Meng Jie, Wang Wenxiong, Li Li, Yin Qi, Zhang Guofan
Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, 266071, Shandong, China.
Laboratory for Marine Fisheries and Aquaculture, Qingdao National Laboratory for Marine Science and Technology, Qingdao, Shandong, China.
Sci Rep. 2017 Sep 15;7(1):11716. doi: 10.1038/s41598-017-11894-7.
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.
包括牡蛎在内的海洋软体动物能够在其软组织中富集高浓度的镉(Cd),但其毒性的分子机制仍具有推测性。在本研究中,将太平洋牡蛎(太平洋牡蛎)暴露于镉中9天,并对其鳃进行蛋白质组学分析,通过转录组学分析进一步证实。共定量了4964种蛋白质,并鉴定出515种响应镉暴露的差异表达蛋白质。基因本体富集分析表明,过量的镉影响DNA和蛋白质代谢。具体而言,镉毒性导致碱基切除修复途径中DNA糖基化酶以及缺口填充和连接酶表达的抑制,这可能降低了DNA修复能力。在蛋白质水平上,镉诱导热休克蛋白反应、蛋白质重折叠的启动以及通过泛素蛋白酶体途径的降解等作用。过量的镉还诱导抗氧化反应,特别是谷胱甘肽代谢,其在镉螯合和抗氧化中起重要作用。本研究首次在蛋白质水平上提供了镉对DNA和蛋白质代谢毒性的分子机制,并鉴定了牡蛎中镉毒性的分子生物标志物。