氧化应激在硝基苯致小鼠肾损伤中的作用

为探讨硝基苯对小鼠肾的毒性作用，采用灌胃法对试验小鼠用硝基苯进行染毒，染毒剂量分别为26、52、105mg／kg，每天染毒1次，共30d。于末次染毒后第2d将小鼠脱颈处死，立即取出肾通过相应处理用于抗氧化指标检测及显微和超微结构的观察。结果，染毒小鼠主要表现为近曲小管上皮细胞不同程度水样变性，线粒体肿胀，脊断裂；内质网脱核糖颗粒；细胞核发生形变；肾小球血管内皮细胞肿胀，血管扩张；随着染毒剂量的加大，肾和血清中MDA含量逐渐升高，SOD和GSH—Px酶活性不断降低，与对照组比较，均差异显著（P〈0．05）或极显著（P〈0．01）。结果表明，硝基苯能够诱发小鼠肾细胞发生氧化胁迫，并诱导细胞凋亡的发生。

Effect of oxidative stress on the nitrobenzene-damaged murine kidneys

In order to investigate the toxic effect of nitrobenzene on kidney of mice,the mice were subjected to nitrobenzene by intragastric administration. According to body weight of the mice,the doses of 26 mg/kg, 52 mg/kg and 105 mg/kg were administrated, respectively,once time per day for 30 consecutive days. The mice were sacrificed on day 2 post-final administration. The kidneys were collected for the detection of antioxidant indexes and the observations of microstructure and ultrastructure. The results revealed that the epithelial cells of the proximal convoluted tubule was in different water-apomorphosis under the microscope. Under the electron microscope, the pathological changes were mitochondria swell, lophos breakage,endoplasmic reticulum dis-ribose particle, cellular nucleus deformation, vascular endothelial cell swell and vasodilatation in renal glomerulus. With the increase of dose of nitrobenzene,content of MDA increased gradually, and activities of CAT and SOD decreased gradually in the kidney and serum. The antioxidant indexes were significantly or extremely significantly different between the treatment and the control groups. These results indicated that nitrobenzene could cause the mice renal cells to generate oxidative stress and induce cellular apoptosis.