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机构地区:[1]山东省滨州医学院,山东烟台264003 [2]重庆医科大学,重庆630000
出 处:《广东微量元素科学》2011年第8期12-15,共4页Trace Elements Science
基 金:重庆市"十一五"科技发展规划重大专项(CSTC;2007AB5034)
摘 要:为了解重庆地区自身免疫性甲状腺疾病(AITD)患者体内SOD、MDA的变化情况及其与尿碘的关系,初步探讨碘在AITD发病中的作用机制,采用病例对照研究,检测并分析了各组人群外周血SOD、MDA及尿碘的含量。结果表明:(1)GD与HT组尿碘中位数高于对照组(P<0.000 1);(2)GD与HT患者血清中的MDA含量高于对照组,SOD与MDA比值低于对照组(P<0.01);(3)随着尿碘的升高,血清中MDA的含量升高,SOD与MDA比值下降,SOD无明显变化。提示:AITD患者体内存在高碘营养状况,高碘可能导致机体的脂质过氧化损伤,从而诱发AITD。To know the relationship of SOD, MDA with urinary iodine in Chongqing and its changes in the, serum of patients with autoimmune thyroid disease, and to discuss preliminarily the effect of iodine in the mechanism of the pathogenesis of AITD, taking a case - control study, SOD, MDA and urine iodine levels were detected in each group. The results showed that (1) The median urinary iodine of GD and HT was higher than control group (P 〈 0. 000 1 ) ; (2) The content of MDA of GD and HT was higher than control group, n(SOD)/c(MDA) ratio was lower than the control group (P 〈0. 01 ) ; (3) With the increase of urinary iodine, MDA was increased, n(SOD)/c(MDA) was decreased, and SOD had no significant changes. It concludes: iodine nutritional status may be higher in the AITD patients. High iodine may lead to lipid peroxidative damage to the body, and induce AITD.
关 键 词:自身免疫性甲状腺疾病 Graves病(GD) 桥本甲状腺炎(HT) 超氧化物歧化酶 丙二醛 尿碘
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