期刊文献+

碘缺乏和碘过量大鼠碘代谢及相关基因mRNA表达 被引量:9

The metabolism of iodine and the expression of relative gene mRNA in iodine deficiency and iodine excess at rats
原文传递
导出
摘要 目的观察不同水平的碘摄人对大鼠碘代谢及相关基因表达的影响。方法Wistar大鼠按体质量、性别随机分为低碘组(LI)、适碘组(NI)、5倍碘组(5HI)、10倍碘组(10HI)、50倍碘组(50HI)、100倍碘组(100HI),分别饮用含碘(碘化钾)量不同的水,饲养12个月后处死,采用RT—PCR及酸消化砷铈催化分光光度法检测甲状腺钠碘转运体(NIS)、氯碘转运体(PDS基因编码)mRNA的表达和尿碘、甲状腺组织含碘量。结果U组尿碘(0μg/L)、甲状腺组织含碘量[(0.0l±0.00)mg/g]显著低于NI组[234.5μg/L、(1.40±0.35)mg/g],组间比较差异有统计学意义(尸〈0.01);5HI、10HI、50HI、100HI组尿碘呈成倍升高,甲状腺组织含碘量呈逐渐升高的趋势。均高于NI组(P〈0.01)。U组甲状腺NISmRNA表达水平(1.15±0.16)明显高于NI组(1.11±0.21),组间比较差异有统计学意义(P〈0.01);5HI、10HI、50HI、100HI组呈逐渐下降趋势,与NI组比较差异有统计学意义(P〈0.01)。PDSmRNA水平,U组和5HI、10HI、50HI、100HI组均高于NI组,但仅U组(1.38±0.39)、50HI组(1.10±0.30)和100HI组(1.02±0.50)与NI组(0.79±0.14)比较差异有统计学意义(p〈0.05)。结论大鼠对长期碘过量比碘缺乏有更强的耐受力,NISmRNA的低表达是机体耐受碘过量的主要机制。碘过量可促进PDSmRNA的表达,这可能与碘过量时甲状腺组织含碘量增加,甲状腺球蛋白(取)发生过度碘化,进而诱发自身免疫反应增强的发病机制有关。 Objective To explore the effects of the different iodine intake on iodine metabolism and related gene expression at rats. Methods Wistar rats were divided into low iodine (LI), normal iodine (NI), five fold iodine (5HI), ten-fold iodine(10HI), fifty-fold iodine (50HI), one hundred-fold iodine (100HI). Rats in each group drank tap water containing potassium iodide with different concentration. 12 months after after administration, they were then sacrificed. Urinary iodine, thyroid tissue iodine and sodium iodide symporter (NIS), pendred's syndrome(PDS) mRNA were measured. Results Urinary iodine and thyroid iodine content in LI group [0 μg/L, (0.01 ± 0.00)mg/g] were significantly lower than those in NI group[234.5μg/L, (1.40 ± 0.35)mg/g], the difference had statistical significances (P 〈 0.01). The excessive iodine groups (HI) had significantly high urinary iodine. Thyroid tissue iodine in HI was higher than that in NI (P 〈 0.01 ). Thyroid NIS expression in LI (1.15 ± 0.16) was higher than that in NI (1.11 ± 0.21 ), the difference had statistical significance(P 〈 0.01), and decreased gradually from 5HI to 100HI. The expressions of PDS mRNA in both LI and HI groups were higher than that in NI. However, they were significantly different only in LI (1.38 ± 0.39), 50HI(1.10 ± 0.30) and 100HI(1.02 ± 0.50) from that in NI(0.79 ± 0.14), the difference had statistical significances (P 〈 0.05 ). Conclusions Rats are more tolerant to iodine excess than to iodine deficiency. The down regulation of NIS mRNA is the main mechanism of thyroid being tolerate to iodine excess. Iodine excess can promote PDS mRNA expression, which may be related with the increase of iodine content in thyroid tissue, over-iodization of thyroglobulin (Tg) and the enhance of auto-immunol reactivity when iodine intake is excess.
出处 《中国地方病学杂志》 CAS CSCD 北大核心 2008年第1期41-43,共3页 Chinese Jouranl of Endemiology
基金 国家自然科学基金重点资助项目(30230330)
关键词 代谢 甲状腺 钠碘转运体 Iodine Metabolism Thyroid gland Sodium iodide symporter
  • 相关文献

参考文献7

  • 1Royaux IE, Suzuki K, Moil A, et al. Pendrin the protein encoded by the pendred syndrome gene (PDS), is an apical porter of iodide in the thyroid and is regulated by thyroglobulin in FRTL-5 cells[J]. Endocrinology, 2000,141 ( 2 ) : 839-845.
  • 2Kouk M, Masuko M, Stone S, et al. Increased expression of tumor necrosis factor ot and decreased expression of thyroglobulin and thyroidperoxidase mRNA levels in the thyroid of iodine treated BB/W rat[J]. Eur J Endocrinol, 1998, 139:539-545.
  • 3刘嘉玉,张墨玲,阎玉芹,侯秉璋,叶振坤,林来祥,聂秀玲,孙毅娜,王琨,叶艳,陈祖培.不同碘摄入水平对大鼠甲状腺功能影响的实验研究[J].中国地方病学杂志,2006,25(6):615-617. 被引量:13
  • 4Dohan O, De la Vieja A, Paroder V, et al. The sodium iodide symporter: characterization, regulation, and medical significance [J]. Endocr Rev,2003,24( 1 ) :48-77.
  • 5Schroder-van der Elst JP, van der Heide D, Kastelijn J, et al. The expression of the sodium/iodide symporter is up-regulated in the thyroid of fetuses of iodine-deficient rats[J]. Endocrinology,2001, 142(9) :3736-3741.
  • 6Everett LA, Glaser B, Beck JC, et al. Pendred syndrome is caused by mutations in a putative sulphate transporter gene(PDS)[J]. Nat Genet, 1997,17(4) :411-422.
  • 7聂秀玲,林来祥,叶振坤,阎玉芹,陈祖培.高碘对大鼠甲状腺TPO、TgmRNA表达及血清甲状腺激素的影响[J].中国地方病学杂志,2005,24(3):258-261. 被引量:21

二级参考文献18

  • 1罗玉玉,叶振坤,项建梅,阎玉芹,陈祖培.不同剂量碘酸钾和碘化钾对缺碘大鼠甲状腺肿回缩效果的影响[J].中国地方病学杂志,2004,23(5):435-437. 被引量:8
  • 2卫生部碘缺乏病专家咨询组.卫生部碘缺乏病专家咨询组会议纪要[J].中国地方病学杂志,2004,23(6):632-634. 被引量:3
  • 3聂秀玲,孙云,李兰英,阎玉芹,陈祖培.碘对大鼠体内及体外甲状腺钠碘转运体mRNA表达的调节[J].中国地方病学杂志,2005,24(6):625-627. 被引量:5
  • 4Delange FM. Iodine deficiency[A]. In: Braverman LE, Utiger RD,eds. Werner and Ingbar's the thyroid, a fundamental and clinical text (the 8th edition)[ M ]. Lippincott Williams and Wilkins, 2000.295-304.
  • 5Taurog AM. Hormone synthesis: thyroid iodine metabolism[A]. In:Braverman LE, Utiger RD,eds. Werner and Ingbar's the thyroid, a fundamental and clinical text (the 8th edition)[M ]. Lippincott Williams and Wilkins, 2000. 61-84.
  • 6邱曙东 见:刘新民 潘长玉 张达青 等主编.甲状腺功能的调节[A].见:刘新民,潘长玉,张达青,等主编.实用内分泌学第3版[M].北京:人民军医出版社,2004.195-202.
  • 7Uyttersprot N, Pelgrims N, Carrasco N, et al. Moderate doses of iodide in vivo inhibit cell proliferation and the expression of thyroperoxidase and Na+/I- symporter mRNAs in dog thyroid [J].Mol Cell Endocrinol, 1997,131(2): 195-203.
  • 8Eng PHK, Cardona GR, Fang SL. Escape from the acute Wolffchaikoff effect is associated with a decrease in thyroid sodium/iodide symporter messenger ribonucleic and protein [J ]. Endocrinology, 1999,140(8): 3404-3410.
  • 9于志恒 朱惠民 陈崇义.高碘地方性甲状腺肿研究进展[A].见:陈祖培主编.中国控制碘缺乏病的对策[M].天津:天津科学技术出版社,2002.100-108.
  • 10Suzuki K, Lavaroni S, Mori A, et al. Autoregulation of thyroidspecific gene expression by thyroglobulin [J ]. Proc Nat Sci USA,1999, 95(5) :8251-8256.

共引文献29

同被引文献73

引证文献9

二级引证文献26

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部