【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。更多还原

【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 andζ 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.更多还原