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系统地研究了肟类药物对塔崩抑制的大鼠脑AChE的体外重活化作用,并与梭曼、沙林和VX进行了比较。结果表明,沙林和VX抑制的AChE较易被药物重活化,而塔崩和梭曼抑制的AChE则较难。37℃、pH7.2条件下,塔崩抑制的大鼠脑AChE可浓度依赖性地被TMB_r和LuH_6重活化,2-PAM在高浓度下也有一定作用,但HI-6在所用3个浓度下均无重活化。通过降低抑制温度成功地建立了未老化的梭曼膦酰化AChE模型。药物试验表明,未老化的梭曼膦酰化大鼠脑AChE可被高浓度(1mmol/L)HI-6重活化,而不被2-PAM、TMB_4及LuH_6重活化。提示药物自身内在活性在重活化作用中的重要性。TMB_4和LuH_6对塔崩磷酸化AChE有较强重活化,而对未老化梭曼膦酸化AChE无重活化,HI-6则相反,对未老化梭曼膦酰化AChE重活化效果好,而对塔崩磷酰化AChE无重活化作用。塔崩和梭曼膦酰化AChE在未老化以前对药物的响应就有所不同,毒剂残基的空间效应可能起重要作用。
The in vitro reactivation of AChE induced by tabun inhibition in rat was systematically investigated by oximes and compared with soman, sarin and VX. The results showed that AChE inhibited by sarin and VX was more susceptible to drug reactivation, whereas AChE inhibited by tabun and soman was more difficult. Under the condition of 37 ℃ and pH7.2, AChE was inhibited by Aspergillus tabaci in rat brain and activated by TMB_r and LuH_6 in a concentration-dependent manner. 2-PAM was also effective at high concentration. However, at the three concentrations of HI-6 No heavy activation. The unaged Asoxamylated AChE model was successfully established by lowering the inhibitory temperature. Drug experiments showed that un-aged somatomedin phosphorylation of rat brain AChE can be high concentration (1mmol / L) HI-6 reactivation, but not 2-PAM, TMB_4 and LuH_6 reactivation. Prompted the intrinsic activity of drugs in the reactivation of importance. TMB_4 and LuH_6 had stronger reactivation of the aspergillus phosphorylated AChE, whereas the un-aged somatostated AChE had no reactivation, while HI-6 had the opposite effect on unactivated AChE, Tagun phosphorylation of AChE no heavy activation. Tabuchiin and soman phosphonated AChE respond differently to drugs before they age, and the spatial effect of toxic residues may play an important role.