TY - JOUR
T1 - Effects of acrylonitrile on antioxidant status of different brain regions in rats
AU - Rongzhu, Lu
AU - Suhua, Wang
AU - Guangwei, Xing
AU - Chunlan, Ren
AU - Fangan, Han
AU - Suxian, Chen
AU - Zhengxian, Zhang
AU - Qiuwei, Zhu
AU - Aschner, Michael
N1 - Funding Information:
The authors are grateful to Dr. Sam Kacew at the University of Ottawa, Dr. Jordi Llorens at the University of Barcelona, Dr. Larry Fechter at Jerry Pettis Memorial Veterans Medical Center, Loma Linda, California and Dr. Peter Spencer at Oregon Health and Science University for critical comments and suggestions on the draft manuscript. This work was in part supported by the Natural Science Foundation of China (No. 30872139) (to Lu Rongzhu), the SCI-TECH(2008-018-02) and Nutrition-Disease Team Fund of Jiangsu University, the Natural Science Foundation of Jiangsu Province (No. BK 20040061) (to Lu Rongzhu), and NIEHS ES07331 (to Michael Aschner).
PY - 2009/12
Y1 - 2009/12
N2 - While the adverse effects of acrylonitrile (AN) on the central nervous system (CNS) are known to be mediated, at least in part, by the generation of free radicals and oxidative stress, there is a paucity of data on region-specific alterations in biomarkers of oxidative stress in the brain of AN-exposed animals. The present study was designed to examine the effects of AN on biomarkers of oxidative stress in several brain regions of adult Sprague-Dawley rats. Daily intraperitoneal (i.p.) treatment of animals to 0 (control, normal saline solution), 25, 50 or 75 mg AN/kg body weight for 7 days resulted in statistically significant (p < 0.05) increases in the levels of lipid peroxidation product, malondialdehyde (MDA), in the cortex and cerebellum; a statistically significant (p < 0.05) decrease MDA levels were noted in the striatum. Contents of reduced glutathione (GSH) were significantly (p < 0.05) decreased in cortex, cerebellum and hippocampus. The activities of the antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GPx) were differentially affected by AN and these effects were brain region-specific and AN dose-dependent. Taken together, these data suggest brain region-specific effects of AN on lipid peroxidation, activities of antioxidant enzymes and non-enzymatic antioxidant levels. These effects may provide biochemical evidence for AN-induced neurobehavioral damage and disturbance of monoamine neurotransmitters.
AB - While the adverse effects of acrylonitrile (AN) on the central nervous system (CNS) are known to be mediated, at least in part, by the generation of free radicals and oxidative stress, there is a paucity of data on region-specific alterations in biomarkers of oxidative stress in the brain of AN-exposed animals. The present study was designed to examine the effects of AN on biomarkers of oxidative stress in several brain regions of adult Sprague-Dawley rats. Daily intraperitoneal (i.p.) treatment of animals to 0 (control, normal saline solution), 25, 50 or 75 mg AN/kg body weight for 7 days resulted in statistically significant (p < 0.05) increases in the levels of lipid peroxidation product, malondialdehyde (MDA), in the cortex and cerebellum; a statistically significant (p < 0.05) decrease MDA levels were noted in the striatum. Contents of reduced glutathione (GSH) were significantly (p < 0.05) decreased in cortex, cerebellum and hippocampus. The activities of the antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GPx) were differentially affected by AN and these effects were brain region-specific and AN dose-dependent. Taken together, these data suggest brain region-specific effects of AN on lipid peroxidation, activities of antioxidant enzymes and non-enzymatic antioxidant levels. These effects may provide biochemical evidence for AN-induced neurobehavioral damage and disturbance of monoamine neurotransmitters.
KW - Acrylonitrile
KW - Antioxidant enzymes
KW - Brain regions
KW - Lipid peroxidation
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U2 - 10.1016/j.neuint.2009.05.009
DO - 10.1016/j.neuint.2009.05.009
M3 - Article
C2 - 19463879
AN - SCOPUS:69349083269
SN - 0197-0186
VL - 55
SP - 552
EP - 557
JO - Neurochemistry International
JF - Neurochemistry International
IS - 7
ER -