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首页> 外文期刊>Applied Organometallic Chemistry >Effects of tri-n-butyltin(IV)chloride on neurulation of Ciona intestinalis(Tunicata,Ascidiacea):an ultrastructural study
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Effects of tri-n-butyltin(IV)chloride on neurulation of Ciona intestinalis(Tunicata,Ascidiacea):an ultrastructural study

机译:超微结构研究三氯化三正丁基锡(IV)对小肠短ona(Ciona intestinalis)(Tunicata,Ascidiacea)神经营养的影响

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摘要

This paper reports the cytotoxic effects of tri-n-butyltin(IV)chloride,TBTC1,on the neurulation process of the ascidian Ciona intestinalis.Exposure of the embryos at early neurula stage in 10~(-5)and 10~(-7)M TBT(IV)chloride solutions for 1-2 h provoked the irreversible arrest of their development.Morphological and ultrastructural observations suggested that most probably there are two principal causes determining the neurulation process block.The first is due to the TBT effects of inhibiting the polymerization and/or degradation of microfilaments and microtubules,proteins that constitute the cytoskeleton.The lack of orientation and extension of both microtubules and microfilaments of actin prevent the shape changes and mobility of neural plate blastomeres indispensable to the neurulation process.The second cause is certainly determined by the ultrastructural modification which mitochondria undergo.The ultrastructural anomalies showed by these organules are so serious as to impede their proper functionality with consequent inhibition of oxidative phosphorylation and ATP synthesis,remarkable metabolic processes that occur during ascidian neurulation.
机译:本文报道了氯化三正丁基锡(IV),TBTC1对海鞘Ciona intestinalis神经形成过程的细胞毒性作用。在10〜(-5)和10〜(-7)神经早期的胚胎暴露)M TBT(IV)氯化物溶液1-2 h导致其发展不可逆转地停止。形态学和超微结构观察表明,很可能有两个主要原因决定了神经形成过程的阻滞。首先是由于TBT抑制作用微丝和微管,构成细胞骨架的蛋白质的聚合和/或降解。肌动蛋白的微管和微丝缺乏方向性和延伸性,阻碍了神经板卵裂球的形状变化和迁移,这是神经形成过程中必不可少的。第二个原因是这些线粒体的超微结构异常非常严重,以至于阻碍了它们的发展。具有适当的功能性,因此抑制了氧化磷酸化和ATP合成,在海鞘神经发生过程中发生了明显的代谢过程。

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