F-53B对人肝癌细胞HepG2和Hep3B的细胞毒性效应研究  

Cytotoxic Effects of F-53B on Human Hepatoma Cells HepG2 and Hep3B

作　　者：赵芳 严骁 何绵 王远芳 康亭亭 蔡凤珊 郑晶 谢春[1] Zhao Fang;Yan Xiao;He Mian;Wang Yuanfang;Kang Tingting;Cai Fengshan;Zheng Jing;Xie Chun(School of Public Health,the Key Laboratory of Environmental Pollution Monitoring and Disease Control,Ministry of Education,Guizhou Medical University,Guiyang 561113,China;State Environmental Protection Key Laboratory of Environmental Pollution Health Risk Assessment,Research Center of Emerging Contaminants,South China Institute of Environmental Sciences,Ministry of Ecology and Environment,Guangzhou 510655,China;Scientific Research Center,The Seventh Affiliated Hospital of Sun Yat-sen University,Shenzhen 518000,China)

机构地区：[1]贵州医科大学公共卫生与健康学院,环境污染与疾病监控教育部重点实验室,贵阳561113 [2]生态环境部华南环境科学研究所新污染物研究团队,国家环境保护环境污染健康风险评价重点实验室,广州510655 [3]中山大学第七附属医院科研中心,深圳518000

出　　处：《生态毒理学报》2024年第2期232-241,共10页Asian Journal of Ecotoxicology

基　　金：国家自然科学基金资助项目(42007392,42077404,4222711)。

摘　　要：研究氯化多氟烷基醚磺酸(6:2 chlorinated polyfluorinated ether sulfonate,商品名F-53B)对人肝癌细胞HepG2和Hep3B的毒性效应,并初步探讨其作用机制。选择常用的全氟辛烷磺酸(perfluorooctane sulfonate,PFOS)和全氟辛酸(perfluorooctanoic acid,PFOA)与F-53B同时进行毒性评估,检测细胞形态、细胞活力、凋亡、活性氧(reactive oxygen species,ROS),过氧化氢酶(catalase,CAT)、超氧化物歧化酶(superoxide dismutase,SOD)、凋亡相关因子(Bax、Caspase-3、PARP、Caspase-9等)表达水平。F-53B对细胞活性具有明显的抑制作用且毒力显著大于PFOS,并呈剂量依赖性;F-53B显著诱导ROS释放和细胞凋亡,并降低了抗氧化酶CAT活性;进一步证明促凋亡相关因子(Bax、Caspase-3、PARP、Caspase-9)表达增加,抑制凋亡因子Bcl-2表达水平降低。F-53B可诱导细胞凋亡和氧化应激,且线粒体内在途径可能参与细胞毒性作用。6:2 chlorinated polyfluorinated ether sulfonate,known as F-53B,is widely used as an important substitute of perfluorooctane sulfonate(PFOS)in industry,which may bring serious environmental and health risks.In this study,we will explore the potential hepatotoxic effects and related mechanism induced by F-53B in human hepatoma cells.Three perfluorinated compounds,including F-53B,PFOS and perfluorooctanoic acid(PFOA),were selected to assess their effects on cell morphology,cell viability and apoptosis in HepG2 and Hep3B cells.Markers of oxidative stress,such as reactive oxygen species(ROS),catalase(CAT),superoxide dismutase(SOD),were compared among these three compounds.The protein levels of several apoptosis-related factors were also detected after chemicals exposure.Treatment with F-53B resulted in strong dose-dependent decrease in hepatoma cell viability,the effect of which was significantly higher than those obtained in the group treated with PFOS or PFOA.F-53B induced ROS release and decreased the activity of antioxidant enzyme CAT.F-53B also caused cell apoptosis,which was proved by the increased expression of pro-apoptotic factors(Bax,Caspase-3,PARP,Caspase-9)and decreased expression level of apoptotic factor Bcl-2.F-53B can induce hepatoma cell apoptosis and oxidative stress through mitochondrial intrinsic pathway.

关 键 词：氯化多氟烷基醚磺酸 肝细胞 细胞凋亡 氧化应激 

分 类 号：X171.5[环境科学与工程—环境科学]