钼对小鼠脂质过氧化损伤及肝Smac和Bax表达的影响

通过向饮水中添加不同剂量钼(以钼离子计,0、100、200、400mg/L)建立实验动物模型:分别为对照组、钼100组、钼200组和钼400组。在试验处理的第120天,采集血液及肝组织,用透射电镜(TEM)观察肝细胞超微结构损伤,用免疫组化技术测定Smac和Bax蛋白表达量。结果:在饮水中添加200mg/L和400mg/L钼显著降低了血清超氧化物歧化酶(SOD)活性和谷胱甘肽过氧化物酶(GSH-PX)活性,提高了丙二醛(MDA)含量;高浓度的钼可导致小鼠肝组织细胞数量明显减少,细胞形态结构模糊,细胞核萎缩,内质网扩张,线粒体肿胀、嵴断裂,出现大量空泡化病理变化;添加200mg/L和400mg/L钼显著提高了肝中Smac和Bax蛋白的表达量。结果表明,钼暴露可增加机体脂质过氧化反应的程度,对肝组织的形态学和细胞超微结构产生病理学损伤,促进小鼠肝中Smac和Bax蛋白的高表达。

Effect of molybdenum on lipid peroxidation and expression of Smac and Bax in mice

The animal model was established by adding different doses of Mo into drinking water as the control group(Mo:0 mg/L),the Mo 100 group(Mo:100 mg/L),the Mo 200 group(Mo:200 mg/L) and the Mo 400 group(Mo:400 mg/L).On the 120th day of the treatment,the blood and hepar tissue were collected with the activities of SOD and GSH-Px and the content of MDA in serum determined by spectrophotometer.The histopathological and ultrastructural changes of the liver were observed by light microscope and transmission electron microscope(TEM).The Smac and Bax protein expressions were determined by the method of immunohistochemistry.In result,the activities of SOD and GSH-Px were significantly decreased,and the MDA content in serum was significantly increased in the Mo 200 group and the Mo 400 group,respectively.High Mo induced the hepatocytes swelling degeneration,liver sinusoidal endothelial cells hyperplasia,the structure of liver cells fuzzy,atrophy even necrosis.Under the TEM,swollen mitochondria and expanded endoplasmic reticulum were observed in the Mo 200 group and Mo 400 group.The level of Smac and Bax protein expressions were significantly increased in the Mo 200 group and the Mo 400 group.The result showed that Mo induced lipid peroxidation and the changes were dose-dependent.In addition,high doses of Mo significantly increased expressions of the apoptosis-related protein Smac and Bax.