Permethrin (Per) is a widely used and frequently detected pyrethroid pesticide in agricultural products and the environment. It may pose potential toxicity to non-target organisms. Per has been reported to affect lipid homeostasis, although the mechanism is undefined. This study aims to explore the characteristic transcriptomic profiles and clarify the underlying signaling pathways of Per-induced lipid metabolism disorder in zebrafish liver. The results showed that environmental exposure to Per caused changes in the liver index, histopathology, and oxidative stress in zebrafish. Moreover, transcriptome results showed that Per heavily altered the pathways involved in metabolism, the immune system, and the endocrine system. We conducted a more in-depth analysis of the genes associated with lipid metabolism. Our findings revealed that exposure to Per led to a disruption in lipid metabolism by activating the KRAS-PPAR-GLUT signaling pathways through oxidative stress. The disruption of lipid homeostasis caused by exposure to Per may also contribute to obesity, hepatitis, and other diseases. The results may provide new insights for the risk of Permethrin to aquatic organisms and new horizons for the pathogenesis of hepatotoxicity.

中文翻译：

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氯菊酯暴露通过 KRAS-PPAR-GLUT 信号通路影响斑马鱼脂质代谢，该信号通路由氧化应激介导


氯菊酯（Per）是一种在农产品和环境中广泛使用且经常检测到的拟除虫菊酯类农药。它可能对非目标生物体造成潜在的毒性。据报道，Per 会影响脂质稳态，但其机制尚不清楚。本研究旨在探讨斑马鱼肝脏中Per诱导的脂质代谢紊乱的特征转录组谱并阐明潜在的信号通路。结果表明，环境暴露于 Per 会导致斑马鱼的肝脏指数、组织病理学和氧化应激发生变化。此外，转录组结果表明，Per 严重改变了代谢、免疫系统和内分泌系统所涉及的途径。我们对与脂质代谢相关的基因进行了更深入的分析。我们的研究结果表明，接触 Per 会通过氧化应激激活 KRAS-PPAR-GLUT 信号通路，从而扰乱脂质代谢。接触 Per 引起的脂质稳态破坏也可能导致肥胖、肝炎和其他疾病。这些结果可能为了解氯菊酯对水生生物的风险提供新的见解，并为肝毒性的发病机制提供新的视野。