Behavioral effects and oxidative status in brain regions of adult rats exposed to BDE-99

被引:52
作者
Belles, Montserrat [1 ,2 ]
Alonso, Virginia [1 ,2 ]
Linares, Victoria [1 ,2 ]
Albina, Maria L. [1 ,2 ]
Sirvent, Juan J. [3 ]
Domingo, Jose L. [1 ]
Sanchez, Domenec J. [1 ,2 ]
机构
[1] Univ Rovira & Virgili, Lab Toxicol & Environm Hlth, Sch Med, IISPV, Reus 43201, Catalonia, Spain
[2] Univ Rovira & Virgili, Physiol Unit, Sch Med, IISPV, Reus 43201, Catalonia, Spain
[3] Univ Rovira & Virgili, Pathol Unit, Sch Med, IISPV, Reus 43201, Catalonia, Spain
关键词
BDE-99; Adult rats; Oxidative stress (OS); Neurotoxicity; Brain; POLYBROMINATED DIPHENYL ETHERS; BROMINATED FLAME RETARDANTS; LOW-DOSE PBDE-99; DEVELOPMENTAL EXPOSURE; POLYCHLORINATED-BIPHENYLS; 2,2',4,4',5-PENTABROMODIPHENYL ETHER; IN-VITRO; TISSUE DISTRIBUTION; NEONATAL EXPOSURE; PCB AROCLOR-1254;
D O I
10.1016/j.toxlet.2010.01.010
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
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.
引用
收藏
页码:1 / 7
页数:7
相关论文
共 56 条
  • [1] ALHBOM J, 1995, BRAIN RES, V677, P13
  • [2] [Anonymous], 2004, TOX PROF POL BIPH PO
  • [3] [Anonymous], ENV HLTH CRIT
  • [4] Cerebellar neurocognition:: Insights into the bottom of the brain
    Baillieux, Hanne
    De Smet, Hyo Jung
    Paquier, Philippe F.
    De Deyn, Peter P.
    Marien, Peter
    [J]. CLINICAL NEUROLOGY AND NEUROSURGERY, 2008, 110 (08) : 763 - 773
  • [5] Combined action of uranium and stress in the rat -: I.: Behavioral effects
    Bellés, M
    Albina, ML
    Linares, V
    Gómez, M
    Sánchez, DJ
    Domingo, JL
    [J]. TOXICOLOGY LETTERS, 2005, 158 (03) : 176 - 185
  • [6] Brominated flame retardants: Cause for concern?
    Birnbaum, LS
    Staskal, DF
    [J]. ENVIRONMENTAL HEALTH PERSPECTIVES, 2004, 112 (01) : 9 - 17
  • [7] Polybrominated diphenyl ethers (PBDEs) in foodstuffs:: Human exposure through the diet
    Bocio, A
    Llobet, JM
    Domingo, JL
    Corbella, J
    Teixidó, A
    Casas, C
    [J]. JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY, 2003, 51 (10) : 3191 - 3195
  • [8] BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
  • [9] Early developmental exposure to BDE 99 or Aroclor 1254 affects neurobehavioural profile: Interference from the administration route
    Branchi, I
    Capone, F
    Vitalone, A
    Madia, F
    Santucci, D
    Alleva, E
    Costa, LG
    [J]. NEUROTOXICOLOGY, 2005, 26 (02) : 183 - 192
  • [10] Polybrominated diphenyl ethers: Neurobehavioral effects following developmental exposure
    Branchi, I
    Capone, F
    Alleva, E
    Costa, LG
    [J]. NEUROTOXICOLOGY, 2003, 24 (03) : 449 - 462