Briançon C, Halpern S, Telenczak P, Fragu P
INSERM U66, Institut Gustave-Roussy, Villejuif, France.
Endocrinology. 1990 Sep;127(3):1502-9. doi: 10.1210/endo-127-3-1502.
Analytical ion microscopy was used to evaluate the quantitative changes in thyroid 127I mapping induced by amiodarone in relation to the iodine intake. Mice were maintained on a normal diet (NID), on a low iodine diet (LID) or on a high iodine diet (HID) during 3 months. They received daily ip injections of amiodarone or NaI during the last 10 days. Microanalysis of iodine was performed on thyroid sections. In NID mice, the cellular 127I concentration (mean +/- SE: 0.90 +/- 0.06 micrograms/mg) was lower than that of follicular lumina (6.99 +/- 0.17). Amiodarone increased cellular concentration (2-fold) and decreased follicular concentration; NaI induced the same results. In LID mice, both concentrations, which were decreased 60- to 70-fold in comparison with NID, were restored by amiodarone, while NaI enhanced follicular concentration more than amiodarone. In HID mice, the follicular concentration (1.5-fold higher than normal) returned to a normal range with amiodarone, but cellular concentration (2.5-fold lower than normal) remained low, while NaI increased the cellular concentration 3-fold. These data show that iodine released by amiodarone has a bioavailability different from that of NaI. They indicate that thyroid response to amiodarone is related to dietary iodine intake, which, in turn, determines autoregulatory mechanisms. They also raise the question of the possible existence of an intrinsic property of amiodarone which would explain the specificity of its activity on thyroid iodine organification and the development of amiodarone-induced human thyroid diseases.
采用分析离子显微镜评估胺碘酮诱导的甲状腺127I图谱定量变化与碘摄入量的关系。将小鼠维持正常饮食(NID)、低碘饮食(LID)或高碘饮食(HID)3个月。在最后10天,每天腹腔注射胺碘酮或碘化钠(NaI)。对甲状腺切片进行碘的微量分析。在NID小鼠中,细胞内127I浓度(均值±标准误:0.90±0.06微克/毫克)低于滤泡腔(6.99±0.17)。胺碘酮增加了细胞内浓度(2倍)并降低了滤泡内浓度;NaI也产生了相同的结果。在LID小鼠中,与NID相比降低了60至70倍的两种浓度均通过胺碘酮恢复,而NaI比胺碘酮更能提高滤泡内浓度。在HID小鼠中,滤泡内浓度(比正常高1.5倍)通过胺碘酮恢复到正常范围,但细胞内浓度(比正常低2.5倍)仍较低,而NaI使细胞内浓度增加了3倍。这些数据表明,胺碘酮释放的碘具有与NaI不同的生物利用度。它们表明甲状腺对胺碘酮的反应与饮食碘摄入量有关,而饮食碘摄入量反过来又决定了自身调节机制。它们还提出了胺碘酮可能存在内在特性的问题,这可以解释其对甲状腺碘有机化作用的特异性以及胺碘酮诱导的人类甲状腺疾病的发生。