克百威预处理对毒死蜱神经细胞毒性的影响

研究了氨基甲酸酯农药克百威预处理对有机磷农药毒死蜱神经细胞毒性的影响. 采用噻唑蓝(MTT)法测定克百威对原代培养皮层神经细胞存活率的影响，找出无细胞毒性浓度；采用无细胞毒性浓度的克百威对培养细胞进行不同时间的预处理后，加入毒死蜱(克百威仍存在)染毒48 h测定细胞毒性的变化；采用Western blot方法测定克百威不同时间预处理对毒死蜱激活ERK1/2作用的影响. 结果表明:10 μmol/L的克百威处理72 h显示无细胞毒性，10 μmol/L的克百威预处理(2～24 h)可减轻毒死蜱的毒性，其中预处理8 h时作用最强；克百威预处理降低了毒死蜱对ERK1/2的激活作用，抑制ERK1/2激活作用与细胞毒性减轻相关. 克百威预处理时间过短(0～2 h)，对毒死蜱的细胞毒性及ERK1/2激活影响很小. 克百威预处理一段时间后可拮抗毒死蜱的细胞毒性，该作用机制与抑制ERK1/2激活有关；但克百威预处理时间过短，则不产生拮抗作用. 提示氨基甲酸酯农药与有机磷农药之间的联合作用模式受二者染毒时间间隔的影响. 

Effects of Carbofuran Pretreatment on Chlorpyrifos-Induced Cytotoxicity in Cortical Neural Cells

The effect of carbofuran pretreatment on chlorpyrifos-induced cytotoxicity was investigated. Carbofuran is a kind of carbamate pesticide, while chlorpyrifos is a kind of organophosphorus pesticide. Cellular survival rate was measured by MTT assay in primary cultures of cortical neural cells exposed to carbofuran, and the nontoxic level of carbofuran was determined. The neural cells were pretreated with a nontoxic level of carbofuran for different periods, followed by exposure to chlorpyrifos with the presence of carbofuran for 48 h, and cellularsurvival rates were measured. The effects of carbofuran pretreatment on chlorpyrifos-induced ERK1/2 activation were examined by western blot assay. The nontoxic level of carbofuran was determined to be 10 μmol/L during 72 h exposure. 10 μmol/Lcarbofuran pretreatment for 2-24 h attenuated chlorpyrifos-induced cytotoxicity, and pretreatment for 8 h produced the maximum effect. Carbofuran pretreatment inhibited chlorpyrifos-induced ERK1/2 activation, which was consistent with the finding of cytotoxicity attenuation; however, carbofuran pretreatment for short periods of 0-2 h produced no significant effects on both chlorpyrifos-induced cytotoxicity and ERK1/2 activation. In conclusion, carbofuran pretreatment for acertain period antagonizes chlorpyrifos-induced cytotoxicity, which is relatedto the inhibition of ERK1/2 activation; pretreatment for a relatively short timedoes not produce significant antagonism, suggesting that the mode of interaction between carbamate pesticide and organophosphorus pesticide depends on the interval of exposure between the two pesticides.