Sorimachi K, Robbins J
Horm Metab Res. 1979 Jan;11(1):39-43. doi: 10.1055/s-0028-1092680.
Monkey hepatocarcinoma cell monolayer cultures (NCLP-6E) metabolized thyroxine, 3,5,3'-triiodothyronine, 3,3',5'-triiodothyronine and 3,3'-diiodothyronine by phenolic and nonphenolic ring deiodinations and sulfation of the deiodinated products, as shown in previous work with this system. The effects of the antithyroid drugs, propylthiouracil (PTU) and methylmercaptoimidazole (MMI), on these processes was investigated. PTU, at 0.1 and 1 mM, inhibited only phenolic ring deiodination. MMI at 1 mM had no effect, but 32 mM inhibited deiodination of both rings as well as sulfation. The findings suggest that the increased serum rT3 level caused by PTU in vivo is the result of decreased rT3 deiodination, in contrast to the increased rT3 production which is caused by starvation.
猴肝癌细胞单层培养物(NCLP - 6E)可通过酚类和非酚类环脱碘作用以及脱碘产物的硫酸化作用代谢甲状腺素、3,5,3'-三碘甲状腺原氨酸、3,3',5'-三碘甲状腺原氨酸和3,3'-二碘甲状腺原氨酸,如先前该系统的研究所示。研究了抗甲状腺药物丙硫氧嘧啶(PTU)和甲巯咪唑(MMI)对这些过程的影响。0.1 mM和1 mM的PTU仅抑制酚类环脱碘作用。1 mM的MMI无作用,但32 mM的MMI抑制两个环的脱碘作用以及硫酸化作用。这些发现表明,与饥饿导致的rT3生成增加相反,PTU在体内引起的血清rT3水平升高是rT3脱碘作用降低的结果。