Page 417 - 《环境工程技术学报》2023年第1期
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Vol.13,No.1                        环 境 工 程 技 术 学 报                                  第 13 卷,第 1 期
            Jan.,2023                      Journal of Environmental Engineering Technology         2023 年 1 月

            王京,闫振广,张天旭,等.BDE-20 对斑马鱼肠道的慢性毒性效          应  [J].环境工程技术学报,2023,13(1):413-422.
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            WANG J,YAN Z G,ZHANG T X,et al.Chronic toxic effects of BDE-209 on the intestinal tract of zebrafish (Danio Rerio)[J].Journal of Environmental
            Engineering Technology,2023,13(1):413-422.

                          BDE-20 对斑马鱼肠道的慢性毒性效应
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                                        王京 ,闫振广 ,张天旭 ,王晶 ,李娟英                   1*
                                                       2
                                             1,2
                                                                       3
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                                               1.上海海洋大学海洋生态与环境学院
                                     2.环境基准与风险评估国家重点实验室, 中国环境科学研究院
                                             3.中国环境科学研究院水生态环境研究所
            摘要 以模式生物斑马鱼为研究对象,探究十溴联苯醚(BDE-209)慢性暴露对肠道组织的毒性效应及分子机制。将斑马鱼暴露
            于不同浓度    的  BDE-209〔6、6 和  600 µg/L,二甲基亚砜溶剂对照〕溶液      中  28 d,利用苏木精-伊红染色对斑马鱼肠道组织进行病
                                  0
            理学检查,并通过生物化学指标          和  ELIS 试验对肠道内氧化应激和炎症反应相关生物标志物含量进行分析,通过实时荧光定量
                                          A
            PCR 分析肠道屏障、炎症反应和细胞凋亡相关基因的相对表达量。结果表明:BDE-20 暴露造成了斑马鱼肠壁变薄、肠绒毛和
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            肠壁外纵肌内空泡化增多以及肠壁和肠绒毛纤毛破损,同时通过下调肠道                         内  ZO-1、Claudin- 和  Tjp2 的  mRN 相对表达量影
                                                                                  2
                                                                                         a
                                                                                                A
            响了肠道的物理屏障功能。BDE-20 暴露导致肠道内活性氧、丙二醛、过氧化氢酶和超氧化物歧化酶的含量增加,表                                    明  BDE-
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            20 暴露造成了肠道内氧化应激。此外,BDE-20 暴露导致促炎细胞因子肿瘤坏死因                        子  α  和白细胞介  素  1 的含量以及肠道内
                                                                                             β
              9
                                                 9
            脂多糖含量升高,加重了肠道的炎症反应,并导               致  p53、Bax、Caspase 基因表达上调    和  Bcl 基因表达下调,促进了斑马鱼肠道
                                                                3
                                                                                 2
            的细胞凋亡。
            关键词 斑马鱼;肠道屏障;氧化应激;炎症反应;细胞凋亡;十溴联苯醚(BDE-209)
            中图分类号:X171.5    文章编号:1674-991X(2023)01-0413-10  doi:10.12153/j.issn.1674-991X.20210869
             Chronic toxic effects of BDE-209 on the intestinal tract of zebrafish (Danio Rerio)
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                          WANG Jing ,  YAN Zhenguang ,  ZHANG Tianxu ,  WANG Jing ,  LI Juanying 1*
                                  1.College of Marine Ecology and Environment, Shanghai Ocean University
               2.State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences
                        3.Institute of Water Ecology and Environment, Chinese Research Academy of Environmental Sciences
            Abstract Taking  the  model  organism  zebrafish  (Danio  Rerio)  as  the  research  object,  the  toxic  effects  and
            molecular  mechanism  of  chronic  exposure  of  decabromodiphenyl  ether  (BDE-209)  on  intestinal  tissue  were
            explored. Zebrafish were exposed to different concentrations of BDE-209 (6, 60, and 600 µg/L, dimethyl sulfoxide
            solvent control) for 28 d. The intestinal tissue of zebrafish was pathologically examined by hematoxylin-eosin (H &
            E) staining. The contents of biomarkers related to oxidative stress and inflammatory response in the intestine were
            analyzed  by  biochemical  indicators  and  ELISA  experiments.  The  relative  expression  of  genes  related  to  the
            intestinal barrier, inflammatory response, and apoptosis was analyzed by real-time qPCR. The results showed that
            BDE-209 exposure resulted in thinning of the intestinal wall, increase of vacuolation in intestinal villi and external
            longitudinal muscle, damage of intestinal wall and cilia, and down-regulation of intestinal ZO-1, Claudin-2, and
            Tjp2a  mRNA  relative  expression  to  affect  intestinal  physical  barrier  function.  BDE-209  exposure  increased  the
            contents of reactive oxygen species (ROS), malondialdehyde (MDA), catalase (CAT), and superoxide dismutase
            (SOD) in the intestine, indicating that BDE-209 exposure caused intestinal oxidative stress. In addition, BDE-209
            exposure up-regulated the contents of pro-inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin
            1β (IL-1β) and the content of lipopolysaccharide (LPS) in the intestine, leading to increased intestinal inflammatory
            response,  and  increased  the  expression  of p53,  Bax,  Caspase 3  gene  and  down-regulated Bcl 2  gene  expression,


            收稿日期:2021-12-29
            基金项目:国家自然科学基金项       目  (41991315)
            作者简介:王   京  (1995—),男,硕士研究生,研究方向为健康风险及污染物分子毒理机制,steviewang123@163.com
            * 责任作者:李娟  英  (1978—),女,教授,博士,研究方向为环境中有毒有害物质的迁移转化及环境毒理,jyli@shou.edu.cn
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