残肾致慢性肾功能衰竭大鼠抗氧化酶基因的表达。

C Van Den Branden, B Ceyssens, D De Craemer, P De Bleser, K Hellemans, A Geerts, D Verbeelen
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引用次数: 16

摘要

活性氧中间体在慢性肾损伤和肾小球硬化中起作用。我们研究了慢性肾功能衰竭大鼠残肾模型中肾皮质抗氧化酶基因表达的变化,并将新数据与早期发表的酶活性进行了比较。利用过氧化氢酶、含铜/锌超氧化物歧化酶和谷胱甘肽过氧化物酶的cDNA探针,对皮质mRNA进行Northern blot分析,评估抗氧化酶基因的表达。过氧化氢酶基因表达在肾功能衰竭过程中降低;在残肾模型的肾小球硬化阶段,这种降低伴随着过氧化氢酶活性的降低。铜/锌超氧化物歧化酶和谷胱甘肽过氧化物酶基因表达在模型发展过程中保持正常水平,而其活性在早期残肾中出现暂时下降。在残肾模型中,过氧化氢酶似乎比超氧化物歧化酶和谷胱甘肽过氧化物酶更容易受到活性氧中间体的影响。我们的研究结果表明,在疾病发展过程中,抗氧化酶活性和基因表达并不是在同一方向上发生变化,所有的抗氧化酶也不是以相同的方式做出反应。
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Antioxidant enzyme gene expression in rats with remnant kidney induced chronic renal failure.

Reactive oxygen intermediates play a role in chronic renal injury and glomerulosclerosis. We investigate changes in renal cortex antioxidant enzyme gene expression in the rat remnant-kidney model of chronic renal failure and compare the new data to enzyme activities published earlier. Antioxidant enzyme gene expression is evaluated by Northern blot analysis of cortex mRNA, using cDNA probes for catalase, copper/zinc-containing superoxide dismutase, and glutathione peroxidase. Catalase gene expression decreases during development of renal failure; this decrease is accompanied by decreased catalase activity during the glomerulosclerosis phase of the remnant-kidney model. Copper/zinc superoxide dismutase and glutathione peroxidase gene expression remain at a normal level during progression of the model, whereas their activities show a temporary decrease in the early remnant kidney. In the remnant-kidney model, catalase seems to be more vulnerable to reactive oxygen intermediates than superoxide dismutase and glutathione peroxidase. Our results show that antioxidant enzyme activity and gene expression do not change in the same direction at all times during disease development and that all antioxidant enzymes do not respond in the same way.

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