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目的 :为研究有机磷化合物的细胞毒性及其在缺氧或低氧环境中毒性升高的机理 ,为高原有机磷中毒的预防和治疗用药提供依据。方法 :利用MTT比色法、放免技术及荧光分析法测定缺氧条件下梭曼中毒PC12细胞存活率、cAMP含量和细胞内游离钙浓度 (〔Ca2 +〕i)的变化。结果 :单纯梭曼中毒组PC12细胞存活率无明显改变 ,缺氧及缺氧中毒组细胞存活率显著下降 ;缺氧组、梭曼中毒组及缺氧梭曼中毒组的细胞cAMP含量〔Ca2 +〕i水平均明显升高 ,且缺氧中毒组的变化较单纯缺氧、梭曼中毒组更为显著 (P <0 .0 1)。结论 :缺氧导致细胞信号传导增强 ,加重神经性毒剂的细胞损伤 ,可能是缺氧或低氧环境中有机磷化合物毒性升高的重要原因之一
OBJECTIVE: To study the cytotoxicity of organophosphorus compounds and their mechanism of toxicity in hypoxia or hypoxia environment, and to provide a basis for the prevention and treatment of organophosphate poisoning in plateau. Methods: MTT assay, radioimmunoassay and fluorescence analysis were used to determine the changes of survival rate, cAMP content and intracellular free calcium concentration ([Ca2 +] i) in soman poisoned PC12 cells. Results: The survival rate of PC12 cells in pure soman intoxication group had no significant change, and the cell survival rate in hypoxia and hypoxia poisoning group decreased significantly. The content of cAMP in cells of hypoxia, soman and so on ([Ca2 + 〕 I levels were significantly higher, and hypoxia poisoning group than the simple hypoxia, soman poisoning group was more significant (P <0.01). CONCLUSION: Hypoxia leads to enhanced cell signaling and aggravates cell injury of neurotoxic agents, which may be one of the important reasons for the increased toxicity of organophosphorus compounds in hypoxia or hypoxia