中文摘要：

本试验旨在研究辛硫磷（Phoxim）对大鼠的毒性作用,探讨辛硫磷中毒的氧化应激机制.将36只SD大鼠分成对照组和2个染毒组,染毒组大鼠分别以30（低剂量组）和300μmol/kg体重剂量（高剂量组）灌服辛硫磷,连续灌服15、30 d后,分别测定血浆和肝脏胆碱酯酶（ChE）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活性和丙二醛（MDA）含量,并观察肝脏组织学变化.结果表明：辛硫磷染毒后大鼠血浆和肝脏ChE活性均极显著降低（P＜0.01）,尤其是高剂量染毒组,大鼠血浆ChE最大降低至对照组的22%,肝匀浆中ChE活性降低至对照组的75%.大鼠血浆和肝脏SOD、GSH Px活性变化随染毒时间延长呈下降趋势,血浆和肝脏MDA含量均呈上升趋势.组织学检查显示辛硫磷可造成肝细胞脂肪变性.本研究表明,大鼠辛硫磷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,说明氧化应激在辛硫磷的肝脏毒性中发挥着重要作用.

英文摘要：

In order to study the toxicity of phoxim on rats, and explore the role of oxidative stress in the mechanism of phoxim intoxication, phoxim was administrated intragastrically to SD rats with the concentrations of 30 and 300μmol/kg body weight. After 15 and 30 days, the content of malondialdehyde （MDA） and the activity of cholinesterase（ChE）, superoxide dismutase（SOD）, glutathione peroxidase（GSH-Px）in liver tissue and plasma were determined and histopathological changes were detected. Results showed that activity of ChE in the plasma and liver were sighificant lower than that in the control group（P〈0.01）. Especially , the activity of ChE in high dosage group decreased to 22Y00 in plasma and 75% in liver compared to the control. The activity of SOD and GSH-Px both decreased in plasma, the content of MDA increased in plasma and liver along with the exposed time extended. Histopathological changes showed that fatty degeneration in hepatocytes of rats. The results indicated that phoxim can induce enhanced lipid peroxidation on SD rats and lesions of structure in the liver. The oxidative stress plays an important role in the mechanism of hepatotoxicity.