Beckett G J, Peterson F E, Choudhury K, Rae P W, Nicol F, Wu P S, Toft A D, Smith A F, Arthur J R
University Department of Clinical Chemistry, Royal Infirmary, Edinburgh, Scotland, United Kingdom.
J Trace Elem Electrolytes Health Dis. 1991 Dec;5(4):265-7.
Labelling of rat kidney microsomes in vitro with [125I]-bromoacetyl T4 produced two bands on SDS/PAGE with Mr of 55 kDa and 27.5 kDa representing protein disulphide isomerase and type I iodothyronine deiodinase (ID-I) respectively. The amount of the 55 kDa band was unchanged by selenium (Se) deficiency but the 27.5 kDa protein was markedly decreased in kidney microsomal fraction obtained from Se-deficient rats. Concurrent Se and iodine deficiency produced a significant increase in thyroid weight, plasma thyrotrophin (TSH) and a decrease in thyroidal iodine when compared with either single Se or iodine deficiency. These results suggest that ID-I is a selenoprotein and that Se deficiency can exacerbate the hypothyroidism observed in iodine deficiency. In man, blood glutathione peroxidase and blood Se levels were decreased in hyperthyroidism due to Graves' disease whilst normal levels of these analytes were found in patients treated for Graves' disease. These results suggest that thyroid status can affect Se balance rather than Se deficiency predisposes to Graves' disease.
用[125I] - 溴乙酰甲状腺素在体外标记大鼠肾微粒体,在SDS/PAGE上产生两条带,分子量分别为55 kDa和27.5 kDa,分别代表蛋白二硫键异构酶和I型碘甲状腺原氨酸脱碘酶(ID-I)。55 kDa条带的量不受硒(Se)缺乏的影响,但在从缺硒大鼠获得的肾微粒体组分中,27.5 kDa的蛋白质明显减少。与单独的硒缺乏或碘缺乏相比,同时缺乏硒和碘会导致甲状腺重量显著增加、血浆促甲状腺激素(TSH)升高以及甲状腺碘含量降低。这些结果表明ID-I是一种硒蛋白,并且硒缺乏会加剧碘缺乏时观察到的甲状腺功能减退。在人类中,格雷夫斯病所致甲状腺功能亢进患者的血液谷胱甘肽过氧化物酶和血液硒水平降低,而接受格雷夫斯病治疗的患者这些分析物水平正常。这些结果表明甲状腺状态会影响硒平衡,而不是硒缺乏易患格雷夫斯病。