Beckett G J, Russell A, Nicol F, Sahu P, Wolf C R, Arthur J R
University Department of Clinical Chemistry, Royal Infirmary, Edinburgh, U.K.
Biochem J. 1992 Mar 1;282 ( Pt 2)(Pt 2):483-6. doi: 10.1042/bj2820483.
Selenium deficiency in rats for a period of up to 6 weeks inhibited both the production of 3,3',5-tri-iodothyronine (T3) from thyroxine (T4) (5'-deiodination) and also the catabolism of T3 to 3,3'-di-iodothyronine (5-deiodination) in liver homogenates. The hepatic stores of T3 were decreased by only 8% in selenium deficiency, despite the T3 production rate from T4 being only 7% of the rate found in selenium-supplemented rats. Hepatic glutathione S-transferase (GST) activity was increased in both hypothyroidism and selenium deficiency, but apparently by different mechanisms, since mRNA expression for this family of enzymes was lowered by hypothyroidism and increased in selenium deficiency. It is concluded that, since both T3 production and catabolism are inhibited by selenium deficiency, there is little change in hepatic T3 stores, and therefore the changes in the activity of certain hepatic enzymes, such as GST, that are found in selenium deficiency are not the result of tissue hypothyroidism.
大鼠缺硒长达6周会抑制肝脏匀浆中甲状腺素(T4)生成3,3',5-三碘甲状腺原氨酸(T3)的过程(5'-脱碘作用),以及T3分解为3,3'-二碘甲状腺原氨酸的过程(5-脱碘作用)。尽管缺硒时T4生成T3的速率仅为补硒大鼠的7%,但肝脏中T3的储存量仅减少了8%。甲状腺功能减退和缺硒时肝脏谷胱甘肽S-转移酶(GST)活性均升高,但机制明显不同,因为该酶家族的mRNA表达在甲状腺功能减退时降低,而在缺硒时升高。得出的结论是,由于缺硒既抑制T3的生成又抑制其分解代谢,肝脏中T3的储存量变化不大,因此缺硒时某些肝脏酶(如GST)活性的变化并非组织甲状腺功能减退的结果。