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Toxicity of nickel and cobalt in Japanese flounder

文献类型： 外文期刊

作者： Sun, Zhaohui 1 ; Gong, Chunguang 3 ; Ren, Jiangong 2 ; Zhang, Xiaoyan 2 ; Wang, Guixing 2 ; Liu, Yufeng 2 ; Ren, Yuqin 2 ;

作者机构： 1.Minist Agr, Key Lab Aquat Genom, Beijing 100141, Peoples R China

2.Chinese Acad Fishery Sci, Beidaihe Cent Expt Stn, Qinhuangdao 066100, Hebei, Peoples R China

3.Agr Univ Hebei, Ocean Coll, Qinhuangdao 066009, Hebei, Peoples R China

关键词： Paralichthys olivaceous; Lethal concentration; Oxidative stress; Transcriptome; Ferroptosis

期刊名称：ENVIRONMENTAL POLLUTION （ 影响因子：8.071； 五年影响因子：8.35 ）

ISSN： 0269-7491

年卷期： 2020 年 263 卷

页码：

收录情况： SCI

摘要： Nickel and cobalt are essential elements that become toxic at high concentrations. Little is known about nickel and cobalt toxicity in aquatic animals. This study aimed to investigate acute and chronic toxicity of nickel and cobalt in Japanese flounder (Paralichthys olivaceous), with emphasis on oxidative stress reactions, histopathological changes, and differences in gene expression. The lethal concentration for 50% mortality (LC50) in 3 and 8 cm Japanese flounder exposed to nickel for 96 h was found to be 86.2 +/- 0.018 and 151.3 +/- 0.039 mg/L; for cobalt exposure, LC50 was 47.5 +/- 0.015 and 180.4 +/- 0.034 mg/L, respectively. Chronic nickel and cobalt exposure caused different degrees of oxidative enzyme activity changes in gill, liver, and muscle tissues. Erythrocyte deformations were detected after acute or chronic exposure to nickel and cobalt. the nickel and cobalt exposure also caused pathological changes such as spherical swelling over other gill patches, rod-like proliferations in the gill patch epithelial cell layer, and disorder in hepatocyte arrangement, cell swelling, and cytoplasm loosening. RNA-Seq indicated that there were 184 upregulated and 185 downregulated genes in the liver of Japanese flounder exposed to 15 mg/L nickel for 28 d. For cobalt, 920 upregulated and 457 downregulated genes were detected. Among these differentially expressed genes, 162 were shared by both nickel and cobalt exposure. In both nickel and cobalt, pathways including fatty acid elongation, steroid biosynthesis, unsaturated fatty acid biosynthesis, fatty acid metabolism, PPAR signaling, and ferroptosis were significantly enriched. Taken together, these results aided our understanding of the toxicity of nickel and cobalt in aquatic animals. (C) 2020 Elsevier Ltd. All rights reserved.

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