Integration of Multi-Omics, Histological, and Biochemical Analysis Reveals the Toxic Responses of Nile Tilapia Liver to Chronic Microcystin-LR Exposure
文献类型： 外文期刊
作者： Li, Yichao 1 ; Yang, Huici 2 ; Fu, Bing 3 ; Kaneko, Gen 4 ; Li, Hongyan 2 ; Tian, Jingjing 2 ; Wang, Guangjun 2 ; Wei, Mingken 5 ; Xie, Jun 2 ; Yu, Ermeng 2 ;
作者机构： 1.Shanghai Ocean Univ, Fac Fisheries & Life Sci, Shanghai 201306, Peoples R China
2.Chinese Acad Fishery Sci, Pearl River Fisheries Res Inst, Guangzhou 510380, Peoples R China
3.South China Agr Univ, Coll Marine Sci, Guangzhou 510640, Peoples R China
4.Univ Houston, Coll Nat & Appl Sci, Victoria, TX 77901 USA
5.Guangdong Lab Lingnan Modern Agr, Maoming Branch, Maoming 525000, Peoples R China
关键词： microcystin-LR; nile tilapia; hepatotoxicity; bile acid biosynthesis; molecular mechanism
期刊名称：TOXINS （ 影响因子：4.2； 五年影响因子：4.7 ）
ISSN：
年卷期： 2024 年 16 卷 3 期
页码：
收录情况： SCI
摘要： Microcystin-LR (MC-LR) is a cyanobacterial metabolite produced during cyanobacterial blooms and is toxic to aquatic animals, and the liver is the main targeted organ of MC-LR. To comprehensively understand the toxicity mechanism of chronic exposure to environmental levels of MC-LR on the liver of fish, juvenile Nile tilapia were exposed to 0 mu g/L (control), 1 mu g/L (M1), 3 mu g/L (M3), 10 mu g/L (M10), and 30 mu g/L (M30) MC-LR for 60 days. Then, the liver hepatotoxicity induced by MC-LR exposure was systematically evaluated via histological and biochemical determinations, and the underlying mechanisms were explored through combining analysis of biochemical parameters, multi-omics (transcriptome and metabolome), and gene expression. The results exhibited that chronic MC-LR exposure caused slight liver minor structural damage and lipid accumulation in the M10 group, while resulting in serious histological damage and lipid accumulation in the M30 group, indicating obvious hepatotoxicity, which was confirmed by increased toxicity indexes (i.e., AST, ALT, and AKP). Transcriptomic and metabolomic analysis revealed that chronic MC-LR exposure induced extensive changes in gene expression and metabolites in six typical pathways, including oxidative stress, apoptosis, autophagy, amino acid metabolism, primary bile acid biosynthesis, and lipid metabolism. Taken together, chronic MC-LR exposure induced oxidative stress, apoptosis, and autophagy, inhibited primary bile acid biosynthesis, and caused fatty deposition in the liver of Nile tilapia.
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