首页 | 期刊简介 | 编委会 | 投稿要求 | 化学品管理信息动态 | 学术会议 | 专辑 | 毒理学测试技术设备 | 订购本刊 | 联系我们 | English version

许梦川1,2,谈勇2,李小满2,李前2,*,吴跃峰1,李东明1,#. 百草枯急性暴露对肝细胞L-O2的毒理研究[J]. 生态毒理学报, 2018, 13(5): 163-170
百草枯急性暴露对肝细胞L-O2的毒理研究
Toxicological Effects of Acute Paraquat Exposure on L-O2 Hepatocytes
投稿时间:2017-12-05  修订日期:2018-01-04
DOI:10.7524/AJE.1673-5897.20171205002
中文关键词:  百草枯  细胞,L-O2  细胞凋亡,碳酸酐酶9
英文关键词:paraquat  L-O2 hepatocytes  apoptosis  carbonic anhydrase 9
基金项目:国家自然科学基金(31672292);河北省自然科学基金(C2017205059)
作者单位
许梦川1,2,谈勇2,李小满2,李前2,*,吴跃峰1,李东明1,# 1. 河北师范大学生命科学学院 河北省动物生理生化与分子生物学重点实验室石家庄 050024 2. 军事科学院军事医学研究院毒物药物研究所 抗毒药物与毒理学国家重点实验室北京 100850 
摘要点击次数: 58
全文下载次数: 38
中文摘要:
      百草枯(paraquat, PQ)是目前农业生产上使用较为广泛的除草剂,PQ毒性极大,能造成人和动物多器官损伤。因肝脏是主要的受损器官之一,故以肝细胞L-O2为研究对象,探讨PQ急性暴露对肝细胞产生的毒理影响。结果显示在40~640 μmol L-1暴露浓度下作用24 h,PQ显著抑制肝细胞L-O2的增殖活性(P<0.01),半抑制浓度(IC50)为263.2 μmol L-1。将肝细胞L-O2暴露于不同浓度的PQ(60、120、180和250 μmol L-1),作用24 h后,与对照组相比,PQ暴露组的活性氧(ROS)累积和细胞凋亡率都表现出明显的浓度依赖性升高(P<0.01;P<0.05),细胞周期阻滞在S期。Western blot结果显示,除60 μmol L-1外的其他暴露组中活化的胱天蛋白酶9(caspase-9)表达显著上调,Bax和Bcl-2的比值显著增大,提示细胞凋亡机制可能与内源性线粒体通路的激活有关。此外,碳酸酐酶9(CA9)mRNA表达显著升高,提示PQ暴露下可能引起酸性代谢产物出现,对细胞产生酸毒害,但其内在的机制还需进一步研究。
  
AuthorAffiliation
Xu Mengchuan1,2, Tan Yong2, Li Xiaoman2, Li Qian2,*, Wu Yuefeng1, Li Dongming1,#1.Key Laboratory of Animal Physiology, Biochemistry and Molecular Biology of Hebei Province, College of Life Sciences, Hebei Normal University, Shijiazhuang 050024, China 2. State Key Laboratory of Toxicology and Medical Countermeasures, Institute of Pharmacology and Toxicology, Academy of Military Medical Sciences, Beijing 100850, China
英文摘要:
      Paraquat (PQ) is one of the most widely used herbicides, but with ultrahigh toxicity. Its toxic effect was suggested to be related to the effect of oxidation-responsive stress, leading to multi-organ dysfunctions. As liver is the most important detoxification organ, here we reported the toxicological effects of PQ on L-O2 hepatocytes when it was acutely exposed to PQ. Our results showed that PQ was highly toxic to L-O2 hepatocytes with IC50 of 263.2 μmol L-1 for 24 h (P< 0.01). When L-O2 hepatocytes were exposed to PQ of different concentrations (60, 120, 180, 250 μmol L-1) for 24 h, the concentration-dependent increase of ROS accumulation and apoptosis rate of L-O2 hepatocytes were observed, compared to the control group (with P<0.01, P<0.05, respectively). The cell cycle was blocked in S phase. Further mechanistic studies were conducted on the toxicity and the apoptotic pathways. The abnormal high level of the activated caspase-9 and the ratio of Bax to Bcl-2 might indicate that an endogenous mitochondrial apoptosis could be responsible for the increased apoptosis rate of L-O2, and the distinct mRNA relative expression of carbonic anhydrase 9 (CA9) indicated the acidic toxicity inside the cells, but it is necessary to study further.
查看全文  查看/发表评论  下载PDF阅读器
关闭

您是第4942336位访问者   京ICP备 09058833 号

主办单位:中国科学院生态环境研究中心     单位地址:北京市海淀区双清路18号

 服务热线:010-62941072       传真:010-62923563       邮编:100085    Email: stdlxb@rcees.ac.cn

    本系统由北京勤云科技发展有限公司设计

0463美女美女3764美女美女ktv