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产前传递多溴联苯醚(PBDEs)导致斑马鱼幼体发育神经毒性。

Prenatal transfer of polybrominated diphenyl ethers (PBDEs) results in developmental neurotoxicity in zebrafish larvae.

机构信息

State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China.

出版信息

Environ Sci Technol. 2012 Sep 4;46(17):9727-34. doi: 10.1021/es302119g. Epub 2012 Aug 17.

Abstract

Parental exposure to polybrominated diphenyl ethers (PBDEs) in animals has been found to be transferred to the offspring. The environmental health risk and toxicity to the offspring are still unclear. The objective of the present study was to identify environmentally relevant concentrations of PBDEs for parental exposure that would cause developmental neurotoxicity in the offspring. Adult zebrafish were exposed to environmentally relevant concentrations of DE-71 (0.16, 0.8, 4.0 μg/L) via water. The results showed that PBDE exposure did not affect larvae hatching, malformation, or survival. The residue of PBDEs was detected in F1 eggs upon parental exposure. Acetylcholinesterase (AChE) activity was significantly inhibited in F1 larvae. Genes of central nervous system development (e.g., myelin basic protein, synapsin IIa, α1-tubulin) were significantly downregulated in larvae. Protein levels of α1-tubulin and synapsin IIa were also reduced. Decreased locomotion activity was observed in the larvae. This study provides the first evidence that parental exposure to environmentally relevant concentrations of PBDEs could cause adverse effects on neurodevelopment in zebrafish offspring.

摘要

动物体内母体暴露于多溴二苯醚(PBDEs)已被发现会传递给后代。其对后代的环境健康风险和毒性仍不清楚。本研究的目的是确定母体暴露于环境相关浓度的 PBDEs 会导致后代发育神经毒性。通过水,成年斑马鱼被暴露于环境相关浓度的 DE-71(0.16、0.8、4.0μg/L)中。结果表明,PBDE 暴露不会影响幼虫孵化、畸形或存活。母体暴露后,F1 卵中检测到 PBDE 残留。F1 幼虫中的乙酰胆碱酯酶(AChE)活性显著受到抑制。中枢神经系统发育的基因(如髓鞘碱性蛋白、突触素 IIa、α1-微管蛋白)在幼虫中显著下调。α1-微管蛋白和突触素 IIa 的蛋白水平也降低。幼虫的运动活性下降。本研究首次提供证据表明,母体暴露于环境相关浓度的 PBDEs 可能导致斑马鱼后代神经发育的不良影响。

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