Analysis of ethanol developmental toxicity in zebrafish.

Analysis of ethanol developmental toxicity in zebrafish.
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乙醇对斑马鱼的发育毒性分析。

DOI:
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发表时间:
2008
影响因子:
--
通讯作者:
M. Reimers
M. Reimers
中科院分区:
--
文献类型:
--
作者:
Robert L. Tanguay;M. Reimers

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人们普遍认为,脊椎动物在生命早期阶段更容易受到化学伤害。这意味着,如果一种化学物质,如乙醇是发育毒性,它必须干扰,或调制,关键的信号通路。对胚胎易感性增加的可能的分子解释是,在动物的整个生命周期中,没有其他时期的分子信号是活跃的。了解乙醇暴露破坏脊椎动物胚胎发育的机制是非常具有挑战性的;它需要彻底了解正常的分子程序,以了解短暂的乙醇暴露如何破坏信号传导并导致有害的长期影响。在过去的几年里,研究人员已经认识到斑马鱼模型的优势,发现编排胚胎发育的信号事件。外部发展加上众多的分子和遗传学方法使这个模型成为一个有价值的工具,以解开乙醇破坏胚胎发育的机制。在这一章中,我们描述的程序用于评估和定义的形态,细胞和分子的反应,乙醇在斑马鱼。
It is largely accepted that vertebrates are more susceptible to chemical insult during the early life stage. It is implied that if a chemical such as ethanol is developmentally toxic, it must interfere with, or modulate, critical signaling pathways. The probable molecular explanation for increased embryonic susceptibility is that collectively there is no other period of an animal's lifespan when the full repertoire of molecular signaling is active. Understanding the mechanism by which ethanol exposure disrupts vertebrate embryonic development is enormously challenging; it requires a thorough understanding of the normal molecular program to understand how transient ethanol exposure disrupts signaling and results in detrimental long-lasting effects. During the past several years, investigators have recognized the advantages of the zebrafish model to discover the signaling events that choreograph embryonic development. External development coupled with the numerous molecular and genetic methods make this model a valuable tool to unravel the mechanisms by which ethanol disrupts embryonic development. In this chapter we describe procedures used to evaluate and define the morphological, cellular and molecular responses to ethanol in zebrafish.
DOI: 10.1016/j.ntt.2004.06.012
发表时间: 2004-11-01
影响因子: 2.9
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