摘要
目的探讨胺碘酮(am iodarone,AMD)改变碘的生物利用度对于所致甲状腺功能失调的机理。方法用原代培养的猪甲状腺细胞分别给予不同浓度的AMD和碘化钾(K I)培养,来测定TSH所致cAMP的生成量。结果当AMD的浓度大于100μmol/L时,cAMP的生成量有明显的下降,与AMD相比含等量碘的K I对cAMP生成的影响很小,只有超生理计量的K I才可以抑制cAMP的生成。结论AMD本身的毒性作用和其释放的碘共同所致甲状腺功能失调,在碘含量相同的情况下AMD与K I相比对体外培养甲状腺细胞呈现出潜在的抑制作用。
Objective To observe the genrsis of thyroid dysfunction. Methods hypothesis that altered bioavailablity of iodine is the pathoPrimary cultured porcine thyroid ceils were treated with various amiodarone or inorganic iodide, duing the period they were routinely monitored for cAMP production and iodide uptake. Results When the concentration of AMD was more than 100p.mol/L, there was a striking fall in cAMP production. In comparison to AMD, equivalent doses of inorganic iodide had negligible effects on cAMP production until supraphysiological doses were used. Conclusions The roles of iodine and the toxicity of AMD lead to the pathogenesis of thyroid dysfunctiong. At equimolar concentrations of iodinde, AMD exerts a significant inhibition on porcine thyroid ceil in vitro.
出处
《锦州医学院学报》
2006年第4期41-43,共3页
Journal of Jinzhou Medical College
作者简介
李小明（1976-），男，内蒙古集宁市人，在读硕士研究生，主要研究方向为蛋白质生化。
