Evaluation of mitochondrial toxicity of cadmium in clam Ruditapes philippinarum using iTRAQ-based proteomics. (August 2019)

• Record Type: Journal Article
• Authors: Ji, Chenglong; Lu, Zhen; Xu, Lanlan; Li, Fei; Cong, Ming; Shan, Xiujuan; Wu, Huifeng
• Is Part Of: Environmental pollution. Volume 251(2019)
• Page Start: 802
• Page End: 810
• Publication Date: 2019-08
• Subjects: Cadmium -- iTRAQ -- Proteomics -- Mitochondrial toxicity -- Ruditapes philippinarum; Pollution -- Periodicals; Pollution -- Environmental aspects -- Periodicals; Environmental Pollution -- Periodicals; Pollution -- Périodiques; Pollution -- Aspect de l'environnement -- Périodiques; Pollution -- Effets physiologiques -- Périodiques; Pollution; Pollution -- Environmental aspects; Periodicals; Electronic journals; 363.73
• DOI: 10.1016/j.envpol.2019.05.046
• Languages: English
• ISSNs: 0269-7491

Abstract

Abstract: Cadmium 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 μg/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 ( △Ψm ) was observed in clams treated with the high concentration (50 μg/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 β-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. Graphical abstract: Image 1 Highlights: Mitochondrion was the target organelle of Cd toxicity. Cd dissipated mitochondrial membrane potential. Cd induced mitochondrial elongations. Abstract : Cd induced mitochondrial toxicity in clam gills. Dynamical regulations in mitochondria might play essential roles in Cd tolerance.