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目的了解急性弓形虫病对宿主体内是否发生氧化损伤.方法用小鼠建立急性弓形虫病模型,采用羟胺法测定小鼠血浆及心、肝、肺组织中超氧化物歧化酶(SOD)活性;采用薄层聚丙烯酸胺凝胶等电聚焦技术对SOD同工酶进行分析.结果小鼠于感染弓形虫后第3天其SOD活性呈反应性升高,于第6天显著下降;正常小鼠血浆及.心、肝、肺组织的SOD同工酶带分别为6、2、4与3条,感染弓形虫6d后的小鼠肝脏少一条酶带(PI＝8.1).结论氧自由基参与了急性弓形虫病的病理生理过程.“,”Aim Attempts had been made to know whether the oxidation injury by free radicals takes place in the body of the host with acute toxoplasmosis. Methods Hydroxylamine oxidation procedure was used to detect superoxide dismutase activity and TLPAG-IEF(thin layer polyacrylamide gel isoelectric focusing) was carried out to determine SOD isoenzymes after a murine model of experimental acute toxoplasmosis has been established by peritoneally injection of RH strain Toxoplasmsa gondii tachyzoites. Results SOD activity obviously increased on the third day post infection but markedly decreased after 6 days of the infection. SOD isoenzyme bands of the blood plasma and the homogenates of hearts,livers,and lungs of the normal mice were 6,2,4 and 3,respectively.The SOD band with PI8. 1 was not found in the liver homogenates of the mice with 6 day's infection. Conclusion These findings indicated that oxygen free radicals may play an important role in the pathophysiological process of acute toxoplasmosis.