乙体氯氰菊酯对小鼠脑组织中Glu、GABA水平及GABA-T活力的影响

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目的探讨拟除虫菊酯(pyrethroid,PD)类农药乙体氯氰菊酯的神经毒性,为该类农药的中毒防治提供理论依据。方法选取120只健康初成年昆明种小鼠,按体质量随机分为4组,雌雄各半。染毒组小鼠以1次经口灌胃方式分别给予20、40、80mg/kg剂量的乙体氯氰菊酯,以食用玉米油稀释受试物质,对照组给予等量色拉油。分别于灌胃后1、2、4h以分光光度法检测小鼠脑组织中谷氨酸(glutamate,Glu)、γ-氨基丁酸(γ-aminobutyric acid,GABA)水平及γ-氨基丁酸转氨酶(GABA transaminase,GABA-T)活力(n=10)。结果各时点各染毒组小鼠脑组织中Glu水平与对照组比较,差异均无统计学意义(P>0.05)。染毒后2、4h,80mg/kg剂量组小鼠脑组织中GABA水平高于对照组(分别为P<0.05、P<0.01)。80mg/kg剂量组小鼠于染毒后4h,脑组织中Glu/GABA比值低于对照组(P<0.01)。染毒后2h,40、80mg/kg剂量组小鼠脑组织中GABA-T活力低于对照组(分别为P<0.05、P<0.01)。结论乙体氯氰菊酯可使小鼠脑组织中GABA水平增加,导致Glu/GABA平衡紊乱,其原因可能是GABA-T活力降低所致。 Objective To investigate the neurotoxicity of pyrethroid beta-cypermethrin and provide a theoretical basis for the prevention and control of these pesticides. Methods A total of 120 healthy adult Kunming mice were randomly divided into 4 groups according to their body weight, with half male and one female. The mice in the exposure group were given the dosage of beta cypermethrin of 20, 40, and 80 mg / kg by oral gavage. The test substance was diluted with edible corn oil, and the control group was given the same amount of salad oil. The levels of glutamate (Glu), γ-aminobutyric acid (GABA) and γ-aminobutyrate aminotransferase (GABA) were measured by spectrophotometry at 1, GABA transaminase, GABA-T) activity (n = 10). Results There was no significant difference in Glu levels in brain tissue of all exposure groups at any time point between the two groups (P> 0.05). The levels of GABA in the brain tissue of mice treated with 80mg / kg 2,4,4d were higher than that of the control group (P <0.05, P <0.01, respectively). The ratio of Glu / GABA in brain tissue in 80mg / kg dose group was lower than that in control group 4h after exposure (P <0.01). The activity of GABA-T in brain tissue of 40 and 80 mg / kg dose groups was lower than that of the control group 2 h after exposure (P <0.05, P <0.01). Conclusion Beta-cypermethrin can increase the level of GABA in brain tissue of mice, resulting in the imbalance of Glu / GABA. The reason may be the decrease of GABA-T activity.
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