Behavioral effects and oxidative status in brain regions of adult rats exposed to BDE-99
Behavioral effects and oxidative status in brain regions of adult rats exposed to BDE-99
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DOI：
10.1016/j.toxlet.2010.01.010
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发表时间：
2010-04-15
影响因子：
3.5
通讯作者：
Sanchez, Domenec J.
中科院分区：
文献类型：
--
作者：
Belles, Montserrat;Alonso, Virginia;Sanchez, Domenec J.
多溴联苯醚(PBDEs)被用作阻燃剂。尽管已经对多溴二苯醚的发育神经毒性进行了研究，但对其在成年后的潜在神经毒性作用仍知之甚少。在这项研究中，我们评估了脑切片的氧化损伤和暴露于2，2‘，4，4’，5-五溴二苯醚(BDE-99)可能引起的行为影响。成年雄性大鼠(10只/组)按0、0.6、1.2 mg/kg体重单次灌胃BDE-99。染毒45d后，分别进行旷场活动、被动回避和Morris水迷宫测试。此外，还检测了大脑皮层、海马区和小脑的氧化应激指标：还原型谷胱甘肽、氧化型谷胱甘肽、谷胱甘肽还原酶、谷胱甘肽过氧化物酶、谷胱甘肽-S转移酶、超氧化物歧化酶、过氧化氢酶和硫代巴比妥酸反应物质。在小脑中，BDE-99在最高剂量时可显著降低小鼠的SOD、CAT和GR活性。皮层和海马区的CAT和SOD活性也分别下降。在行为测试中，没有观察到BDE-99的影响，而脑区的组织病理学检查是正常的。目前的结果表明，BDE-99暴露对大脑的抗氧化能力有影响，主要是在小脑。氧化损伤可能是BDE-99成年大鼠神经毒性的机制之一。(C)2010年，爱思唯尔爱尔兰有限公司出版。
Polybrominated diphenyl ethers (PBDEs) are used as flame retardants. Although developmental neurotoxicity of PBDEs has been already investigated, little is still known about their potential neurotoxic effects in adulthood. In this study, we assessed the oxidative damage in brain sections and the possible behavioral effects induced by exposure to 2,2',4,4',5-pentabromodiphenyl ether (BDE-99). Adult male rats (10/group) received BDE-99 by gavage at single doses of 0, 0.6 or 1.2 mg/kg/body weight. Forty-five days after exposure, the following behavioral tests were conducted: open-field activity, passive avoidance and Morris water maze. Moreover, cortex, hippocampus and cerebellum were processed to examine the following oxidative stress (OS) markers: reduced glutathione (GSH), oxidized glutathione (GSSG), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), superoxide dismutase (SOD), catalase (CAT) and thiobarbituric acid reactive substances (TBARS). In cerebellum, BDE-99 significantly decreased SOD, CAT and GR activities at the highest BDE-99 dose. A decrease in CAT and SOD activities was also observed in cortex and hippocampus, respectively. In the behavioral tests, no BDE-99 effects were observed, while histopathological examination of the brain regions was normal. The current results show that the brain antioxidant capacity is affected by BDE-99 exposure, mainly in cerebellum. Oxidative damage could be a mechanism for BDE-99 neurotoxicity in adult rats. (C) 2010 Published by Elsevier Ireland Ltd.