Study On The Effects On Oxidative Stress Of Decabromodiphenylether On Mice Brain Tissue And Changes In The MAPK Signaling Pathway Proteins

BackgroundTo study the oxidative stress induced by Decabromodiphenylether (PBDE-209) in cortex,hippocampus,striatum and cerebellum of mice and the protein changes in MAPK signaling pathway,for further study of the neural toxicity mechanism of PBDE-209.MethodsTwenty eight male BALB/c mice we studied were randomizedly divided into four groups with seven mice in each:saline group,solvent group,low(200mg/kg) and high(500mg/kg) dose groups.Test substances were administered by gavage and mice were sacrificed 6 weeks after treatment.Malonyldialdehyde(MDA),supemxide dismutase (SOD) and glutathione(GSH) in cortex,hippocampus,cerebellum and striatum were examined and the protein expression was assayed by Western blot in hippocampus and cortex.ResultsThe difference content of MDA,SOD,GSH between solvent group and saline group was not statistically significant,so in this study we use saline group as control group.Compared with the saline group,the content of MDA in cortex, cerebellum,striatum and hippocampus in exposed mice were increased(P<0.05) while SOD activity decreased significantly(P<0.05).The content of GSH in cortex,cerebellum and striatum were decreased(P<0.05).Western blot results showed that compared with the saline group,the ratio of p-p38/p38,p-ERK/ERK,Bax/Bcl-2 in exposed mice hippocampus were higher and the difference was significant(P<0.05):the ratio of p-ERK/ERK was increased significantly(P<0.05).The cell shape,structure was normal and the nuclear staining was light blue in saline group.In exposed group the nerve cell structure is unclear,smaller size,deformation,nuclear pyknosis,anachromasis,ill-defined nuclear envelope membrane and perinuclear vacuolization.ConclusionPBDE-209 could induced oxidative stress in brain tissue and the proteins abnormal expression in MAPK pathway in the hippocampus,indicate that PBDE-209 may cause oxidative damage to body tissues and further to activate the MAPK signaling pathway and induce Bax,Bcl-2 changed in the hippocampus.The tissue oxidative damage might be one of the primary mechanisms of neurotoxicity of PBDE-209. BackgroundDecabromodiphenyl ether (PBDE-209) is a persistent organic pollutants and has the potential threats to ecological environment and biological.In our previous study we confirmed that PBDE-209 can cause oxidative damage to brain tissue and protein changes in the hippocampus.So our research focus on the effects of N-acetyl-cysteine antioxidants on mice's brain tissue oxidative injury and MAPK-related protein changes in the hippocampus induced by formaldehyde.MethodsTwenty one male BALB/c mice we studied were randomizedly divided into three groups with seven mice in each: saline group,PBDE-209(500 mg·kg-1·d-1) group and (500 mg·kg-1·d-1,PBDE-209+100 mg·kg-1·d-1,NAC) group.Test substances were administered by gavage and mice were sacrificed 6 weeks after treatment.Malonyldialdehyde(MDA),supemxide dismutase (SOD) and glutathione(GSH) in cortex,hippocampus,cerebellum and striatum were examined and the protein expression was assayed by Western blot in hippocampus and cortex.ResultsCompared with the saline group and PBDE-209+NAC group,the content of MDA in cerebellum,striatum and hippocampus in PBDE-209 group was increased(P<0.05) while SOD activity decreased significantly in striatum and hippocampus (P<0.05).The content of GSH in cortex,cerebellum and striatum were decreased(P<0.05).Western blot results showed that compared with the saline group and PBDE-209+NAC group:the ratio of p-p38/p38,p-ERK/ERK,Bax/Bcl-2 in exposed mice hippocampus were higher and the difference was significant(P<0.05).The cell shape,structure was normal and the nuclear staining was light blue in saline group.In exposed group the nerve cell structure is unclear,smaller size,deformation,nuclear pyknosis,anachromasis,ill-defined nuclear envelope membrane and perinuclear vacuolization.The morphology and structure in brain tissue cells was normal in intervention group.ConclusionAntioxidant N-acetylysteine might be beneficial in preventing PBDE-209-induced the mice brain injury and the MAPK-related protein.