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桥本甲状腺炎中的氧化应激增强:与甲状腺功能生物标志物的相互关系。

Enhanced oxidative stress in Hashimoto's thyroiditis: inter-relationships to biomarkers of thyroid function.

机构信息

Department of Clinical Biochemistry and Nutrition, Urmia University of Medical Sciences, Urmia, Iran.

出版信息

Clin Biochem. 2013 Mar;46(4-5):308-12. doi: 10.1016/j.clinbiochem.2012.11.021. Epub 2012 Dec 4.

Abstract

OBJECTIVES

Oxidative stress has been implicated in the pathogenesis of several inflammatory and immune-mediated disorders including Hashimoto's thyroiditis (HT). The objectives of the present cross-sectional investigation were to estimate serum glutathione (GSH) status and the activities of its recycling enzymes in HT and to explore their interrelationships with biomarkers of autoimmunity and thyroid function.

DESIGN AND METHODS

Newly diagnosed females with HT (n=44) and 58 matched control subjects were recruited. Thyroid hormone profile, anti-thyroperoxidase anti-body (TPO-AB), anti-thyroglublin antibody (Tg-AB), thyroid volume (Tvol), urinary iodine excretion (UIE), GSH and the activities of glutathione peroxidase (GPx), glutathione reductase and gamma-glutamyltransferase were assessed.

RESULTS

Median UIE in HT was slightly but not significantly higher than that of controls. HT group exhibited higher levels of TSH, TPO-AB, Tg-AB and larger Tvol when compared with controls (P<0.001). The means of GSH and GPx in HT patients were significantly different from those of controls (P<0.001). In HT subjects, significant associations were seen between Tvol on TSH, GSH on TPO-AB, GSH on TSH and TPO-AB titers on TSH, respectively.

CONCLUSIONS

This is the first study to demonstrate a substantial reduction in GSH status in HT subjects. Secondly, the interrelationship between the GSH contents and TPO-AB titers in HT provides a preliminary data to support the notion that GSH diminution is a hallmark of in the events leading to oxidative stress activation and the development of immunological intolerance in HT. Further studies are required to elucidate the role of GSH in the etiology of down-regulation of thyroid function.

摘要

目的

氧化应激与几种炎症和免疫介导的疾病的发病机制有关,包括桥本甲状腺炎(HT)。本横断面研究的目的是评估 HT 患者的血清谷胱甘肽(GSH)状态及其循环酶的活性,并探讨其与自身免疫和甲状腺功能的生物标志物的相互关系。

设计和方法

招募了 44 名新诊断的 HT 女性患者和 58 名匹配的对照者。评估甲状腺激素谱、抗甲状腺过氧化物酶抗体(TPO-AB)、抗甲状腺球蛋白抗体(Tg-AB)、甲状腺体积(Tvol)、尿碘排泄量(UIE)、GSH 以及谷胱甘肽过氧化物酶(GPx)、谷胱甘肽还原酶和γ-谷氨酰转移酶的活性。

结果

HT 组的 UIE 略高于对照组,但无统计学意义。HT 组的 TSH、TPO-AB、Tg-AB 水平和 Tvol 均高于对照组(P<0.001)。HT 患者的 GSH 和 GPx 均值与对照组有显著差异(P<0.001)。在 HT 患者中,Tvol 与 TSH、GSH 与 TPO-AB、GSH 与 TSH 和 TPO-AB 滴度与 TSH 之间均存在显著相关性。

结论

这是第一项表明 HT 患者 GSH 状态显著降低的研究。其次,HT 患者 GSH 含量与 TPO-AB 滴度之间的相互关系为 GSH 减少是氧化应激激活和免疫耐受发展的标志性事件提供了初步数据。需要进一步研究阐明 GSH 在甲状腺功能下调病因中的作用。

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