Chronic Cr(VI) exposure-induced biotoxicity involved in liver microbiota-gut axis disruption in Phoxinus lagowskii Dybowski based on multi-omics technologies
文献类型: 外文期刊
作者: Shang, Xinchi 1 ; Che, Xinghua 1 ; Ma, Kai 1 ; Guo, Wenxue 2 ; Wang, Shanshan 3 ; Sun, Zhi Peng 1 ; Xu, Wei 1 ; Zhang, Yongquan 1 ;
作者机构: 1.Chinese Acad Fishery Sci, Heilongjiang River Fisheries Res Inst, Harbin 150070, Peoples R China
2.Rongcheng Marine Econ Dev Ctr, Rongcheng 264300, Peoples R China
3.Heilongjiang Aquat Anim Resource Conservat Ctr, Harbin, Peoples R China
4.Northeast Agr Univ, Coll Life Sci, Harbin 150036, Peoples R China
关键词: Hepatic metabolome; Cr(VI) stress; Gut microbial; LPS; Antioxidant
期刊名称:ENVIRONMENTAL POLLUTION ( 影响因子:7.3; 五年影响因子:8.1 )
ISSN: 0269-7491
年卷期: 2025 年 368 卷
页码:
收录情况: SCI
摘要: Cr(VI) is widely used in industry and has high toxicity, making it one of the most common environmental pollutants. Long-term exposure to Cr(VI) can cause metabolic disorders and tissue damage. However, the effects of Cr(VI) on liver and gut microbes in fish have rarely been reported. In this study, 240 fish were randomly divided into 3 groups: the control group, low-dose Cr(VI) group (0.5 mg/L), and high-dose Cr(VI) group (2 mg/ L). The mechanism by which Cr(VI) affects the enterohepatic axis of common carp was elucidated via multiomic analysis, serology, histomorphology, and physiological and biochemical indices. The results revealed that Cr(VI) stress led to hepatocyte damage, nuclear lysis, inflammatory cell infiltration, and vacuolated degeneration. The structure of the intestinal villi was severely damaged, and the length and width of the intestinal villi were significantly reduced. We also found that the accumulation of Cr(VI) in tissues increased in a concentrationdependent manner, and the content of Cr(VI) in each tissue increased in the order of gut > gill > liver > muscle. Multiple omics studies have revealed that chronic Cr(VI) stress leads to disturbances in the intestinal flora, with a significant reduction in the abundance of the beneficial bacterium Akkermansia and a significant increase in the abundance of the harmful bacterium Escherichia/Shigella. Intestinal injury and dysbiosis lead to an increase in blood LPS levels, further inducing metabolic disorders in the liver. The metabolites in the liver, including geniposide, leucine, C17 sphingosine, and 9,10-DiHODE, were significantly increased, whereas the beneficial metabolites, such as carnitine propionate and palmitoyl ethanolamide, were significantly reduced. In conclusion, our results suggest that chronic Cr(VI) stress leads to disturbances in gut microbial homeostasis and disturbed fatty acid and amino acid metabolism in the liver. LPS released into the bloodstream reaches the liver through the portal circulation, further exacerbating Cr(VI) stress-induced hepatotoxicity. This study revealed the mechanism of Cr(VI) toxicity to the liver-microbiota-gut axis of common carp. Our study provides new insights into the effects of Cr(VI) on the liver-microbiota-gut axis.
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