{"title":"Hepatotoxicity in Carp (<i>Carassius auratus</i>) Exposed to Perfluorooctane Sulfonate (PFOS): Integrative Histopathology and Transcriptomics Analysis.","authors":"Lin Tang, Guijie Hao, Dongren Zhou, Yunpeng Fan, Zihao Wei, Dongsheng Li, Yafang Shen, Haoyu Fang, Feng Lin, Meirong Zhao, Haiqi Zhang","doi":"10.3390/ani15040610","DOIUrl":null,"url":null,"abstract":"<p><p>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<sub>50</sub>) 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.</p>","PeriodicalId":7955,"journal":{"name":"Animals","volume":"15 4","pages":""},"PeriodicalIF":2.7000,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11851982/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Animals","FirstCategoryId":"97","ListUrlMain":"https://doi.org/10.3390/ani15040610","RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"AGRICULTURE, DAIRY & ANIMAL SCIENCE","Score":null,"Total":0}
引用次数: 0
Abstract
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 (LC50) 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.
全氟辛烷磺酸污染由于其广泛分布和持续存在，对环境构成重大威胁。然而，全氟辛烷磺酸对关键水生物种（如鲫鱼）的肝毒性作用仍未得到充分研究。本研究系统研究了全氟辛烷磺酸对鲫鱼的肝毒性及其潜在的分子机制，为期21天。96 h 50%致死浓度为23.17 mg/L。组织病理学和转录组学分析证实了全氟辛烷磺酸引起的鲤鱼肝损伤，其特征是静脉充血、核仁溶解和细胞空泡化。转录组学分析进一步确定了1036个差异表达基因（deg），涉及脂质和能量代谢、免疫和内分泌调节相关的关键途径。这些途径对于非酒精性脂肪性肝病（NAFLD）的发展是不可或缺的。具体而言，与脂质代谢相关的deg发生了显著变化，而与能量代谢相关的deg则表明ATP产生和线粒体功能受到破坏。与免疫应答相关的基因显示了促炎标志物的上调，激素调节基因强调了内分泌信号的改变。我们的研究结果强调，全氟辛烷磺酸对鲫鱼具有急性毒性，可能通过破坏多种生理系统引起肝毒性。该研究为减轻水生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学和保护生物学讨论。
AnimalsAgricultural and Biological Sciences-Animal Science and Zoology
CiteScore
4.90
自引率
16.70%
发文量
3015
审稿时长
20.52 days
期刊介绍：
Animals (ISSN 2076-2615) is an international and interdisciplinary scholarly open access journal. It publishes original research articles, reviews, communications, and short notes that are relevant to any field of study that involves animals, including zoology, ethnozoology, animal science, animal ethics and animal welfare. However, preference will be given to those articles that provide an understanding of animals within a larger context (i.e., the animals'' interactions with the outside world, including humans). There is no restriction on the length of the papers. Our aim is to encourage scientists to publish their experimental and theoretical research in as much detail as possible. Full experimental details and/or method of study, must be provided for research articles. Articles submitted that involve subjecting animals to unnecessary pain or suffering will not be accepted, and all articles must be submitted with the necessary ethical approval (please refer to the Ethical Guidelines for more information).
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