水胺硫磷亚急性暴露对小鼠肝脏氧化应激的影响

为探讨水胺硫磷对小鼠肝脏损伤作用机制,设置0.11、1.08、2.16 mg·kg-13个低、中、高不同剂量组,以灌胃方式对昆明种小鼠进行染毒7 d后,测定小鼠肝脏组织超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)2种抗氧化酶的活性,以及抗氧化物质谷胱甘肽(GSH)和膜脂质过氧化物丙二醛(MDA)含量,同时观察肝脏的组织学变化。结果表明,除低剂量组外,中、高剂量组小鼠肝脏SOD和GSH-Px活性与对照组相比均受到显著抑制(P0.05),GSH的含量与对照组相比显著下降(P0.05),MDA含量与对照组相比却呈显著上升趋势(P0.01),同时各指标的变化均呈一定的剂量-效应关系。组织学观察显示中、高剂量组肝细胞出现明显水肿和坏死,肝窦狭窄甚至闭塞。结果表明氧化损伤可能是水胺硫磷致小鼠肝脏毒性损伤的作用机制之一。

Oxidative Stress of Isocarbophos on the Liver of Mice in A Subacute Exposure

To investigate the mechanism of liver damage caused by isocarbophos, kunming mice were intragastric administered with isocarbophos for 7 days at 0.11, 1.08, 2.16 mg·kg^-1, respectively. Then, the activity of antioxidative enzymes: superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) in the liver tissues, as well as levels of antioxidative substance of glutathione (GSH) and the membrane lipid peroxide of malonaldehyde (MDA) were measured, and compared among the treated groups and the control group. Histopathological changes of liver were also observed. The results showed that compared with the control group, the activity of both SOD and GSH-Px were significantly inhibited (P<0.05), and the level of GSH was decreased dramatically (P<0.05), whereas the level of MDA was significantly increased (P<0.01) in all treated groups except for the low-dosage group (0.11 mg·kg^-1). All the biological indicators changed in dose-effect manners. At the same time, histological observations in the medium and high-dosage groups showed edema and necrosis in hepatocytes, and stenosis or even occlusion in hepatic sinusoids. In summary, our results indicate that oxidative damage might be involved in hepatic toxicity after exposure to isocarbophos.