Abstract：
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.
摘要：
乙炔是一种多环芳烃（PAH），是一种广泛分布的环境污染物，在生物体中积累并导致人类健康风险。虽然有报道称对水生生物有毒,其对这些生物肝脏的影响尚未被评估。这里,以斑马鱼为实验模型。斑马鱼幼虫暴露于4.5、5.5和6.5mg/L的ε2中72小时，而成年斑马鱼暴露于1.5、2和2.5mg/L的ε2中28天。我们研究了吖啶在斑马鱼中引起肝毒性的机制。研究结果表明,吖啶通过促进活性氧(ROS)的产生导致氧化应激,影响斑马鱼早期发育,并导致线粒体损伤。分析炎症和凋亡相关基因的表达,观察促炎因子IL-8、TNF-α、IL-6促凋亡基因p53、Caspase-3、Bax和Bax/Bcl-2比值上调,而抗凋亡基因Bcl-2下调。此外,我们研究了吖啶对肝脏代谢的影响。当暴露于萘时，肝脏的糖原含量下降，而脂质积累随着肝脏代谢相关指标的改变而增加。总之,萘通过ROS产生诱导氧化应激，导致线粒体损伤和激活与炎症和细胞凋亡相关的途径，导致肝毒性。这会影响正常的肝脏代谢。我们的研究结果揭示了斑马鱼的肝毒性机制，并为更全面地了解吖啶的肝毒性提供了新的证据。
