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.
出处
《中国地方病学杂志》
CAS
CSCD
1992年第1期12-14,共3页
Chinese Jouranl of Endemiology
关键词
克汀病
核T3受体
脱碘酶
Endemic cretinism
Nuclear T_3 receptor
T_4 5′-deiodinase
