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有机锗干预大鼠矽肺形成及其抗氧化应激机制的研究
引用本文:王明臣,李玉山,肖培义,王俊萍,文春和,高琦.有机锗干预大鼠矽肺形成及其抗氧化应激机制的研究[J].中国职业医学,2003,30(1):43-45.
作者姓名:王明臣  李玉山  肖培义  王俊萍  文春和  高琦
作者单位:1. 河南医科大学生物化学教研室,河南,郑州,450052
2. 河南医科大学三附院生化室,450052
3. 鹤壁市职业病防治研究所,456600
4. 河南省职业病防治研究所,450052
摘    要:目的:探讨有机锗(^132Ge)对大鼠矽肺形成的干预作用及对性氧化酶活性,脂质过氧化物(LPO)水平及肝Kupffer细胞功能的影响。方法:将实验大鼠随机分为A、B、C三组。A、B两组气管内注入石英尘混悬液,C组注入生理盐水。B组饮用含^132Ge水进行干预。A、C两组饮用自来水。6个月后取心脏血,进行超氧化物歧化酶(SOD)同工酶,谷胱甘肽过氧化物酶(GSH-Px)过氧化氢(CAT)活力及还原型谷胱甘肽(GSH)、LPO含量测定,并用肝Kupffer细胞诱生肿瘤坏死因子(TNF)实验测定矽肺鼠细胞免疫功能,结果:矽肺大鼠血清LPO含量显著高于对照组,而总SOD、CuZnSOD、GSH-Px、CAT活性均显著下降。GSH水平显著升高。矽肺鼠肝Kupffer细胞诱导TNF的功能略有下降。使用^132Ge可明显升高矽肺大鼠抗氧化酶系的活力,使肝Kupffer细胞诱生TNF的能力有所上升。结论:^132Ge可减轻由矽尘介导的氧化应激损伤,对免疫功能低下有一定的改善作用。并可明显干预矽肺病变的形成。

关 键 词:大鼠  矽肺  氧化应激  Kupffer细胞  ^132Ge
文章编号:1000-6486(2003)01-0043-03
修稿时间:2002年7月23日

Studies on interference of organic germanium in the formation of silicosis of rats and its mechanism of antioxidative stress
WANG Ming-chen,LI Yu-shan,XIAO Pei-yi,et al.Studies on interference of organic germanium in the formation of silicosis of rats and its mechanism of antioxidative stress[J].China Occupational Medicine,2003,30(1):43-45.
Authors:WANG Ming-chen  LI Yu-shan  XIAO Pei-yi  
Abstract:Objective To explore the blocking effect of organic germanium (132Ge) in the formation of silicosis and the influence on antioxidase activities, level of LPO and function of liver Kupffer cells in rats with silicosis. Methods Experimental rats were randomly divided into three groups. Group A and B were instilled intratracheally with suspension of mixed quartz dust, and group C with normal saline. Group B was fed with water containing 132Ge and group A and C were fed with tap water. After six months, blood specimens were collected from animal hearts. The activities of antioxidase (SOD isoenzymes, GSH-Px, CAT), level of LPO and GSH and cellular immunity of silicosis rats was determined by tumor necrosis factor (TNF) test. Results The serum LPO levels in rats with silicosis were significantly higher than those of the control group, while the activities of total SOD, CuZnSOD, GSH-Px and CAT were significantly lower. The ability to induce TNF in liver Kupffer cells reduced slightly in rats with silicosis. Administration of 132Ge could obviously enhance the activities of antioxidase and increase the ability to induce TNF in liver Kupffer cells. Conclusion 132Ge can alleviate quartz dust-mediated oxidative stress, improve the immune function and interfere markedly in the formation of silicosis lesions.
Keywords:Rat  Silicosis  Oxidative stress  Kupffer cell  132Ge
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