庄娟¹,
李梦秋²,
洪法水¹,
胡卫成¹,
张萌萌¹,
周颖君¹,
罗艳¹,
张建梅¹,
郑元林²
1. 淮阴师范学院生命科学学院江苏省环洪泽湖生态农业生物技术重点实验室;淮阴师范学院江苏省高校区域现代农业与环境保护协同创新中心, 淮安 223300;
2. 江苏师范大学江苏省药用植物生物技术重点实验室, 江苏师范大学生命科学学院, 徐州 221116

作者简介: 庄娟(1977-),女,博士,讲师,研究方向为环境毒理学,E-mail:dajiangsky@163.com.

基金项目: 总理基金项目“大气重污染成因与治理攻关(DQGG0305)”


中图分类号: X171.5

2,2′,4,4′-Tetrabromodiphenyl Ether-induced Neurotoxicity in Mice

Zhuang Juan¹,
Li Mengqiu²,
Hong Fashui¹,
Hu Weicheng¹,
Zhang Mengmeng¹,
Zhou Yingjun¹,
Luo Yan¹,
Zhang Jianmei¹,
Zheng Yuanlin²
1. Jiangsu Key Laboratory for Eco-Agricultural Biotechnology around Hongze Lake, Jiangsu Collaborative Innovation Center of Regional Modern Agriculture & Environmental Protection, School of Life Science, Huaiyin Normal University, Huaian 223300, China;
2. Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, China

CLC number: X171.5

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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。
关键词: BDE-47/
海马组织/
神经毒性/
PKC/
caspase-3

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.
Key words:BDE-47/
hippocampus/
neurotoxicity/
PKC/
caspase-3.