peoples R China
Department海岸带环境过程实验室
AbstractCadmium is one of the most serious metal pollutants in the Bohai Sea. Previous studies revealed that mitochondrion might be the target organelle of Cd toxicity. However, there is a lack of a global view on the mitochondrial responses in marine animals to Cd. In this work, the mitochondrial responses were characterized in clams Ruditapes philippinarum treated with two concentrations (5 and 50 mu g/L) of Cd for 5 weeks using tetraethylbenzimidazolylcarbocyanine iodide (JC-1) staining, ultrastructural observation and quantitative proteomic analysis. Basically, a significant decrease of mitochondrial membrane potential (Delta Psi m) was observed in clams treated with the high concentration (50 mu g/L) of Cd. Cd treatments also induced specific morphological changes indicated by elongated mitochondria. Furthermore, iTRAQ-based mitochondrial proteomics showed that a total of 97 proteins were significantly altered in response to Cd treatment. These proteins were closely associated with multiple biological processes in mitochondria, including tricarboxylic acid (TCA) cycle, oxidative phosphorylation, fatty acid beta-oxidation, stress resistance and apoptosis, and mitochondrial fission. These findings confirmed that mitochondrion was one of the key targets of Cd toxicity. Moreover, dynamical regulations, such as reconstruction of energy homeostasis, induction of stress resistance and apoptosis, and morphological alterations, in mitochondria might play essential roles in Cd tolerance. Overall, this work provided a deep insight into the mitochondrial toxicity of Cd in clams based on a global mitochondrial proteomic analysis. (C) 2019 Elsevier Ltd. All rights reserved.
SubtypeArticle
Indexed BySCI
Language英语
WOS KeywordMUSSELS MYTILUS-GALLOPROVINCIALIS ; VIRGINICA GMELIN BIVALVIA ; SHRIMP CRANGON-AFFINIS ; METABOLIC-RESPONSES ; OXIDATIVE STRESS ; METAL POLLUTION ; MEMBRANE ; INSIGHTS ; FISSION ; BOHAI
WOS Research AreaEnvironmental Sciences
WOS IDWOS:000474329700088
Citation statistics
Cited Times:7[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.yic.ac.cn/handle/133337/24896
Collection中科院海岸带环境过程与生态修复重点实验室_海岸带环境过程实验室
Affiliation1.Chinese Acad Sci, CAS Key Lab Coastal Environm Proc & Ecol Remediat, Yantai Inst Coastal Zone Res YIC, Shandong Key Lab Coastal Environm Proc,YICCAS, Yantai 264003, Peoples R China;
2.Qingdao Natl Lab Marine Sci & Technol, Lab Marine Fisheries Sci & Food Prod Proc, Qingdao 266237, Shandong, Peoples R China;
3.Univ Chinese Acad Sci, Beijing 100049, Peoples R China
Recommended Citation
GB/T 7714
Ji, CL,Lu, Z,Xu, LL,et al. Evaluation of mitochondrial toxicity of cadmium in clam Ruditapes philippinarum using iTRAQ-based proteomics[J]. ENVIRONMENTAL POLLUTION,2019,251:802-810.
APA Ji, CL.,Lu, Z.,Xu, LL.,Li, F.,Cong, M.,...&Wu, HF.(2019).Evaluation of mitochondrial toxicity of cadmium in clam Ruditapes philippinarum using iTRAQ-based proteomics.ENVIRONMENTAL POLLUTION,251,802-810.
MLA Ji, CL,et al."Evaluation of mitochondrial toxicity of cadmium in clam Ruditapes philippinarum using iTRAQ-based proteomics".ENVIRONMENTAL POLLUTION 251(2019):802-810.
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