摘要
目的研究高碘性甲状腺损伤的机制并寻求合适的硒干预剂量。方法50只Wistar大鼠分为5组正常组、高碘组(饮水含碘酸钾48mg/L)和3个补硒组(饮水含碘酸钾48mg/L,亚硒酸钠分别为0.5、1.0、2.0mg/L),共喂养36周。放射免疫法测定甲状腺激素水平,测定肝脏和肾脏组织Ⅰ型脱碘酶(IDI)活性,以RT-PCR测定IDImRNA水平。结果与正常组比较,高碘组肝、肾IDI活性[(17.1±2.1,2.67±1.10)pmolI·mg-1·min-1vs(13.0±2.9,1.52±0.44)pmolI·mg-1·min-1]、mRNA水平(1.78±0.14,1.55±0.17vs0.90±0.05,0.58±0.12,均P<0.05)下降(均P<0.05),而补充0.5mg/L硒组上述指标与正常组差异无统计学意义。结论IDI活力、mRNA水平下降可能是高碘性甲状腺损伤的机制之一,而补充硒应选择合适的干预剂量。
Objective To study the mechanism of the thyroid damage resulted from iodine excess and to seek suitable dosage of selenium for intervention. Methods Fifty Wistar rats were divided into five groups, normal control group, high iodine group （drinking water containing potassium iodate 48 mg/L） and three selenium groups （drinking water containing potassium iodate 48 mg/L and sodium selenite 0.5, 1.0, 2.0 mg/L）. These rats were fed for 36 weeks. The levels of thyroid hormones were assayed by RIA, type Ⅰ deiodinase（IDI） activities of liver and kidney were determined and the levels of mRNA of IDI in liver and kidney were detected by RT-PCR. Results As compared with normal control group, hepatic and renal IDI activity [ （ 17.1±2.1,2.67±1.10） pmol I·mg^-1·min^-1 vs （13.0±2.9,1.52±0.44）pmol I·mg^-1·min^-1] and mRNA level （1.78±0.14,1.55±0.17 vs 0.90±0.05,0.58±0.12, all P 〈0.05） in high-iodine group decreased significantly （all P 〈0. 05）. There was no difference between normal control group and the group that took water containing 0.5 mg/L selenium. Condusion Declines of IDI activities and mRNA levels in liver and kidney seem to be one of the mechanisms of the damage resulted from iodine excess and should be effectively intervened by suitable dosage of selenium.
出处
《中华内分泌代谢杂志》
CAS
CSCD
北大核心
2006年第2期136-138,共3页
Chinese Journal of Endocrinology and Metabolism
基金
国家自然科学基金资助项目(30230330)
关键词
碘
硒
Ⅰ型脱碘酶
大鼠
Iodine
Selenium
Deiodinase, type Ⅰ
Rats, Wistar
