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高同型半胱氨酸血症对小鼠金属硫蛋白合成的影响 被引量:3

Homocysteine induces metallothionein formation in mice
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摘要 目的 :观察高同型半胱氨酸 (Hcy)血症时小鼠组织金属硫蛋白 (MT)含量的变化。方法 :小鼠腹腔注射Hcy复制高Hcy血症模型。观察肝、心和肾组织的MT和丙二醛 (MDA)水平。结果 :肝、心和肾组织在Hcy组MT水平较对照组分别高 2 10 % (P <0 0 1)、133 % ((P <0 0 5 )和 6 0 % (P <0 0 1)。而丙二醛水平则分别高6 %、5 2 % (P <0 0 5 )和 6 9% (P <0 0 5 )。注射Hcy同时用超氧化物歧化酶 (SOD)处理的动物 ,肝、心和肾组织MT含量较Hcy组分别低 2 2 % (P <0 0 5 )、33 % (P <0 0 5 )和 13% (P >0 0 5 )。丙二醛含量则分别降低 2 4% (P <0 0 5 )、2 1% (P <0 0 5 )和 48% (P <0 0 1)。组织MT水平与MDA含量呈显著正相关。结论 AIM: To observe the changes of metallothionein (MT) in various tissues of mice during hyperhomocysteinemia. METHODS: Intraperitoneal injection of homocysteine into mice induced hyperhomocysteinemia. The contents of tissue MT and malondialdehyde (MDA) in liver, heart and kidney were determined. RESULTS: Compared with control group, tissue MT levels in Hcy-group animals were increased by 210% ( P <0.01) for liver, by 133% ( P <0.05) for heart and by 60% ( P <0.01) for kidney. Tissue MDA contents were increased by 6%, 52% ( P <0.05) and 69% ( P <0.05), respectively. However, in treated animals with Hcy plus superoxide dismutase (SOD), the tissue MT contents in liver, heart and kidney were decreased by 22% ( P <0.05),33% ( P <0.05) and 13% ( P >0.05),respectively, compared with Hcy alone group. Tissue MDA contents were decreased by 24% ( P <0.05), 21% ( P <0.05) and 48% ( P <0.01). There was a positive correlation between tissue MT content and MDA level. CONCLUSION: Hcy could induce tissue MT formation through oxidative stress.
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2000年第8期678-680,共3页 Chinese Journal of Pathophysiology
基金 国家自然科学基金资助! (No .39730 2 2 0 )
关键词 金属硫蛋白 应激 高同型半胱氨酸血症 小鼠 Homocysteine Metallothionein Stress
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  • 1卜瑞芳,邓振霞,沈泓,许岚,吴懿玲,蒋艳敏,华嘉临,张稷.血浆同型半胱氨酸水平与2型糖尿病合并脑梗死的关系[J].中华内分泌代谢杂志,2004,20(5):444-445. 被引量:39
  • 2高平,秦绍森,肖路延,蔡晓杰.高同型半胱氨酸血症与Alzheimer病的关系[J].中国神经免疫学和神经病学杂志,2005,12(3):125-127. 被引量:5
  • 3李保华,毛利忠,王克义,雷志锴,牛国忠.脑梗死与高同型半胱氨酸血症的相关性研究[J].中国实用神经疾病杂志,2006,9(1):8-10. 被引量:97
  • 4Harding H P, Ron D. Endoplasmic reticulum stress and the development of diabetes: a review. Diabetes ,2002, 51(supple 3) :S455 - 461
  • 5Mouw G. Activation of caspase-12, an endoplasmic reticulum resident caspase, after permanent focal ischemia in rat. Neuroreport, 2003, 14:183 - 186
  • 6Mattson M P. Excitotoxic and excitoprotective mechanisms: abundant targets for the prevention and treatment of neurodegenerative disorders.Neuromol Med, 2003, 3: 65 - 94
  • 7Watanabe Y, Suzuki O, Haruyama T, Akaike T. Interferon-gamma induces reactive oxygen species and endoplasmic reticulum stress at the hepatic apoptosis. J Cell Biochem, 2003,89(2): 244 - 253
  • 8Lawrence de Koning A B, Werstuck G H, Zhou J, Austin RC.Hyperhomocysteinemia and its role in the development of atherosclerosis. Clin Biochem ,2003,36(6): 431 - 441
  • 9Ermak G, Davies K J. Calcium and oxidative stress: from cell signaling to cell death. Mol lmmunnol, 2002, 38(10): 713 - 721
  • 10Ferri K F, Kroemer G. Organelle-specific initiation of cell death pathways. Nat Cell Biol, 2001, 3( 11 ): E255 - 263

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