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
赵芳 1严骁 1何绵 2王远芳 2康亭亭 2蔡凤珊 3郑晶 1谢春4
作者信息
- 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;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
- 2. 中山大学第七附属医院科研中心,深圳 518000
- 3. 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
- 4. 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
- 折叠
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.
Abstract
6:2 chlorinated polyfluorinated ether sulfonate,known as F-53B,is widely used as an important substi-tute 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 com-pared 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 de-creased 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Key words
F-53B/hepatocytes/apoptosis/oxidative stress引用本文复制引用
基金项目
国家自然科学基金资助项目(42007392)
国家自然科学基金资助项目(42077404)
国家自然科学基金资助项目(4222711)
出版年
2024
NETL
NSTL
万方数据