{"title":"Oxidant/Antioxidant status in relation to thyroid hormone metabolism in selenium- and/or iodine-deficient rats","authors":"Belma Giray, Jacqueline Riondel, Marie-Jean Richard, Alain Favier, Filiz Hıncal","doi":"10.1002/jtra.20001","DOIUrl":null,"url":null,"abstract":"Iodine and selenium are essential components of normal thyroid hormone metabolism and are involved in the modulation of antioxidant defense system. This study was designed to evaluate the extent of peroxidation of lipids and activities of antioxidant enzymes (AOEs) in various tissues of iodine- and/or selenium-deficient rats in relation to thyroid hormone metabolism. Iodine deficiency caused marked enhancements in glutathione peroxidase (GSHPx), superoxide dismutase (SOD), and catalase (CAT) activities in thyroid but did not cause lipid peroxidation (LP), indicating the occurrence of an adaptive response that protected the gland against oxidative stress induced by high levels of thyroid stimulating hormone (TSH). Except significant reduction in CAT activity in liver and kidney and an enhancement of SOD in kidney, iodine deficiency did not cause any other alterations in other tissues. Selenium deficiency and combined iodine and selenium deficiency caused significant alterations in AOE activities in all tissues and caused significantly high levels of LP in thyroid, liver, brain, and plasma, but not in kidney. Alterations in selenium-involved deficiencies appeared to be mainly caused by substantial losses of GSHPx activity; however, compensatory changes in SOD and CAT activities were also observed. J. Trace Elem. Exp. Med. 17:109–121, 2004. © 2004 Wiley-Liss, Inc.","PeriodicalId":101243,"journal":{"name":"The Journal of Trace Elements in Experimental Medicine","volume":"17 2","pages":"109-121"},"PeriodicalIF":0.0000,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/jtra.20001","citationCount":"14","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Journal of Trace Elements in Experimental Medicine","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/jtra.20001","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 14
硒和/或碘缺乏大鼠的氧化/抗氧化状态与甲状腺激素代谢的关系
碘和硒是甲状腺激素正常代谢的重要成分,参与抗氧化防御系统的调节。本研究旨在评估碘和/或硒缺乏大鼠不同组织中脂质过氧化程度和抗氧化酶(AOEs)活性与甲状腺激素代谢的关系。碘缺乏导致甲状腺谷胱甘肽过氧化物酶(GSHPx)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性显著增强,但没有引起脂质过氧化(LP),这表明发生了一种适应性反应,保护腺体免受高水平促甲状腺激素(TSH)诱导的氧化应激。除了肝脏和肾脏中CAT活性显著降低和肾脏中SOD活性增强外,碘缺乏没有引起其他组织的任何其他变化。硒缺乏和碘硒联合缺乏导致所有组织中AOE活性的显著改变,并导致甲状腺、肝脏、大脑和血浆中LP水平显著升高,但肾脏中没有。硒缺乏症的改变似乎主要是由GSHPx活性的大量损失引起的;SOD和CAT活性也出现了代偿性变化。J.Trace Elem。Exp.Med.17:109-1212004。©2004 Wiley-Liss,股份有限公司。
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