乐果亚长期暴露对大鼠肝脏氧化应激的影响

本试验旨在研究乐果(Dimethoate)对大鼠的毒性作用,探讨乐果中毒的氧化应激机制.将24只SD大鼠分成对照组和3个染毒组,分别以0、1、6、30 mg/kg体质量剂量灌服乐果,连续灌服30 d后,测定血浆和肝脏胆碱酯酶(ChE)活性及肝脏中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活性和丙二醛(MDA)含量,并观察肝脏组织学和超微结构变化.结果显示,乐果染毒后大鼠血浆和肝脏ChE活性均极显著降低(P<0.01);大鼠肝脏SOD活性呈上升趋势,而GSH-Px、CAT活性随染毒剂量增加呈先下降后上升趋势;各染毒组肝脏MDA含量均呈上升趋势;组织学和超微结构检查显示肝细胞脂肪变性、凋亡等.结果表明.大鼠乐果持续染毒可以诱导机体脂质过氧化增强,并导致肝脏结构损伤,说明氧化应激在乐果的肝脏毒性中发挥重要作用.

Effects of sub-chronic exposure to dimethoate on oxidative stress in the liver of rats

In order to study the toxicity of dimethoate on rats and explore its oxidative stress mechanism,twenty-four SD rats were divided to four groups with one control and three experimental groups;dimethoate was intragastrically administrated everyday with concentration of 0,1,6 and 30 mg/kg body weight,respectively.After thirty days,the activity of cholinesterase(ChE) in plasma and liver,and that of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px) and catalase(CAT),as well as the content of malondialdehyde(MDA) in liver tissue were determined;histopathological and ultrastructural changes in liver were observed.Results showed that plasma and liver ChE activity decreased significantly(P<0.01),liver SOD activity and MDA content increased,GSH-Px and CAT activity increased at first and then decreased with increasing dosage of dimethoate;adipose degeneration and apoptosis in liver cells were observed.To conclude,sub-exposure to dimethoate can increase lipid peroxidation and lead to the damage of liver structure;therefore,oxidative stress plays an important role in liver toxicity induced by dimethoate.