不能将值 NULL 插入列 'id',表 'aje_website.dbo.t_web_site_access';列不允许有空值。INSERT 失败。 语句已终止。 欢迎访问《生态毒理学报》编辑部网站!

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

-. 水环境中镍毒性的机制研究:有害结局路径(AOP)分析[J]. 生态毒理学报, 2017, 12(3):
水环境中镍毒性的机制研究:有害结局路径(AOP)分析
The Mechanisms of Nickel Toxicity in Aquatic Environments: An Adverse Outcome Pathway (AOP) Analysis
  
DOI:10.7524/AJE.1673-5897.201720etc
中文关键词:  
英文关键词:Nickel  Adverse outcome pathway  Biotic ligand model  Mechanism  Risk assessment
基金项目:
作者单位
- - 
摘要点击次数: 420
全文下载次数: 
中文摘要:
      目前对镍(Ni)生态风险评估和水质法规采用了基于机制的预测工具,如生物配体模型(BLMs)。然而,尽管有许多具体细致的研究,Ni对水生生物毒性的精确机制仍然难以确定。对Ni行为机制的不确定性导致了大家在一些管理设置中应用像BLM这样的工具时,有所顾虑。为了解决这一认知差距,作者使用了有害结局路径(AOP)分析,也是第一个用于金属的AOP分析,来确定Ni毒性的多种潜在机制以及它们与淡水水生生物的相互作用。在金属的分子起始事件(molecular initiating events)在分类群中可能存在的前提下,在许多不同种水生和陆生生物数据的基础上,考虑建立一种潜在的行为机制。通过分析,作者识别了Ni可能对水生生物产生毒性的5个潜在的分子起始事件:Ca2+体内平衡的破坏,Mg2+体内平衡的破坏,Fe2+/3+体内平衡的破坏,活性氧类物质引起的氧化损伤,以及呼吸上皮细胞的过敏反应。在生物组织的器官水平,这5个潜在的分子起始事件会分解成3个可能的途径:支持外骨骼、外壳和骨骼生长的Ca2+减少;呼吸受损;细胞毒性和肿瘤形成。在整个生物体的水平,器官水平的反应将可能导致生长、繁殖的降低和/或能量代谢的改变,并且在每个通路之间有几个潜在的反馈回路。总体来说,目前的AOP分析可指导Ni的毒性机制研究,并为其他金属开发AOPs提供了有效的参考。
精选自Brix, K. V., Schlekat, C. E. and Garman, E. R. (2017), The mechanisms of nickel toxicity in aquatic environments: An adverse outcome pathway analysis. Environmental Toxicology and Chemistry, 36: 1128–1137. doi: 10.1002/etc.3706
详情请见http://onlinelibrary.wiley.com/wol1/doi/10.1002/etc.3706/full
  
AuthorAffiliation
Kevin V. Brix 1,2,*, Christian E. Schlekat 3, Emily R. Garman 31. EcoTox, Miami, Florida, USA 2. RSMAS, University of Miami, Miami, Florida, USA 3. NiPERA, Durham, North Carolina, USA
英文摘要:
      Current ecological risk assessment and water quality regulations for nickel (Ni) use mechanistically based, predictive tools such as biotic ligand models (BLMs). However, despite many detailed studies, the precise mechanism(s) of Ni toxicity to aquatic organisms remains elusive. This uncertainty in the mechanism(s) of action for Ni has led to concern over the use of tools like the BLM in some regulatory settings. To address this knowledge gap, the authors used an adverse outcome pathway (AOP) analysis, the first AOP for a metal, to identify multiple potential mechanisms of Ni toxicity and their interactions with freshwater aquatic organisms. The analysis considered potential mechanisms of action based on data from a wide range of organisms in aquatic and terrestrial environments on the premise that molecular initiating events for an essential metal would potentially be conserved across taxa. Through this analysis the authors identified 5 potential molecular initiating events by which Ni may exert toxicity on aquatic organisms: disruption of Ca2+?homeostasis, disruption of Mg2+?homeostasis, disruption of Fe2+/3+ homeostasis, reactive oxygen species–induced oxidative damage, and an allergic-type response of respiratory epithelia. At the organ level of biological organization, these 5 potential molecular initiating events collapse into 3 potential pathways: reduced Ca2+?availability to support formation of exoskeleton, shell, and bone for growth; impaired respiration; and cytotoxicity and tumor formation. At the level of the whole organism, the organ-level responses contribute to potential reductions in growth and reproduction and/or alterations in energy metabolism, with several potential feedback loops between each of the pathways. Overall, the present AOP analysis provides a robust framework for future directed studies on the mechanisms of Ni toxicity and for developing AOPs for other metals.?
View more in http://onlinelibrary.wiley.com/wol1/doi/10.1002/etc.3706/full
查看全文  查看/发表评论  下载PDF阅读器
关闭

您是第3317599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