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氧化应激与 GST-T1 基因与儿童支气管哮喘的关系。

Association of oxidative stress and GST-T1 gene with childhood bronchial asthma.

机构信息

Department of Medical Biochemistry, Comenius University in Bratislava, Jessenius Faculty of Medicine, Martin, Slovakia.

出版信息

J Physiol Pharmacol. 2009 Nov;60 Suppl 5:27-30.

Abstract

There is increasing evidence that bronchial asthma is associated with increased oxidative stress. Reactive oxygen species are produced in each organism as by-products of several essential reactions and can damage biomolecules. Asthma is a complex chronic inflammatory disorder of the airways, with many candidate genes suspected as being important in its development. Glutathione S-transferase (GST) is such a gene due to its role in protection against oxidative stress. In the present study, we examined the hypothesis that increased oxidative stress and polymorphism in the GST-T1 gene are associated with childhood asthma. We found that the amount of sulfhydryl groups significantly decreased and the content of thiobarbituric acid-reactive substances increased in the group of asthmatic children, compared with healthy controls. The GST-T1 null genotype was more frequent among the asthma patients. These results suggest that the GST-T1 null genotype and increased oxidative stress may play a role in the asthma pathogenesis in children.

摘要

越来越多的证据表明,支气管哮喘与氧化应激增加有关。活性氧在每个生物体中作为几种必需反应的副产物产生,并且可以破坏生物分子。哮喘是一种复杂的慢性气道炎症性疾病,许多候选基因被怀疑在其发展中起重要作用。谷胱甘肽 S-转移酶 (GST) 就是这样一种基因,因为它在对抗氧化应激中起作用。在本研究中,我们检验了这样一个假设,即氧化应激增加和 GST-T1 基因多态性与儿童哮喘有关。我们发现,与健康对照组相比,哮喘儿童组的巯基含量显著降低,硫代巴比妥酸反应物质的含量增加。GST-T1 无效基因型在哮喘患者中更为常见。这些结果表明,GST-T1 无效基因型和氧化应激增加可能在儿童哮喘发病机制中起作用。

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