Institutional Repository of Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences
Tissue-specific molecular and cellular toxicity of Pb in the oyster (Crassostrea gigas): mRNA expression and physiological studies | |
Meng, Jie1,2,4; Wang, Wen-Xiong5; Li, Li1,2,4; Zhang, Guofan1,3,4 | |
2018-05-01 | |
发表期刊 | AQUATIC TOXICOLOGY |
ISSN | 0166-445X |
卷号 | 198期号:2018页码:257-268 |
通讯作者 | Li, Li ; Zhang, Guofan |
摘要 | Lead (Pb) is one of the ubiquitous and toxic elements in aquatic environment. In oysters, gills and digestive glands are the main target organs for Pb-induced toxicity, but there is limited information on the molecular mechanisms underlying its toxicity. The present study investigated the Pb-induced toxicity mechanisms in the Pacific oyster (Crassostrea gigas) based on transcriptome, phenotypic anchoring, and validation of targeted gene expression. Gene ontology and pathway enrichment analyses revealed the differential Pb toxicity mechanisms in the tissues. In the gills, Pb disturbed the protein metabolism, with the most significant enrichment of the "protein processing in endoplasmic reticulum" pathway. The main mechanism comprised of a Pb-stimulated calcium (Ca2+) increase by the up-regulation of transporter-Ca-ATPase expression. The disturbed Ca2+ homeostasis then further induced high expressions of endoplasmic reticulum (ER) chaperones, leading to ER stress in the oysters. Unfolded proteins induced ER associated degradation (ERAD), thereby preventing the accumulation of folding incompetent glycoproteins. However, Pb mainly induced oxidative reduction reactions in the digestive gland with high accumulation of lipid peroxidation products and high expression of antioxidant enzymes. Further, Pb induced fatty acid beta-oxidation and CYP450 catalyzed co-oxidation due to increased metabolic expenditure for detoxification. The increased content of arachidonic acid indicated that Pb exposure might alter unsaturated fatty acid composition and disturb cellular membrane functions. Taken together, our results provided a new insight into the molecular mechanisms underlying Pb toxicity in oysters. |
关键词 | Crassostrea Pb Exposure Er Stress Fatty Acid Oxidation Transcriptome |
DOI | 10.1016/j.aquatox.2018.03.010 |
语种 | 英语 |
资助项目 | Shandong Provincial Natural Science Foundation, China[ZR2016DQ13] ; National Natural Science Foundation of China[31530079] ; Earmarked Fund for Modern Agro-industry Technology Research System[CARS-48] ; Qingdao National Laboratory for Marine Science and Technology[2015ASKJ02-03] ; Strategic Priority Research Program of |
WOS研究方向 | Marine & Freshwater Biology ; Toxicology |
WOS类目 | Marine & Freshwater Biology ; Toxicology |
WOS记录号 | WOS:000430630100026 |
出版者 | ELSEVIER SCIENCE BV |
引用统计 | |
文献类型 | 期刊论文 |
版本 | 出版稿 |
条目标识符 | http://ir.qdio.ac.cn/handle/337002/154489 |
专题 | 实验海洋生物学重点实验室 |
通讯作者 | Li, Li; Zhang, Guofan |
作者单位 | 1.Chinese Acad Sci, Inst Oceanol, Key Lab Expt Marine Biol, Qingdao 266071, Shandong, Peoples R China 2.Qingdao Natl Lab Marine Sci & Technol, Lab Marine Fisheries & Aquaculture, Qingdao, Shandong, Peoples R China 3.Qingdao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao 266071, Shandong, Peoples R China 4.Natl & Local Joint Engn Lab Ecol Mariculture, Qingdao 266071, Shandong, Peoples R China 5.HKUST Shenzhen Res Inst, Marine Environm Lab, Shenzhen 518057, Peoples R China |
第一作者单位 | 中国科学院海洋研究所 |
通讯作者单位 | 中国科学院海洋研究所 |
推荐引用方式 GB/T 7714 | Meng, Jie,Wang, Wen-Xiong,Li, Li,et al. Tissue-specific molecular and cellular toxicity of Pb in the oyster (Crassostrea gigas): mRNA expression and physiological studies[J]. AQUATIC TOXICOLOGY,2018,198(2018):257-268. |
APA | Meng, Jie,Wang, Wen-Xiong,Li, Li,&Zhang, Guofan.(2018).Tissue-specific molecular and cellular toxicity of Pb in the oyster (Crassostrea gigas): mRNA expression and physiological studies.AQUATIC TOXICOLOGY,198(2018),257-268. |
MLA | Meng, Jie,et al."Tissue-specific molecular and cellular toxicity of Pb in the oyster (Crassostrea gigas): mRNA expression and physiological studies".AQUATIC TOXICOLOGY 198.2018(2018):257-268. |
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