乙体氯氰菊酯对小鼠脑组织GS活力的影响及其机制探讨  

Effects and Mechanisms of Beta-cypermethrin on the Activity of Glutamine Synthetase in Mice Brain

作　　者：安丽[1] 鲍清[2] 孙静[1] 赵越[1] 刘莉[1] 于飞[1] 任亚浩[1] 杨军[1] 

机构地区：[1]中国医科大学公共卫生学院,辽宁沈阳110001 [2]化学工业农药安全评价质量监督检验中心,辽宁沈阳110021

出　　处：《工业卫生与职业病》2009年第6期329-331,共3页Industrial Health and Occupational Diseases

基　　金：国家自然科学基金(30872144)

摘　　要：目的初步探讨拟除虫菊酯类农药致哺乳动物兴奋性神经毒作用机制。方法将健康成年小鼠按体重随机分成1个对照组、3个染毒组和1个干预组,每组10只,雌雄各半。染毒组小鼠以灌胃方式分别给予20、40、80 mg/kg剂量的乙体氯氰菊酯,食用色拉油稀释受试物质;对照组小鼠给予等量色拉油;干预组小鼠以80 mg/kg剂量的乙体氯氰菊酯灌胃染毒的同时,腹腔注射给予300 mg/kg还原型谷胱甘肽(Glutathione,GSH)。3 h后处死小鼠,检测脑组织谷氨酰胺合成酶(glutamine synthetase,GS)活力及其mRNA水平。结果80 mg/kg剂量组和干预组全部小鼠以及40 mg/kg剂量组个别小鼠于染毒2 h后陆续出现不同程度的兴奋症状;与80 mg/kg剂量组小鼠相比,GSH干预组小鼠的中毒症状明显减轻。各染毒组小鼠脑组织GS活力随着剂量的增加而逐渐降低,其中40、80 mg/kg剂量组小鼠脑组织GS活力明显低于对照组,差异有统计学意义(P<0.01);干预组小鼠脑组织GS活力高于80 mg/kg剂量组,但差异无统计学意义(P>0.05)。各染毒组小鼠脑组织GS mRNA水平与对照组相比,差异均无统计学意义(P>0.05)。结论乙体氯氰菊酯对小鼠脑组织GS活力的抑制与GS基因转录调控无关;外源性GSH可明显减轻乙体氯氰菊酯染毒小鼠的中毒症状,但在改善该药抑制GS活力方面作用不明显。Objective To explore the effects and mechanisms of pyrethroids on excitatory neurotoxicity in mammal. Methods According to their body weights, healthy adult mice were randomly divided into five groups with 10 in each （5 males and 5 females）. Four groups of mice were administrated by gastro-gavage with 0, 20, 40 and 80 mg/kg of beta-cypermethrin, diluted with salad oil respectively. Another group of mice was immediately given 300 mg/kg of reduced glutathione（GSH）by intraperitoneal injection after administration with 80 mg/kg of betacypermethrin. Three hours after administration, the activity and the mRNA expression of glutamine synthetase（GS） in brains were determined by colorimetric assay and RT-PCR, respectively. Results Two hours after administration, some excitotoxic symptoms were observed in the group of 40 and 80 mg/kg with or without GSH intervention, and the toxic symptoms were alleviated in mice by GSH intervention. There were no obvious symptoms in the group of 20 mg/kg. With the increasing of administrated dosage, the activity of GS in mice brain decreased. Statistical treatment showed that the GS activity of mice brain in groups of 40 mg/kg and 80 mg/kg were remarkably different with the control group （P〈0. 001, P〈0. 01）. The GS activity of mice brain in the intervention group was higher than that in the group of 80 mg/kg, however, the difference was not significant（P〉0. 05）. In addition, GS rnRNA levels had no remarkable difference （P 〉0. 05） among each group. Conclusions The suppression of GS activity in mice brain induced by beta-eypermethrin was not mediated by GS gene transcriptional regulation. Toxic symptoms were alleviated obviously in mice, but the GS activity was not significantly improved by exogenetie GSH treatment.

关 键 词：拟除虫菊酯 谷氨酰胺合成酶 神经毒性 

分 类 号：R139.3[医药卫生—劳动卫生]