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目的 为研究槟榔碱 (Arecoline)灭螺增效的作用机制。方法 用加入和未加入增效剂的灭螺药物浸泡钉螺 2 4h后 ,观察不同浓度的Are单用或与杀螺剂合用对钉螺中枢神经节Mg2 + -ATPase、ChE、SDH、LDH的变化。结果 6 2 5mg/LAre浸泡钉螺 2 4h后 ,其中枢神经节Mg2 + -ATPase被明显破坏 ,ChE轻度破坏 ;1 5 6mg/LAre与 1 2 5mg/LNaPCP、 0 2 5mg/LNic、 15 6 2 5mg/LSG合用时 ,对钉螺中枢神经节Mg2 + -ATPase的破坏作用大于后三种药物单用时的作用 ;各实验组SDH、LDH无明显改变 ,与正常对照组无显著性差异 (P >0 0 5 )。结论 槟榔碱的增效作用机制在于增强其它杀螺药的药效作用 ,药物的杀螺位点在于阻断氧化磷酸化偶联生成ATP ,进而影响能量代谢 ,可能最终因ATP生成和利用障碍而使钉螺丧失机械运动及生物合成等生命功能而死亡。
Aim To study the mechanism of action of Arecoline on snail-killing efficiency. Methods The snails were immersed in snails for 24 hours with and without synergists. The changes of Mg2 + -ATPase, ChE, SDH and LDH in the central nervous ganglia of Oncomelania snails were observed with different concentrations of Are alone or combined with snail. Results After soaking snails for 24 h, the Mg2 + -ATPase in the central ganglion was damaged obviously and the ChE was mildly destroyed. When 165mg / LAre and 125mg / LNaPCP, 0.255mg / LNic and 1562 5mg / LSG, the destructive effect on Mg2 + -ATPase in the central nervous system of Oncomelania snails was greater than that of the latter three drugs alone. There was no significant difference in SDH and LDH between the experimental groups and the normal control group (P> 0 0 5). Conclusion The synergistic mechanism of arecoline is to enhance the efficacy of other molluscicides. The killing point of the drug is to block the oxidative phosphorylation and coupling of ATP to generate energy metabolism, which may eventually lead to the formation and utilization of ATP. To snail loss of mechanical movement and biosynthesis and other life functions and death.