Integration of Multi-Omics, Histological, and Biochemical Analysis Reveals the Toxic Responses of Nile Tilapia Liver to Chronic Microcystin-LR Exposure

dc.contributor.authorLi, Yichao
dc.contributor.authorYang, Huici
dc.contributor.authorFu, Bing
dc.contributor.authorKaneko, Gen
dc.contributor.authorLi, Hongyan
dc.contributor.authorTian, Jingjing
dc.contributor.authorWang, Guangjun
dc.contributor.authorWei, Mingken
dc.contributor.authorXie, Jun
dc.contributor.authorYu, Ermeng
dc.date.accessioned2024-03-27T13:15:51Z
dc.date.available2024-03-27T13:15:51Z
dc.date.issued2024-03-14
dc.date.updated2024-03-27T13:15:52Z
dc.description.abstractMicrocystin-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 μg/L (control), 1 μg/L (M1), 3 μg/L (M3), 10 μg/L (M10), and 30 μg/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.
dc.identifierdoi: 10.3390/toxins16030149
dc.identifier.citationToxins 16 (3): 149 (2024)
dc.identifier.urihttps://hdl.handle.net/10657/16612
dc.titleIntegration of Multi-Omics, Histological, and Biochemical Analysis Reveals the Toxic Responses of Nile Tilapia Liver to Chronic Microcystin-LR Exposure

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