四溴联苯醚对小鼠的神经毒性
2,2´,4,4´-Tetrabromodiphenyl Ether-induced Neurotoxicity in Mice
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摘要: 为探讨持久性有机污染物 2,2’,4,4’-四溴联苯醚(BDE-47)对小鼠海马组织的神经毒性，将小鼠每日灌胃25或50 mg·kg-1剂量的BDE-47，6周后检测其记忆能力、海马组织病理学变化、蛋白激酶C(PKC)表达量和半胱氨酸天冬氨酸蛋白酶-3(caspase-3)活性。结果显示，BDE-47损伤了小鼠被动回避实验的记忆保持能力，导致海马安蒙角(CA1)区锥体细胞排列紊乱，神经元胞体体积变小，形态不规则。BDE-47对小鼠海马组织PKCα、β、γ和ζ的表达无影响，但显著上调了PKCδ和PKCλ的表达，促进了caspase-3活性。这些结果提示，BDE-47导致的海马神经毒性可能与PKCδ和PKCλ表达异常及caspase-3活性升高有关。本实验结果为进一步了解BDE-47神经毒作用机制提供了实验依据。Abstract: This study was aimed to investigate the neurotoxicity induced by persistent organic pollutant 2,2´,4,4´-tetrabromodiphenyl ether (BDE-47) in mice. Mice were received BDE-47 (25 or 50 mg·kg-1) by oral gavage daily for 6 weeks. At the end of treatment, memory function, hippocampal histopathological changes, the expression of protein kinase C (PKC) and cysteinyl aspartate specific proteinase-3 (caspase-3) activity in mouse hippocampus was evaluated. The results showed that BDE-47 led to memory retention impairment in the passive avoidance task in mice. Moreover, the pyramidal cells in the hippocampal cornu ammonis 1 (CA1) were irregularly arranged and exhibited shrunken and irregular shape in BDE-47-treated mice. There was no significant change in PKCα, β, γ and ζ expressions compared with the control. The expression of PKCδ and PKCλ and the activity of caspase-3 was increased in the hippocampus of BDE-47-treated mice. These findings suggested that BDE-47-induced neurotoxicity was associated with the abnormal expression of PKCδ and PKCλ, along with the increased caspase-3 activity. Our results also provide an experimental basis for further understanding the neurotoxicity mechanisms of BDE-47.
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Key words:
- BDE-47 /
- hippocampus /
- neurotoxicity /
- PKC /
- caspase-3
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