Beckett G J, Beddows S E, Morrice P C, Nicol F, Arthur J R
University Department of Clinical Chemistry, Royal Infirmary, Edinburgh, U.K.
Biochem J. 1987 Dec 1;248(2):443-7. doi: 10.1042/bj2480443.
Selenium (Se) deficiency produced up to a 14-fold decrease in hepatic tri-iodothyronine (T3) production from thyroxine (T4) in vitro. The T3 production rate could not be restored by the addition of a variety of cofactors, nor by the addition of control homogenate. The impairment in hepatic T3 production observed in Se deficiency was reflected in the concentrations of thyroid hormones circulating in plasma, T4 being increased approx. 40% and T3 being decreased by 30%. However, the fall in plasma T3 concentrations was smaller than might be expected in view of the marked decreased in T3 production. Se deficiency had no measurable effect on plasma reverse-tri-iodothyronine concentrations. The data suggest that Se deficiency produces an inhibition of both 5- and 5'-deiodination, consistent with the widely held view that these reactions are catalysed by the same enzyme complex. The mechanism of inhibition appears not be mediated by changes in thiol levels, but a direct role of Se in the activity of the deiodinase complex cannot be excluded.
硒（Se）缺乏在体外使肝脏从甲状腺素（T4）生成三碘甲状腺原氨酸（T3）的量减少了多达14倍。添加多种辅助因子以及添加对照匀浆均无法恢复T3的生成率。硒缺乏时观察到的肝脏T3生成受损反映在血浆中循环的甲状腺激素浓度上，T4大约增加了40%，而T3下降了30%。然而，鉴于T3生成显著减少，血浆T3浓度的下降幅度小于预期。硒缺乏对血浆反式三碘甲状腺原氨酸浓度没有可测量的影响。数据表明，硒缺乏会抑制5-脱碘和5'-脱碘，这与普遍认为这些反应由同一酶复合物催化的观点一致。抑制机制似乎不是由巯基水平的变化介导的，但不能排除硒在脱碘酶复合物活性中起直接作用。
