Monaco F, Santolamazza C, De Ros I, Andreoli A
Acta Endocrinol (Copenh). 1980 Jan;93(1):32-6. doi: 10.1530/acta.0.0930032.
The effect of 6-propyl-2-thiouracil (PTU), and 1-methyl-2-mercaptoimidazole (MMI) on thyroglobulin (Tg) biosynthesis has been studied in vivo and in vitro. In vivo experiments were performed in rats treated for 20 days with PTU or MMI, analyzing soluble and particulate, cold and 125I-labelled, Tg. Thyroglobulin biosynthesis was also investigated by in vitro experiments, incubating thyroid tissue with labelled amino acid and carbohydrate in the presence of antithyroid compounds. It has been found that in vivo antithyroid agents decrease the amount of soluble Tg and increase the proportion of particulate Tg. Tg from treated animals is poorly iodinated being mainly represented by its 12S subunit. In vitro studies demonstrate that PTU and MMI inhibit Tg biosynthesis which is impaired in the polypeptide synthesis as well as in carbohydrate chains addition. Thus the inhibition of the hormonogenetic processes induced by antithyroid treatment leading to a depressed iodinating activity also appears to be related to a significant impairment of the production of the Tg molecule, the specific iodine acceptor.
研究了6-丙基-2-硫氧嘧啶（PTU）和1-甲基-2-巯基咪唑（MMI）对甲状腺球蛋白（Tg）生物合成的体内和体外作用。在给大鼠用PTU或MMI治疗20天的体内实验中，分析了可溶性和颗粒性、冷态和125I标记的Tg。还通过体外实验研究甲状腺球蛋白的生物合成，即将甲状腺组织在抗甲状腺化合物存在的情况下与标记氨基酸和碳水化合物一起孵育。已发现体内抗甲状腺药物可减少可溶性Tg的量并增加颗粒性Tg的比例。来自经治疗动物的Tg碘化不足，主要由其12S亚基代表。体外研究表明，PTU和MMI抑制Tg生物合成，这在多肽合成以及碳水化合物链添加过程中均受到损害。因此，抗甲状腺治疗诱导的激素生成过程的抑制导致碘化活性降低，这似乎也与Tg分子（特定碘受体）产生的显著损害有关。
