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脂多糖对化学诱癌大鼠抗氧化系统的选择性损害作用
引用本文:杨金明,韩德五,赵严. 脂多糖对化学诱癌大鼠抗氧化系统的选择性损害作用[J]. 中国病理生理杂志, 1999, 15(3): 214-216
作者姓名:杨金明  韩德五  赵严
作者单位:山西医科大学病理生理学教研室,太原,030001
基金项目:山西省科委归国人员资助
摘    要:目的:观察脂多糖对化学诱癌大鼠抗氧化系统的影响。方法:用03g/L硫代乙酰胺给大鼠饮用6个月,诱发肝硬化癌变模型。大鼠在实验前作脾切除造成肠源性内毒素血症或/和在肝硬化形成时给予外源性脂多糖。结果:无论是外源性或/和肠源性内毒素均可提高肝硬化大鼠内毒素血症水平和肝癌发生率增加趋势。肝内丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性不同程度地增高、而谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)活性呈降低趋势,并与MDA浓度呈明显负相关(P<005)。结论:抗氧化酶类代谢紊乱、特别是CAT活性降低可能与肝硬化癌变的发生发展有关

关 键 词:脂多糖类;自由基;肝肿瘤.实验性;大鼠

Selective impairment of lipopolysaccharide on antioxidant system in rat hepatocarcinogenesis induced by thioacetamide
YANG Jin-Ming,HAN De-Wu,ZHAO Yan. Selective impairment of lipopolysaccharide on antioxidant system in rat hepatocarcinogenesis induced by thioacetamide[J]. Chinese Journal of Pathophysiology, 1999, 15(3): 214-216
Authors:YANG Jin-Ming  HAN De-Wu  ZHAO Yan
Abstract:AIM:To study the effect of lipopolysaccharide on antioxidant system in rat hepatocarcinogenesis.METHODS:Hepatocarcinoma in rats was induced by oral intake of 0.3 g/L thioacetamide(TAA) for six months.The TAA-induced rats were treated additionally with splenectomy before commencement of the experiment and/or administration of 8 mg/L lipopolysaccharide(LPS) underlying cirrhosis RESULTS:The intestinal endotoxin from splenectomy and/or exo-endotoxin from LPS oral administration elevated endotoxemia levels ( P <0 05) and increase hepatoma rate;The increased MDA content in liver was inversely correlated to the activities of GSH-Px and catalase (CAT) instead of SOD.CONCLUSION:The impaired GSH-Px and CAT possibly contributed to hepatocarcinogenesis in cirrhotic rats.
Keywords:Lipopolysaccharides  Free radicals  Live neoplasms  experimental  Rat  
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