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机构地区:[1]北京医科大学劳动卫生学教研室
出 处:《中华劳动卫生职业病杂志》1998年第3期129-132,共4页Chinese Journal of Industrial Hygiene and Occupational Diseases
基 金:高等学校博士学科点专项科研基金
摘 要:目的研究间二硝基苯(m-DNB)对肝脏的损伤并探讨其中毒机制。方法采用整体与离体实验相结合的方式对大鼠进行m-DNB染毒,观察大鼠肝脏脂质过氧化情况。结果随染毒剂量的增加和染毒时间的延长,染毒组大鼠肝脏丙二醛(MDA)含量明显增加,呈良好的剂量-效应关系和时间-效应关系;低剂量、短时间染毒时,谷胱甘肽(GSH)含量增加,大剂量、长时间染毒时,其含量降低;氧化型谷胱甘肽(GSSG)及GSSG/GSH比值均随染毒剂量和时间的增加而增加;肝细胞的超氧阴离子自由基(O-2·)、羟自由基(·OH)的产生量明显增加。结论诱发脂质过氧化及产生自由基是m-DNB的主要中毒机制之一。Objective The study was designed to examine the damage induced by m DNB to hepatocytes. Methods Two ways of exposure to m DNB were carried out:(1)rats were administered in vivo with different doses of m DNB;(2)cultured rat hepatocytes were exposed to different concentrations of m DNB.Then the changes of indices in lipid peroxidation were observed. Results The contents of MDA increased significantly in a manner dependent on exposure time and concentration of m DNB ;the contents of GSH increased as a response to a stress for short period of exposure and at lower doses,but decreased for longer period of exposure and at higher doses;the contents of GSSG and especially the ratio of GSSG/GSH increased with the rise of doses;the production of hydroxy free radicals and superoxide radicals were elevated obviously. Conclusion The study demonstrated that the lipid peroxidation might play an important role in m DNB toxicity.
分 类 号:R135.1[医药卫生—劳动卫生] R992[医药卫生—公共卫生与预防医学]
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