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金慧英, 李法卿, 谭维国, 陈华标, 房德兴, 李素芹. 镉中毒肝脏过氧化氢(H2O2)定位及抗氧化系统的变化[J]. 中国公共卫生, 2000, 16(1): 15-16. DOI: 10.11847/zgggws2000-16-01-10
引用本文: 金慧英, 李法卿, 谭维国, 陈华标, 房德兴, 李素芹. 镉中毒肝脏过氧化氢(H2O2)定位及抗氧化系统的变化[J]. 中国公共卫生, 2000, 16(1): 15-16. DOI: 10.11847/zgggws2000-16-01-10
Jin Huiying, . Study on Hydrogen Preoxide(H2O2) Localization and Antioxidative System Changes of Hepatocytes After Cadmium exposure[J]. Chinese Journal of Public Health, 2000, 16(1): 15-16. DOI: 10.11847/zgggws2000-16-01-10
Citation: Jin Huiying, . Study on Hydrogen Preoxide(H2O2) Localization and Antioxidative System Changes of Hepatocytes After Cadmium exposure[J]. Chinese Journal of Public Health, 2000, 16(1): 15-16. DOI: 10.11847/zgggws2000-16-01-10

镉中毒肝脏过氧化氢(H2O2)定位及抗氧化系统的变化

Study on Hydrogen Preoxide(H2O2) Localization and Antioxidative System Changes of Hepatocytes After Cadmium exposure

  • 摘要: 为探讨急性镉中毒后自由基产生和损伤的部位及机理,给予大鼠尾静脉注射氯化镉建立急性镉中毒模型,电镜观察自由基过氧化氢(H2O2)的定位及细胞损伤,并测定抗氧化酶和氧化剂的变化.结果表明:H2O2-CeCl3的阳性颗粒沉积在肝细胞膜上,最早出现在中毒后1h,3h最严重,24h消失;抗氧化酶活力受抑,以3h最严重(p<0.01),6h后渐渐恢复;而GSH的含量在3h前均高于正常(p<0.05),以后逐步减少.提示自由基是急性镉中毒所致肝脏损伤的重要因素.

     

    Abstract: To study the localization and mechanism of free radical production and injury by cadmium,we set up the toxical model by intravenous injecting cadmium chloride into rats.Then injury of hepatocytes and free radical(H2O2) localization were studied by electron microscopy,and contents of antioxidation were determinated.Results Showed H2O2 CeCl3 positive precipitation on outer plasma membrane of hepatocytes first appeared at 1h after cadmium exposure,increased obviously at 3h and disappeared at 24h.Activities of antioxidase decreased clearly and with the serious in 3h(p<0.01),recovered progressively in 6h.But GSH content increased obviously before 3h(p<0.05),and decreased step by step.Conclusion:Free radical production is the important factor on injury of hepatocytes after cadmium exposure.

     

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