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目的 研究碘过量摄入对小鼠肝脏I型脱碘酶 (IDI)活性的影响及硒的干预作用。方法 将 4 0只Balb c小鼠按体重随机分为 5组 :正常对照组、碘过量I组 (3mg L)、碘过量I+Se(1mg L)组、碘过量II组 (5mg L)以及碘过量II+Se(1mg L)组 ,分别喂饲碘过量水或碘过量 +硒水以及正常鼠饲料。 3个月后 ,取血、尿及脏器测定相关指标。结果 碘过量组小鼠出现了弥漫胶质性甲状腺肿 ;与正常对照组相比 ,两个碘过量的血清TT4水平显著升高 ,而碘过量II组血清TT3水平显著降低 ;碘可显著降低肝硒水平及I型脱碘酶活性 ,补硒可明显增加碘过量小鼠的肝硒储备 ,抑制碘过量I组脱碘酶活性的降低。结论 碘过量摄入降低小鼠肝硒水平及肝脏I型脱碘酶活性 ,可能是引起血清TT4升高、出现甲状腺肿的原因 ,补硒具有一定的干预作用。
Objective To study the effects of excessive iodine intake on the activity of type I deiodinase (IDI) in mice liver and the intervention effect of selenium. Methods 40 Balb c mice were randomly divided into 5 groups according to body weight: normal control group, iodine excess group I (3 mg L), iodine excess I + Se (1 mg L) group, iodine excess group II (5 mg L) Iodine excess II + Se (1mg L) group were fed with excess iodine or iodine + selenium and normal mouse feed, respectively. After 3 months, take blood, urine and organs related indicators. Results Compared with the normal control group, the serum TT4 levels of two iodine excess groups were significantly increased, whereas the serum TT3 levels of the iodine excess group II group were significantly reduced. Iodine significantly reduced the liver Selenium level and type I deiodinase activity, selenium supplementation can significantly increase the hepatic selenium reserve of iodine excess mice, inhibition of iodine excess group I deiodinase activity decreased. Conclusions Iodine excess intake can reduce hepatic selenium level and liver type I deiodinase activity in mice, which may be the cause of elevated thyroid serum level and occurrence of goiter. Selenium supplementation may have some preventive effects.