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Tissue-specific molecular and cellular toxicity of Pb in the oyster (Crassostrea gigas): mRNA expression and physiological studies.
Aquat Toxicol. 2018 May; 198:257-268.AT

Abstract

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 β-oxidation and CYP450 catalyzed ω-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.

Authors+Show Affiliations

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; National & Local Joint Engineering Laboratory of Ecological Mariculture, Qingdao 266071, Shandong, China.Marine Environmental Laboratory, HKUST Shenzhen Research Institute, Shenzhen 518057, China.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; National & Local Joint Engineering Laboratory of Ecological Mariculture, Qingdao 266071, Shandong, China. Electronic address: lili@qdio.ac.cn.Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, Shandong, China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, Qingdao 266071, Shandong, China; National & Local Joint Engineering Laboratory of Ecological Mariculture, Qingdao 266071, Shandong, China. Electronic address: gfzhang@qdio.ac.cn.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29562214

Citation

Meng, Jie, et al. "Tissue-specific Molecular and Cellular Toxicity of Pb in the Oyster (Crassostrea Gigas): mRNA Expression and Physiological Studies." Aquatic Toxicology (Amsterdam, Netherlands), vol. 198, 2018, pp. 257-268.
Meng J, Wang WX, Li L, et al. Tissue-specific molecular and cellular toxicity of Pb in the oyster (Crassostrea gigas): mRNA expression and physiological studies. Aquat Toxicol. 2018;198:257-268.
Meng, J., Wang, W. X., Li, L., & Zhang, G. (2018). Tissue-specific molecular and cellular toxicity of Pb in the oyster (Crassostrea gigas): mRNA expression and physiological studies. Aquatic Toxicology (Amsterdam, Netherlands), 198, 257-268. https://doi.org/10.1016/j.aquatox.2018.03.010
Meng J, et al. Tissue-specific Molecular and Cellular Toxicity of Pb in the Oyster (Crassostrea Gigas): mRNA Expression and Physiological Studies. Aquat Toxicol. 2018;198:257-268. PubMed PMID: 29562214.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tissue-specific molecular and cellular toxicity of Pb in the oyster (Crassostrea gigas): mRNA expression and physiological studies. AU - Meng,Jie, AU - Wang,Wen-Xiong, AU - Li,Li, AU - Zhang,Guofan, Y1 - 2018/03/13/ PY - 2017/12/06/received PY - 2018/03/08/revised PY - 2018/03/09/accepted PY - 2018/3/22/pubmed PY - 2018/6/5/medline PY - 2018/3/22/entrez KW - Crassostrea KW - ER stress KW - Fatty acid oxidation KW - Pb exposure KW - Transcriptome SP - 257 EP - 268 JF - Aquatic toxicology (Amsterdam, Netherlands) JO - Aquat Toxicol VL - 198 N2 - 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 β-oxidation and CYP450 catalyzed ω-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. SN - 1879-1514 UR - https://www.unboundmedicine.com/medline/citation/29562214/Tissue_specific_molecular_and_cellular_toxicity_of_Pb_in_the_oyster__Crassostrea_gigas_:_mRNA_expression_and_physiological_studies_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0166-445X(18)30240-6 DB - PRIME DP - Unbound Medicine ER -