丙烯酰胺染毒大鼠步态及脑组织某些生化指标的变化  

Acrylamide-induced gait abnormality and changes of some biochemical indicators in rat brain

作　　者：朱兰兰[1] 严汉英 郭雄雄[1] 曾立爱[1] 严红[1] 

机构地区：[1]华中科技大学同济医学院公共卫生学院教育部环境与健康重点实验室,湖北武汉430030 [2]武钢安全环保部安全环保研究所

出　　处：《毒理学杂志》2011年第5期336-339,共4页Journal of Toxicology

基　　金：国家自然科学基金资助项目(30771822)

摘　　要：目的探讨丙烯酰胺(acrylamide,ACR)亚急性经口染毒对大鼠步态及脑组织的氧化损伤和血清中神经元特异性烯醇化酶(neuron specific enolase,NSE)活性的影响。方法 16只健康成年雄性SD大鼠按体重随机分为对照组和ACR组,每组8只,单笼饲养。ACR组按40 mg/kg灌胃,对照组灌等容量的生理盐水,连续12 d。观察大鼠一般行为体重并进行步态评分。在第12天染毒24 h后,两组大鼠均断头处死,在冰盘上分离大脑皮层和小脑并分离血清,全能酶标仪比色法测定大脑皮层和小脑组织的丙二醛(MDA)含量、总超氧化物歧化酶(T-SOD)活性、还原型谷胱甘肽(GSH)含量和谷胱甘肽过氧化物酶(GSH-Px)的活性,ELISA法测定血清中的NSE含量。结果试验期间对照组大鼠体重持续稳定增长,ACR组则持续下降;对照组大鼠呈正常步态,ACR组的步态分值随着染毒时间的延长而持续增高。第3～12天,与对照组相比,ACR组的步态分值显著增加(P<0.01);与对照组相比,ACR组的大脑皮层T-SOD活力显著降低(P<0.01);小脑MDA含量显著增高(P<0.05);T-SOD活性和GSH含量均显著降低(P<0.01);血清中的NSE浓度显著增高(P<0.05)。结论 ACR亚急性染毒可引起大鼠的步态异常,小脑组织发生脂质过氧化以及血清中的NSE浓度升高。氧化损伤可能介导ACR的神经毒作用。Objective To explore the effect of the gait,brain oxidative damage and serum NSE after subacute oral exposure to Acrylamide（ACR） in rats.Methods Sixteen male SD rats were divided randomly into two groups（8 per group） ：control group and ACR group.All rats were housed one per cage.ACR group was orally gavaged with 40 mg/kg ACR solution and control group was treated with equivalent volume of NS for 12 days.The body weights and gait scores were determined every three days.After 24h from the last treatment,all rats were decapitated,blood were collected and brain tissue were separated on ice and preserved in refrigerator at-80℃.Malondialdehyde（MDA）,the total superoxide dismutase（SOD）,glutathione（GSH） and glutathione peroxidase（GSH-Px） in cerebral cortex and cerebellum were assayed by almighty microplate assay,NSE concentration in serum was determined by ELISA.Results Gait score in control group was normal,but ACR group was increased with exposure time.The body weight in control group continued to increase steadily,but ACR group decreased.Compared with control group,the gait score in ACR group were significantly increased（P0.01） from 3 to 12 days.Compared with control group,T-SOD activity in Cerebral cortex in ACR group was significantly decreased（P0.01）,while MDA in cerebellum was significantly increased（P0.05）,and T-SOD and GSH significantly were decreased in cerebellum（P0.01）.NSE concentration in serum was significantly higher in ACR group than that in control group（P0.05）.Conclusion ACR subacute exposure could cause gait abnormality,oxidative damage in cerebellum,and serum NSE enhancement in rats.Oxidative stress might mediate the neurotoxic effect of ACR.

关 键 词：丙烯酰胺 脑氧化损伤 神经元特异性烯醇化酶 步态评分 

分 类 号：R99[医药卫生—毒理学]