摘要
目的观察对乙酰氨基酚(acetaminophen,AP)过量及饥饿条件下治疗剂量对乙酰氨基酚对小鼠的肝毒性作用。方法随机将纯种小鼠分成3组,即正常动物组、对乙酰氨基酚过量组(AP 250mg/kg,ip)、饥饿条件下对乙酰氨基酚治疗剂量小鼠组(AP 100mg/kg,ip),用对乙酰氨基酚诱发小鼠肝损伤,测定各组血清转氨酶、肝匀浆组织中谷胱甘肽含量及观察肝脏病理学改变,评价对乙酰氨基酚对肝脏的毒性作用和探讨其引起肝损伤的机制。结果对乙酰氨基酚过量组及饥饿条件下治疗剂量小鼠组的血清转氨酶升高,分别为(372.65±210.70)IU/L,(180.06±45.54)IU/L,明显高于正常对照组(40.05±19.80)IU/L,P<0.01;两组肝匀浆谷胱甘肽含量明显低于正常组(132.99±39.97)nmol/mg,分别为(22.89±18.63)nmol/mg,(64.60±20.62)nmol/mg,P<0.01;肝脏出现肝细胞损伤的病理改变。结论对乙酰氨基酚过量及饥饿条件下治疗剂量对乙酰氨基酚对小鼠有肝毒性作用。
Objective To study the effect of acetaminophen hepatotoxicity in groups of fed and fasted mice received various doses of acetaminophen. Methods Sixty purebred mice were seperatcd into 3 groups : normal controls, overdosage in fed group, therapeutic dosage in fasted group. When the hepatic injury in mice were induced with acetaminophen, the serum aminotransferase level, the concentration of glutathione in liver homogenate and liver tissue damage were determined for evaluating the effect and the mechanism of AP induced liver injury in mice. Results The serum aminotransferase levels increased in fed mice received overdosage and fasted mice received theraputic dosage of AP with the concentration of glutathione in liver homogenate decreaed and liver tissue damaged simultaneously. Conclusion AP has induced hepatic injury in fed and fasted mice received various doses of AP.
出处
《四川医学》
CAS
2006年第9期888-889,共2页
Sichuan Medical Journal