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首页> 外文期刊>The Science of the Total Environment >Reactive oxygen species (ROS) and the calcium-(Ca~（2+）) mediated extrinsic and intrinsic pathways underlying BDE-47-induced apoptosis in rainbow trout (Oncorhynchus mykiss) gonadal cells
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Reactive oxygen species (ROS) and the calcium-(Ca~（2+）) mediated extrinsic and intrinsic pathways underlying BDE-47-induced apoptosis in rainbow trout (Oncorhynchus mykiss) gonadal cells

机译：活性氧（ROS）和钙（Ca〜（2+））介导的BDE-47诱导虹鳟鱼性腺细胞凋亡的外在和内在途径

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摘要

The brominated flame retardant, 2,2',4,4'-tetrabromodiphenyl ether (BDE-47), is well documented to exert potential negative impacts on different marine biota. However, the responsible mechanism remains unknown. The rainbow trout gonadal cell line RTG-2 was used as a model, and the mechanism and pathway underlying BDE-47 (6, 12.5 and 25 mu M)-induced apoptosis and toxicity were examined in vitro. Apoptosis occurred in the RTG-2 cells exposed to BDE-47 in a clear concentration-dependent manner. The morphology of the mitochondrial alterations was observed using transmission electron microscopy. BDE-47 exposure decreased the cellular mitochondrial membrane potential, increased the cytochrome c released into the cytoplasm and elevated Fas protein expression. The mRNA expressions of Fas-associated death domain-containing protein (FADD), CHOP and GRP78 were also elevated, and similar increases were found in the activities of intracellular caspase-8, caspase-12, caspase-9 and caspase-3. These results indicated that the mitochondrial, endoplasmic reticulum and deathreceptor pathways were involved in apoptosis in RTG-2 cells following BDE-47 exposure. ROS and Ca2+ were responsible for these changes because their overproduction was detected prior to apoptosis. However, the addition of the ROS scavenger N-acetyl-L-cysteine (NAC) and the intracellular calcium chelator (acetoxymethyl)-1,2-bis-(o-aminophenoxy)-ethane-N, N, N', N'-tetraacetic acid (BAPTA-AM) did not significantly alleviate the apoptosis rate. The results of the present study show that BDE-47 exposure induced apoptosis in RTG-2 cells via ROS-and Ca-2-mediated mitochondrial, endoplasmic reticulum and death-receptor apoptotic pathways. (c) 2018 The Author(s). Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license
机译：溴化阻燃剂2,2'，4,4'-四溴二苯醚（BDE-47）有充分的文献证明会对不同的海洋生物群产生潜在的负面影响。但是，负责任的机制仍然未知。以虹鳟鱼性腺细胞RTG-2为模型，体外研究了BDE-47（6、12.5和25μM）诱导的细胞凋亡和毒性的机制和途径。暴露于BDE-47的RTG-2细胞以明显的浓度依赖性方式发生凋亡。使用透射电子显微镜观察线粒体改变的形态。 BDE-47暴露会降低细胞线粒体膜电位，增加释放到细胞质中的细胞色素c并提高Fas蛋白表达。 Fas相关死亡域含蛋白（FADD），CHOP和GRP78的mRNA表达也升高，并且细胞内caspase-8，caspase-12，caspase-9和caspase-3的活性也有类似的升高。这些结果表明，线粒体，内质网和死亡受体途径参与了BDE-47暴露后RTG-2细胞的凋亡。 ROS和Ca2 +是造成这些变化的原因，因为在细胞凋亡之前就检测到了它们的过度生产。然而，添加了ROS清除剂N-乙酰基-L-半胱氨酸（NAC）和细胞内钙螯合剂（乙酰氧基甲基）-1,2-双-（邻氨基苯氧基）-乙烷-N，N，N'，N' -四乙酸（BAPTA-AM）没有显着降低细胞凋亡率。本研究结果表明，BDE-47暴露通过ROS和Ca-2介导的线粒体，内质网和死亡受体凋亡途径诱导RTG-2细胞凋亡。 （c）2018作者。由Elsevier B.V.发布。这是CC BY-NC-ND许可下的开放获取文章

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  • 来源
    《The Science of the Total Environment》 |2019年第15期|778-788|共11页
  • 作者

    Zhou Zhongyuan; Zhou Bin; Chen Hongmei; Tang Xuexi; Wang You;

  • 作者单位

    Ocean Univ China, Coll Marine Life Sci, Dept Marine Ecol, Qingdao 266003, Peoples R China;

    Ocean Univ China, Coll Marine Life Sci, Dept Marine Ecol, Qingdao 266003, Peoples R China|Pilot Natl Lab Marine Sci & Technol, Lab Marine Ecol & Environm Sci, Qingdao 266237, Peoples R China;

    Shihezi Univ, Sch Pharm, Dept Pharmacol, Key Lab Xinjiang Endem Phytomed Resources,Minist, Shihezi 832002, Peoples R China;

    Ocean Univ China, Coll Marine Life Sci, Dept Marine Ecol, Qingdao 266003, Peoples R China|Pilot Natl Lab Marine Sci & Technol, Lab Marine Ecol & Environm Sci, Qingdao 266237, Peoples R China;

    Ocean Univ China, Coll Marine Life Sci, Dept Marine Ecol, Qingdao 266003, Peoples R China|Pilot Natl Lab Marine Sci & Technol, Lab Marine Ecol & Environm Sci, Qingdao 266237, Peoples R China;

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  • 正文语种 eng
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  • 关键词

    Apoptotic pathway; Reactive oxygen species; Calcium; Rainbow trout; RTG-2 cells; 2,2 ',4,4 '-Tetrabromodiphenyl ether;

    机译：凋亡途径;活性氧;钙;虹鳟鱼;RTG-2细胞;2,2';4,4'-四溴二苯醚;

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