先天性碘缺乏对新生大鼠脑内 T_3T_4核 T_3受体与 T_45′-脱碘酶活性的影响  

Effects of inborn iodine deficiency on T_3 T_4 nuclear T_3 receptor and T_45'-deiodinase activity in neonatal rat brain

作　　者：杨康[1] 赵学勤[1] 陈祖培[1] 苏学良[1] 王嘉仪[2] 

机构地区：[1]天津市内分泌研究所 [2]天津医学院生化教研室

出　　处：《中国地方病学杂志》1992年第1期12-14,共3页Chinese Jouranl of Endemiology

摘　　要：用地甲肿与地克病高发区粮食饲养大鼠复制地克病动物模型,观察和比较了先天性碘缺乏第一代和第五代仔鼠20日龄时脑内甲状腺激素及其受体与 T_45′-脱碘酶活性动态变化的实验结果。发现第一代仔鼠存在有限的代偿机制;而第五代仔鼠脑核 T_3减少极为显著,T_45′-脱碘酶活性降低非常显著,与核 T_3受体浓度明显下降,表明机体失代偿。在大脑 T_3含量不足时,推测受体的下行调节可能是地克病发病的始动环节。An animal model of cretinism was prepared in rat by feeding grain got froma high morbidity district of endemic goiter and cretinism.The dynamic changesof T_3,T_4,nuclear T_3 receptor and T_4 5′-deiodinase activity were observedand those in critical period of brain development in the first and the fifthfilial generations compared.There was limited compensatory mechanism in thefirst filial generation,but in the fifth filial generation,the contents ofnuclear T_3 in brain were significantly decreased,the concentration of nuclearT_3 receptors was significantly lower,and the T_4 5′-deiodinase activity wasreduced markedly too,showing decompensation in organism.The down-regulation of T_3 receptor may be the initial step of endemic cretinism causedby severe iodine-deficiency during brain T_3 was in insufficiency.

关 键 词：克汀病 核T3受体 脱碘酶 

分 类 号：R581.210.2[医药卫生—内分泌]