Laboratory of Toxicology and Environmental Health, School of Medicine, IISPV Universitat Rovira i Virgili, Sant Llorens 21, 43201 Reus, Catalonia, Spain.
Toxicol Lett. 2010 Apr 15;194(1-2):1-7. doi: 10.1016/j.toxlet.2010.01.010. Epub 2010 Jan 22.
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 1.2mg/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.
多溴联苯醚（PBDEs）被用作阻燃剂。尽管已经研究了 PBDEs 的发育神经毒性，但它们在成年期的潜在神经毒性影响仍知之甚少。在这项研究中，我们评估了脑切片中的氧化损伤以及暴露于 2,2',4,4',5-五溴二苯醚（BDE-99）引起的可能行为效应。成年雄性大鼠（每组 10 只）通过灌胃接受 BDE-99，单次剂量为 0、0.6 或 1.2mg/kg/体重。暴露 45 天后，进行了以下行为测试：旷场活动、被动回避和 Morris 水迷宫。此外，还处理了皮质、海马和小脑，以检查以下氧化应激（OS）标志物：还原型谷胱甘肽（GSH）、氧化型谷胱甘肽（GSSG）、谷胱甘肽还原酶（GR）、谷胱甘肽过氧化物酶（GPx）、谷胱甘肽-S-转移酶（GST）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和硫代巴比妥酸反应物质（TBARS）。在小脑，BDE-99 在最高 BDE-99 剂量下显著降低了 SOD、CAT 和 GR 的活性。在皮质和海马体中，分别观察到 CAT 和 SOD 活性的降低。在行为测试中，未观察到 BDE-99 的影响，而大脑区域的组织病理学检查正常。目前的结果表明，大脑抗氧化能力受到 BDE-99 暴露的影响，主要是在小脑。氧化损伤可能是 BDE-99 对成年大鼠神经毒性的机制之一。
