环境内分泌干扰物二噁英的细胞毒性及锌的保护作用.pdfVIP

环境内分泌干扰物二噁英的细胞毒性及锌的保护作用 刘 刚，卢春凤，孙岩松，彭双清 （军事医学科学院疾病预防控制所毒理学评价研究中心，北京 100071） 摘要：探讨2,3,7,8- 四氯二苯并二噁英（TCDD ）的细胞毒性作用及其机制，并初步探讨锌对TCDD 所致细胞毒性 作用的保护效应，为进一步探索临床防治措施提供理论基础。分别以不同浓度的TCDD 和ZnCl2 染毒HepG2 细 胞，细胞培养24 h 后。荧光探针DCFH-DA 法检测活性氧（ROS ）；酶标仪比色测定细胞中脂质过氧化产物丙二 醛（MDA ）含量、谷胱甘肽 （GSH ）含量、超氧化物歧化酶（SOD）活性；Hoechst 荧光探针检测细胞凋亡情况。 结果表明，各染毒组细胞内ROS 生成量和MDA 含量明显高于对照组（P0.01 ）、细胞内GSH 含量和SOD 活性 显著降低（P0.05 ）；TCDD 可诱导HepG2 细胞发生凋亡。ZnCl2 能使细胞内ROS 生成量和MDA 含量明显降低 （P0.01 ）、细胞内GSH 含量和SOD 活性显著升高（P0.01 ）；并抑制细胞的凋亡发生。本研究结果表明，氧 化损伤在 TCDD 所致的细胞毒性效应中发挥重要的作用；锌作为自由基清除剂，对 TCDD 所致的细胞毒性作用 具有明显的保护效应。 关键词：2,3,7,8- 四氯二苯并对二噁英；锌；氧化应激；细胞凋亡 Studies on the Mechanisms of Cytotoxic Effect Induced by Environmental Endocrine Disrupters-dioxin and Zinc Protection LIU Gang, LU ChunFeng, SUN Yansong, PENG Shuangqing （Evaluation and Research Center for Toxicology, Institute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing 100071, China ） Abstract ：To study the cytotoxic mechanism of 2,3,7,8-Tetrachlorodibenzo-p -dioxin (TCDD) and the protective effect of zinc to TCDD, to provide the rationale for further to explore the clinical prevention and cure measure. HepG2 cells were cultured and treated with diff-concentration TCDD and ZnCl2 for 24 h. DCFH-DA was used for detecting the production of ROS in cells; GSH and MDA content, activity of SOD in cells were measured by colorimetry method; Apoptosis was measured with Hoechst 33258. The results of this study suggest that TCDD significantly increased the formation of intracellular ROS and MDA content (P0.01). The GSH content and activity of SOD in cells significantly decreased exposed by TCDD(P0.05); Obvious apoptosis was induced by TCDD(P0.05). TCDD-induced