蛋白质组学分析显示，镉对牡蛎（Crassostrea gigas）中DNA和蛋白质代谢的影响。,Scientific Reports

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蛋白质组学分析显示，镉对牡蛎（Crassostrea gigas）中DNA和蛋白质代谢的影响。
Scientific Reports ( IF 3.8 ) Pub Date : 2017-Sep-15 , DOI: 10.1038/s41598-017-11894-7
Jie Meng , Wenxiong Wang , Li Li , Qi Yin , Guofan Zhang

海洋软体动物（包括牡蛎）可以在其软组织中富集高水平的镉（Cd），但是Cd毒性的分子机制仍然是推测性的。在这项研究中，太平洋牡蛎（Crassostrea gigas）暴露于镉中9天，其g进行蛋白质组学分析，并通过转录组分析进一步证实。总共对4,964种蛋白质进行了定量，并确定了515种差异表达的蛋白质，以响应Cd暴露。基因本体论富集分析表明，过量的镉会影响DNA和蛋白质的代谢。具体而言，Cd毒性导致碱基切除修复途径中的DNA糖基化酶和间隙填充和连接酶表达受到抑制，这可能会降低DNA修复能力。在蛋白质水平上，Cd诱导了热激蛋白反应，蛋白质重折叠的启动以及泛素蛋白酶体途径的降解等。过量的镉还会诱导抗氧化反应，尤其是谷胱甘肽代谢，这在镉螯合和抗氧化中起重要作用。这项研究提供了在蛋白质水平上Cd毒性对DNA和蛋白质代谢的第一个分子机制，并确定了牡蛎中Cd毒性的分子生物标志物。

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Cadmium effects on DNA and protein metabolism in oyster (Crassostrea gigas) revealed by proteomic analyses.

Marine molluscs, including oysters, can concentrate high levels of cadmium (Cd) in their soft tissues, but the molecular mechanisms of Cd toxicity remain speculative. In this study, Pacific oysters (Crassostrea gigas) were exposed to Cd for 9 days and their gills were subjected to proteomic analysis, which were further confirmed with transcriptomic analysis. A total of 4,964 proteins was quantified and 515 differentially expressed proteins were identified in response to Cd exposure. Gene Ontology enrichment analysis revealed that excess Cd affected the DNA and protein metabolism. Specifically, Cd toxicity resulted in the inhibition of DNA glycosylase and gap-filling and ligation enzymes expressions in base excision repair pathway, which may have decreased DNA repair capacity. At the protein level, Cd induced the heat shock protein response, initiation of protein refolding as well as degradation by ubiquitin proteasome pathway, among other effects. Excess Cd also induced antioxidant responses, particularly glutathione metabolism, which play important roles in Cd chelation and anti-oxidation. This study provided the first molecular mechanisms of Cd toxicity on DNA and protein metabolism at protein levels, and identified molecular biomarkers for Cd toxicity in oysters.

更新日期：2017-09-15

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