Acenaphthene is a polycyclic aromatic hydrocarbon (PAH) that is a widely distributed environmental pollutant that accumulates in organisms and leads to health risks in humans. Although acenaphthene is reported to be toxic to aquatic organisms, its effects of acenaphthene on the livers of these organisms have not been evaluated. Here, zebrafish were used as an experimental model. Zebrafish larvae were exposed to 4.5, 5.5, and 6.5 mg/L acenaphthene for 72 h while adult zebrafish were exposed to 1.5, 2, and 2.5 mg/L acenaphthene for 28 days. We investigated the mechanism by which acenaphthene causes liver toxicity in zebrafish. The results showed that acenaphthene affected the early development of zebrafish and led to mitochondrial damage by promoting the production of reactive oxygen species (ROS) resulting in oxidative stress. The expression of genes related to inflammation and apoptosis was analyzed, observing up-regulation of the pro-inflammatory factors IL-8, TNF-α, and IL-6. The pro-apoptotic genes p53, Caspase-3, and Bax and the Bax/Bcl-2 ratio were up-regulated, while the anti-apoptotic gene Bcl-2 was down-regulated. In addition, we investigated the effects of acenaphthene on liver metabolism. When exposed to acenaphthene, the glycogen content of the liver decreased, while lipid accumulation increased together with alterations in related indicators of liver metabolism. In conclusion, acenaphthene induced oxidative stress through ROS production, leading to mitochondrial damage and activation of pathways associated with inflammation and apoptosis, resulting in hepatotoxicity. This affects normal liver metabolism. Our results revealed the mechanism of hepatotoxicity in zebrafish acenaphthene, and provided new evidence for a more comprehensive understanding of the hepatotoxicity of acenaphthene.
Keywords: Acenaphthene; Cell apoptosis; Hepatotoxicity; Inflammation; Liver metabolic disorder; Oxidative stress.
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