[Oxidative stress of decabromodiphenylether in mice brain tissue].
OBJECTIVE
To study the oxidative stress induced by decabromodiphenylether (PBDE-209) in the cerebral cortex, hippocampus, cerebellum and striatum of mice.


METHODS
Twenty-eight male BALB/c mice were randomized divided into four groups with seven mice in each: solvent control, blank control, low (200 mg/kg) and high (500 mg/kg) dose groups. Test substances were administered by gavage and mice were sacrificed 6 weeks after treatment. Malonyldialdehyde (MDA), total superoxide dismutase (T-SOD) and glutathione (GSH) in cerebral cortex, hippocampus, cerebellum and striatum were examined.


RESULTS
The content of MDA in cerebral cortex, cerebellum, striatum and hippocampus in high dose group was (92.25 ± 36.64), (4.24 ± 1.15), (12.92 ± 4.30), (12.12 ± 6.39) nmol/mg pro respectively, higher than that in blank group [(56.713 ± 6.44), (2.42 ± 1.41), (4.05 ± 2.23), (4.91 ± 1.60) nmol/mg pro] and the difference was statistically significant (P < 0.05); T-SOD activity in cerebral cortex, cerebellum and striatum in low dose group was (182.48 ± 11.59), (6.67 ± 1.56), (35.48 ± 21.98) U/mg pro respectively, lower than that in blank group [(277.76 ± 106.70), (18.02 ± 16.40), (63.57 ± 20.83) U/mg pro] and the difference was statistically significant (P < 0.05); in high dose group the T-SOD activity in hippocampus was(59.26 ± 37.09) U/mg pro, lower than that in blank group [(93.28 ± 21.75) U/mg pro] and the difference was statistically significant (P < 0.05); The content of GSH in cerebral cortex, cerebellum and striatum in high dose group was (40.98 ± 13.19), (3.55 ± 1.55), (24.46 ± 11.30) mg/g pro respectively, lower than that in blank group [(75.79 ± 26.51), (8.01 ± 3.23), (44.52 ± 13.15) mg/g pro and the difference was statistically significant (P < 0.05); while the content of GSH in hippocampus was not decreased significantly compared with the blank group (P > 0.05).


CONCLUSIONS
PBDE-209 could induce oxidative stress in nervous tissue. The tissue oxidative damage might be one of the primary mechanisms of neurotoxicity of PBDE-209.
Department of Occupational and Environmental Health, School of Public Health, Anhui Medical University, Hefei, 230032, China.
Zhao-Xiang
ZX
Zhang
Xing-Hua
XH
Wang
Li-Wei
LW
Zou
Shu-Shu
SS
Ding
Jin-Xia
JX
Zhai
D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism*; D055768:Halogenated Diphenyl Ethers / Q000633:toxicity*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018384:Oxidative Stress / Q000187:drug effects*
D055768:Halogenated Diphenyl Ethers; C010902:decabromobiphenyl ether