Evaluation of mitochondrial toxicity of cadmium in clam Ruditapes philippinarum using iTRAQ-based proteomics
Evaluation of mitochondrial toxicity of cadmium in clam Ruditapes philippinarum using iTRAQ-based proteomics
复制标题
使用基于 iTRAQ 的蛋白质组学评估菲律宾蛤仔中镉的线粒体毒性
DOI：
10.1016/j.envpol.2019.05.046
复制
发表时间：
2019-08-01
影响因子：
8.9
通讯作者：
Wu, Huifeng
中科院分区：
文献类型：
--
作者：
Ji, Chenglong;Lu, Zhen;Wu, Huifeng
镉是渤海海域最严重的金属污染物之一。以往的研究表明，线粒体可能是镉毒性的靶细胞器。然而，目前对海洋动物线粒体对Cd的反应还缺乏全面的了解。本研究采用四乙基苯并噻唑基碳氰碘（JC-1）染色、超微结构观察和定量蛋白质组学分析，对两种浓度（5和50 μ g/L） Cd处理5周的菲律宾蛤（Ruditapes philipparum）的线粒体反应进行了表征。高浓度（50 μ g/L）镉处理后，蛤体线粒体膜电位（δ Psi m）显著降低。镉处理还引起了线粒体延长的特殊形态变化。此外，基于itraq的线粒体蛋白质组学研究显示，共有97种蛋白质在Cd治疗后发生了显著改变。这些蛋白与线粒体中的多种生物过程密切相关，包括三羧酸（TCA）循环、氧化磷酸化、脂肪酸β -氧化、抗逆性和凋亡以及线粒体裂变。这些发现证实了线粒体是镉毒性的关键靶点之一。此外，线粒体能量稳态的重建、抗逆性和凋亡的诱导以及形态改变等动态调控可能在Cd耐受中起重要作用。总的来说，这项工作基于全球线粒体蛋白质组学分析，为镉对蛤的线粒体毒性提供了深入的了解。(C) 2019 Elsevier Ltd.版权所有。
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 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.