Protective effects of n-acetylcysteine against decabromodiphenyl ether-induced brain oxidative injury in mice.

Zhaoxiang Zhang; Jinxia Zhai

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Protective effects of n-acetylcysteine against decabromodiphenyl ether-induced brain oxidative injury in mice.

Author: Zhaoxiang ZHANG ¹ ; Jinxia ZHAI ²
Author Information

1. Clinical College of An Hui Medical University, Hefei 230032, China.
2. Clinical College of An Hui Medical University, Hefei 230032, China. E-mail: zhaijinxia@sina.com.
Publication Type:Journal Article
MeSH: Acetylcysteine; pharmacology; Animals; Antioxidants; metabolism; pharmacology; Brain; drug effects; metabolism; Extracellular Signal-Regulated MAP Kinases; metabolism; Glutathione; metabolism; Halogenated Diphenyl Ethers; toxicity; Hippocampus; metabolism; Male; Malondialdehyde; metabolism; Mice, Inbred BALB C; Mitogen-Activated Protein Kinases; metabolism; Oxidation-Reduction; Phosphorylation; p38 Mitogen-Activated Protein Kinases; metabolism
From: Chinese Journal of Industrial Hygiene and Occupational Diseases 2014;32(9):674-678
CountryChina
Language:Chinese
Abstract:
OBJECTIVETo study the protective effects of N-acetylcysteine (NAC) against oxidative injury in the brain tissue of mice induced by decabromodiphenyl ether (PBDE-209) and the expression of mitogen activated protein kinase (MAPK)-related proteins in the hippocampus.
METHODSTwenty-one male BALB/c mice were randomly divided into three groups with seven mice in each group: solvent control group, PBDE-209 group with gavage of 500 mg/kg PBDE-209, and PBDE-209 +NAC group which received intraperitoneal injection of 100 mg/kg NAC 0.5 h before exposure to PBDE-209. Mice were sacrificed 6 weeks after exposure. Malondialdehyde (MDA) level, superoxide dismutase (SOD) activity, and glutathione (GSH) level in the cerebral cortex, hippocampus, cerebellum, and striatum, as well as the protein expression of extracellular signal-regulated kinase (ERK), phosphorylated ERK (p-ERK), p38 MAPK (p38), and phosphorylated p38 (p-p38) in the hippocampus, were determined by Western blot.
RESULTSCompared with the hippocampal and cerebellar levels of MDA in control group [(4.91±1.60) and (2.42±1.41) nmol/mg pro] and PBDE-209+NAC group [(6.16±1.03) and (2.83±0.85) nmol/mg pro], the MDA levels in PBDE-209 group [(12.12±6.39) and (4.24±1.15) nmol/mg pro] were significantly increased (P < 0.05). The striatum MDA level in PBDE-209 group [(12.92±4.30) nmol/mg pro] was significantly increased as compared with that of the control group [(4.05±2.23) nmol/mg pro] (P < 0.05). The hippocampal SOD activity of PBDE-209 group [(59.29±37.09) U/mg pro] was reduced significantly as compared with those of the control group [(93.28±21.75) U/mg pro] and PBDE-209+NAC group [(98.92±21.54) U/mgpro] (P < 0.05). The GSH levels in the cerebral cortex, striatum, and cerebellum in PBDE-209 group [(40.98±13.19), (24.46±11.30), and (3.55±1.55) mg GSH/g pro] were significantly reduced as compared with those of the control group [(75.79±26.51), (44.52±13.15) and (8.01±3.23) mg GSH/g pro] and the PBDE-209+NAC group [(89.86±28.39), (39.01±9.05) and (10.34±2.58) mg GSH/g pro] (P < 0.05). Western blot results showed that the ratios of p-p38/p38 and p-ERK/ERK in the hippocampus were significantly higher in the PBDE-209 group than in the control group and PBDE-209+NAC group (P < 0.05).
CONCLUSIONAntioxidant NAC has a protective effect against PBDE-209-induced brain injury in mice to some extent, and reduces the expression of MAPK-related proteins.