十溴联苯醚对小鼠脑组织的氧化应激作用

目的 研究十溴联苯醚(decabromodiphenylether,PBDE-209)对小鼠大脑皮层、海马、纹状体和小脑组织诱导的氧化应激作用.方法 28只雄性BALB/c小鼠,随机分为4组,即溶剂对照组、空白对照组、低剂量染毒组(200mg/kg)和高剂量染毒组(500mg/kg),每组7只,小鼠经口灌胃染毒6周后断头处死,测定小鼠大脑皮层、海马、小脑和纹状体中丙二醛(MDA)含量、总超氧化物歧化酶(T-SOD)活力以及谷胱甘肽(GSH)含量.结果 高剂量染毒组小鼠大脑皮层、小脑、纹状体和海马组织中MDA含量分别为(92.25±36.64)、(4.24±1.15)、(12.92±4.30)、(12.12±6.39)nmol/mgpro,高于空白对照组分别为(56.71±36.44)、(2.42±1.41)、(4.05±2.23)、(4.91±1.60)nmol/mg pro],差异均有统计学意义(P＜0.05);低剂量染毒组小鼠大脑皮层、小脑和纹状体中T-SOD活力分别为(182.48±11.59)、(6.67±1.56)、(35.48±21.98)U/mg pro,低于空白对照组分别为(277.76±106.70)、(18.02±16.40)、(63.57±20.83)U/mg pro],差异均有统计学意义(P＜0.05);高剂量染毒组小鼠海马组织中T-SOD活力为(59.26±37.09)U/mg pro,低于空白对照组(93.28±21.75)U/mg pro],差异有统计学意义(P＜0.05);高剂量染毒组小鼠大脑皮层、小脑、纹状体中GSH含量分别为(40.98±13.19)、(3.55±1.55)、(24.46±11.30)mg/g pro,低于空白对照组分别为(75.79±26.51)、(8.01±3.23)、(44.52±13.15)mg/g pro],差异均有统计学意义(P＜0.05);而染毒小鼠海马组织中GSH含量与溶剂对照组的差异无统计学意义(P＞0.05).结论 PBDE-209可以引起神经组织的脂质过氧化反应增强.PBDE-209导致神经组织的氧化损伤可能在动物神经毒性中起重要作用.

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 randomizedly 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).Conclusion 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.