Cartier L J, Williams I K, Holloszy J, Premachandra B N
Biochim Biophys Acta. 1985 Nov 22;843(1-2):68-72. doi: 10.1016/0304-4165(85)90050-9.
Aminotriazole, a goitrogen, in addition to its known inhibitory effects on the thyroid, demonstrated a unique effect on peripheral deiodination of thyroxine (T4). In contrast to the well-known peripheral effects of goitrogens such as propylthiouracil in inhibiting 5'-deiodinase activity, i.e., to effect a decrease in T4 to triiodothyronine (T3) conversion, aminotriazole had no effect on the 5'-deiodinative pathway. Rather, this goitrogen appeared to stimulate the alternative pathway, viz. T4 5-deiodination, resulting in an increased reverse triiodothyronine (rT3) serum concentration. This was shown in comparisons of serum T4, T3 and rT3 concentrations and serum T3/T4 and rT3/T4 ratios between rats treated with aminotriazole and T4, and rats treated with T4 alone. The finding that aminotriazole may specifically enhance T4 5-deiodination, independently of T4 5'-deiodination, is novel, as this has not been observed in the case of other goitrogens. It is of interest that this goitrogen is devoid of sulphur, which is a prominent constituent of thiourylene compounds which have been noted to affect 5'-deiodination. The potentiating effect of aminotriazole on 5-deiodination of T4 was not attributable to dietary factors.
氨基三唑是一种致甲状腺肿物质，除了对甲状腺有已知的抑制作用外，还对甲状腺素（T4）的外周脱碘表现出独特的作用。与丙硫氧嘧啶等致甲状腺肿物质众所周知的外周作用相反，丙硫氧嘧啶抑制5'-脱碘酶活性，即导致T4向三碘甲状腺原氨酸（T3）的转化减少，而氨基三唑对5'-脱碘途径没有影响。相反，这种致甲状腺肿物质似乎刺激了另一条途径，即T4 5-脱碘，导致血清反三碘甲状腺原氨酸（rT3）浓度升高。在用氨基三唑和T4处理的大鼠与仅用T4处理的大鼠之间，比较血清T4、T3和rT3浓度以及血清T3/T4和rT3/T4比值时，发现了这一点。氨基三唑可能特异性增强T4 5-脱碘，而与T4 5'-脱碘无关，这一发现是新颖的，因为在其他致甲状腺肿物质的情况下尚未观察到这一点。有趣的是，这种致甲状腺肿物质不含硫，硫是已被注意到会影响5'-脱碘的硫脲类化合物的主要成分。氨基三唑对T4 5-脱碘的增强作用并非归因于饮食因素。
