Yue L, Wang F, Li G
Institute of Preclinical Sciences, Norman Bethune University of Medical Sciences, Changchun 130021, China.
Chin Med J (Engl). 1998 Sep;111(9):854-7.
To examine the relationship between selenium (Se)- and vitamin E(VE)-deficiency and thyroid hormone (TH) metabolic disturbance, especially type I iodothyronine 5'-deiodinase (ID-I) activity.
We observed the metabolic changes of TH-3, 3',5-triidothyronine (T3) and thyroxin (T4) and their free radicals-glutathione peroxidase (GSH-Px) and lipid peroxides (LPO) in the peripheral tissues (liver, kidney and blood) of Wistar rats maintained on Se- and VE-deficient artificial semi-synthetic diet for 8 weeks.
In the Se- and VE-deficient rats (compared with Se- and VE-supplement rats): 1). Hepatic and renal ID-I activities decreased by 60% and 50% respectively, serum levels of T3 reduced 36%, and T4 increased by 32%. Hepatic ID-I activity and serum T3 concentration in Se- and VE-supplement rats were significantly higher than those in the Se-supplement and VE-deficient rats. 2). GSH-Px activities in the whole blood and liver decreased by 61% and 82% respectively. LPO concentrations in serum and liver increased by 53% and 40% respectively. When Se content remained the same, changes of VE content did not significantly affect GSH-Px activity, but the combined supplement of Se and VE decreased significantly the LPO concentration.
The data suggests that GSH-Px activity is influenced mainly by Se level, but ID-I activity is influenced by VE concentration in addition to Se level. VE seemed to play a protective role on ID-I and its mechanism might be related to the fact that VE protects the stability of microsomal membrane in which ID-I exists, avoiding from free radical damage as well as the coordinated action and mutual sparing effect of Se and VE.
研究硒（Se）和维生素E（VE）缺乏与甲状腺激素（TH）代谢紊乱之间的关系，尤其是I型碘甲腺原氨酸5'-脱碘酶（ID-I）的活性。
我们观察了以缺Se和VE的人工半合成饲料喂养8周的Wistar大鼠外周组织（肝脏、肾脏和血液）中TH-3、3',5-三碘甲腺原氨酸（T3）和甲状腺素（T4）的代谢变化及其自由基——谷胱甘肽过氧化物酶（GSH-Px）和脂质过氧化物（LPO）。
在缺Se和VE的大鼠中（与补充Se和VE的大鼠相比）：1）肝脏和肾脏的ID-I活性分别降低了60%和50%，血清T3水平降低了36%，T4升高了32%。补充Se和VE的大鼠肝脏ID-I活性和血清T3浓度显著高于补充Se和缺VE的大鼠。2）全血和肝脏中的GSH-Px活性分别降低了61%和82%。血清和肝脏中的LPO浓度分别升高了53%和40%。当Se含量保持不变时，VE含量的变化对GSH-Px活性没有显著影响，但联合补充Se和VE可显著降低LPO浓度。
数据表明，GSH-Px活性主要受Se水平影响，但ID-I活性除受Se水平影响外还受VE浓度影响。VE似乎对ID-I起到保护作用，其机制可能与VE保护ID-I所在的微粒体膜的稳定性、避免自由基损伤以及Se和VE的协同作用和相互节约效应有关。
