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首页> 外文期刊>Chemosphere >Accumulation and developmental toxicity of hexabromocyclododecanes (HBCDs) on the marine copepod Tigriopus japonicus
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Accumulation and developmental toxicity of hexabromocyclododecanes (HBCDs) on the marine copepod Tigriopus japonicus

机译:六溴环十二烷(六溴环十二烷)对海洋co足类Tigriopus japonicus的积累和发育毒性

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摘要

The brominated flame retardants hexabromocyclododecanes (HBCDs) are ubiquitous environmental contaminants, widely distributed in aquatic systems including the marine environment and marine organisms. HBCDs are toxic to the development of both freshwater and marine fish. However, the impacts of HBCDs on marine invertebrates are not well known. In this study, the marine copepod, Tigriopus japonicus, was used to assess the bioaccumulation and developmental toxicity of technical HBCD (tHBCD) through water-borne exposure. The uptake rate constant of tHBCD by T. japonicus was high, which resulted in high bioaccumulation potential. The bioconcentration factors of tHBCD were 8.73 x 10(4) and 6.34 x 10(4) L kg(-1) in T. japonicus, calculated using the kinetic and steady-state methods, respectively. Exposure of T. japonicus nauplii to tHBCD caused significant growth delay. The lowest-observable-effect concentrations of tHBCD induced developmental delay were 30 and 8 mu g L-1 for the F-0 and F-1 generations, respectively, which suggested that the F-1 generation was more sensitive to tHBCD than the FO generation and warranted multiple-generation toxicity tests for future studies. Furthermore, exposure of the adult copepods to tHBCD induced the transcription of oxidative stress response genes and apoptotic genes, e.g., SOD,CAT, GST, OGG1, P53 and Caspase-3. It was therefore speculated that tHBCD exposure induced the generation of reactive oxygen species in T. japonicus, which activated the oxidative stress defense genes and meanwhile resulted in oxidative DNA damage. The damaged DNA activated the transcription of p53 and triggered the caspase-mediated apoptosis pathway, which may be the reason for the tHBCD induced developmental delay in T. japonicus nauplii. (C) 2016 Elsevier Ltd. All rights reserved.
机译:溴化阻燃剂六溴环十二烷(HBCD)是普遍存在的环境污染物,广泛分布在包括海洋环境和海洋生物在内的水生系统中。六溴环十二烷对淡水和海水鱼类的生长都有毒。但是,六溴环十二烷对海洋无脊椎动物的影响尚不清楚。在这项研究中,海洋co足类Tigriopus japonicus被用于通过水接触评估技术六溴环十二烷(tHBCD)的生物积累和发育毒性。日本血吸虫对tHBCD的吸收速率常数很高,因此具有很高的生物蓄积潜力。 tHBCD的生物富集系数分别为8.73 x 10(4)和6.34 x 10(4)L kg(-1),分别通过动力学和稳态方法计算得出。将日本无节幼体暴露于tHBCD会导致明显的生长延迟。对于F-0和F-1代,tHBCD诱导的发育延迟的最低可观察到的浓度分别为30和8μg L-1,这表明F-1代比FO对tHBCD更敏感。代,并保证进行多代毒性试验,以备将来研究。此外,成年co足类动物暴露于tHBCD会诱导氧化应激反应基因和凋亡基因,例如SOD,CAT,GST,OGG1,P53和Caspase-3的转录。因此推测,tHBCD暴露诱导了日本血吸虫中活性氧的产生,从而激活了氧化应激防御基因,同时导致了DNA的氧化损伤。受损的DNA激活了p53的转录并触发了caspase介导的凋亡途径,这可能是tHBCD引起日本无节幼体发育迟缓的原因。 (C)2016 Elsevier Ltd.保留所有权利。

著录项

  • 来源
    《Chemosphere》 |2017年第1期|155-162|共8页
  • 作者单位

    Xiamen Univ, State Key Lab Marine Environm Sci, Xiamen 361102, Fujian, Peoples R China|Xiamen Univ, Environm Sci Res Ctr, Xiamen 361102, Fujian, Peoples R China;

    Xiamen Univ, State Key Lab Marine Environm Sci, Xiamen 361102, Fujian, Peoples R China;

    Xiamen Univ, State Key Lab Marine Environm Sci, Xiamen 361102, Fujian, Peoples R China;

    Xiamen Univ, State Key Lab Marine Environm Sci, Xiamen 361102, Fujian, Peoples R China;

    Xiamen Univ, State Key Lab Marine Environm Sci, Xiamen 361102, Fujian, Peoples R China;

    Xiamen Univ, State Key Lab Marine Environm Sci, Xiamen 361102, Fujian, Peoples R China|Xiamen Univ, Ctr Marine Environm Chem & Toxicol, Xiamen 361102, Fujian, Peoples R China|Xiamen Univ, Environm Sci Res Ctr, Xiamen 361102, Fujian, Peoples R China;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    Hexabromocyclododecanes; Developmental toxicity; Bioaccumulation; Oxidative stress; Marine copepod;

    机译:六溴环十二烷;发育毒性;生物蓄积;氧化应激;海洋co足类;

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