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目的探讨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 80只健康成年昆明种小鼠按体质量随机分为4组,每组20只,雌雄各半。染毒组小鼠以一次经口灌胃方式分别给予20、40、80 mg/kg剂量的乙体氯氰菊酯,食用油稀释受试物质,对照组给予等量食用油。于灌胃后2、4 h,每组各取10只小鼠大脑皮质,HPLC法检测γ-氨基丁酸(γ-aminobutyric acid,GABA)水平(μmol/g),分光光度法检测γ-氨基丁酸转氨酶(GABA transaminase,GABAT)活力(nmol/min.mg.pro),Real time RT-PCR法检测GABA受体(GABA-A、GABA-B)mRNA水平。结果染毒后2、4 h,80 mg/kg剂量组小鼠大脑皮质GABA水平(99.77±13.80、108.29±29.67)高于对照组(72.10±20.51、72.09±20.49)(P<0.05);染毒后2 h,40、80 mg/kg剂量组小鼠大脑皮质GABA-T活力(12.45±2.20、11.48±1.33)低于对照组(14.09±1.64)(分别为P<0.05、P<0.01);染毒后4 h,80 mg/kg剂量组小鼠大脑皮质GABA-A mRNA表达(0.89±0.07)低于对照组(1.00±0.08)(P<0.05),GABA-B mRNA表达与对照组比较,差异均无统计学意义(P>0.05)。结论乙体氯氰菊酯可降低小鼠大脑皮质GABA-T活力,使GABA增多,进而反馈性抑制GABA-A受体mRNA表达。
Objective To investigate the neurotoxicity of beta-cypermethrin and provide a theoretical basis for the prevention and control of such pesticides. Methods Eighty healthy adult Kunming mice were randomly divided into 4 groups according to their body weight, with 20 mice in each group. The mice in the exposure group were given the dose of beta cypermethrin of 20, 40, and 80 mg / kg by oral gavage, the test substance was diluted with edible oil, and the control group was given the same amount of edible oil. At 2 and 4 h after gavage, 10 mice in each group were sacrificed and the cerebral cortex was obtained. The level of γ-aminobutyric acid (GABA) (μmol / g) was determined by HPLC. The γ-amino The GABA receptor (GABA-A, GABA-B) mRNA levels were determined by real time RT-PCR. Results The levels of GABA in the cerebral cortex of mice treated with 80 mg / kg 2,4,4 h were significantly higher than those of the control group (99.97 ± 13.80,108.29 ± 29.67, P <0.05) At 2 h after poisoning, the GABA-T activity in cerebral cortex of mice in the 40 and 80 mg / kg groups was significantly lower than that in the control group (12.09 ± 2.20 and 1.148 ± 1.33, P <0.05, P <0.01, respectively) ; 4 h after exposure, the expression of GABA-A mRNA (0.89 ± 0.07) in the 80 mg / kg group was significantly lower than that in the control group (1.00 ± 0.08) (P <0.05) There was no significant difference between the two groups (P> 0.05). Conclusion Beta-cypermethrin can reduce the activity of GABA-T in mouse cerebral cortex, increase GABA, and then feedback inhibit GABA-A receptor mRNA expression.