Tang Lin, Hao Guijie, Zhou Dongren, Fan Yunpeng, Wei Zihao, Li Dongsheng, Shen Yafang, Fang Haoyu, Lin Feng, Zhao Meirong, Zhang Haiqi
Key Laboratory of Microbial Technology for Industrial Pollution Control of Zhejiang Province, College of Environment, Zhejiang University of Technology, Hangzhou 310014, China.
Key Laboratory of Freshwater Fisheries Healthy Aquaculture, Ministry of Agriculture and Rural Affairs, Key Laboratory of Fish Health and Nutrition of Zhejiang Province, Key Laboratory of Fishery Environment and Aquatic Product Quality and Safety of Huzhou City, Zhejiang Institute of Freshwater Fisheries, Huzhou 313001, China.
Animals (Basel). 2025 Feb 19;15(4):610. doi: 10.3390/ani15040610.
Perfluorooctane sulfonate (PFOS) contamination poses a significant environmental threat due to its widespread distribution and persistence. However, the hepatotoxic effects of PFOS on key aquatic species, such as crucian carp, remain understudied. This study systematically investigated the hepatotoxicity and underlying molecular mechanisms associated with PFOS exposure in crucian carp over a 21 day period. We determined a 96 h 50% lethal concentration (LC) of 23.17 mg/L. Histopathological and transcriptomic analyses confirmed PFOS-induced liver damage in the carp, characterized by venous congestion, nucleolar dissolution and cellular vacuolation. Transcriptomic profiling further identified 1036 differentially expressed genes (DEGs), involving critical pathways related to lipid and energy metabolism, immunity, and endocrine regulation. These pathways are integral to the development of nonalcoholic fatty liver disease (NAFLD). Specifically, DEGs related to lipid metabolism showed significant changes, while those involved in energy metabolism indicated disrupted ATP production and mitochondrial function. Genes associated with immune response revealed an upregulation of pro-inflammatory markers, and hormone regulation genes highlighted alterations in endocrine signaling. Our findings emphasized that PFOS exhibits acute toxicity to crucian carp, potentially inducing hepatotoxicity by disrupting multiple physiological systems. This research provides a theoretical foundation for mitigating aquatic pollution and protecting eco-health, contributing to broader ecological and conservation biology discussions.
全氟辛烷磺酸(PFOS)污染因其广泛分布和持久性而对环境构成重大威胁。然而,PFOS对关键水生物种(如鲫鱼)的肝毒性影响仍未得到充分研究。本研究系统地调查了鲫鱼在21天内接触PFOS后的肝毒性及潜在分子机制。我们确定其96小时50%致死浓度(LC)为23.17毫克/升。组织病理学和转录组分析证实PFOS诱导了鲤鱼肝脏损伤,其特征为静脉淤血、核仁溶解和细胞空泡化。转录组分析进一步鉴定出1036个差异表达基因(DEG),涉及与脂质和能量代谢、免疫及内分泌调节相关的关键途径。这些途径是非酒精性脂肪性肝病(NAFLD)发展所必需的。具体而言,与脂质代谢相关的DEG表现出显著变化,而参与能量代谢的DEG表明ATP生成和线粒体功能受到破坏。与免疫反应相关的基因显示促炎标志物上调,激素调节基因突出了内分泌信号的改变。我们的研究结果强调,PFOS对鲫鱼具有急性毒性,可能通过破坏多个生理系统诱导肝毒性。本研究为减轻水污染和保护生态健康提供了理论基础,有助于更广泛的生态和保护生物学讨论。