崔玉山, 赵亮, 曾强, 王睿, 张磊, 符刚, 冯宝佳, 刘洪亮. 氧化应激在高碘高氟致甲状腺损伤中的作用[J]. 环境与职业医学, 2016, 33(1): 7-12. DOI: 10.13213/j.cnki.jeom.2016.15284
引用本文: 崔玉山, 赵亮, 曾强, 王睿, 张磊, 符刚, 冯宝佳, 刘洪亮. 氧化应激在高碘高氟致甲状腺损伤中的作用[J]. 环境与职业医学, 2016, 33(1): 7-12. DOI: 10.13213/j.cnki.jeom.2016.15284
CUI Yu-shan, ZHAO Liang, ZENG Qiang, WANG Rui, ZHANG Lei, FU Gang, FENG Bao-jia, LIU Hong-liang. Role of Oxidative Stress in High Iodide and/or High Fluoride Induced Thyroid Damage[J]. Journal of Environmental and Occupational Medicine, 2016, 33(1): 7-12. DOI: 10.13213/j.cnki.jeom.2016.15284
Citation: CUI Yu-shan, ZHAO Liang, ZENG Qiang, WANG Rui, ZHANG Lei, FU Gang, FENG Bao-jia, LIU Hong-liang. Role of Oxidative Stress in High Iodide and/or High Fluoride Induced Thyroid Damage[J]. Journal of Environmental and Occupational Medicine, 2016, 33(1): 7-12. DOI: 10.13213/j.cnki.jeom.2016.15284

氧化应激在高碘高氟致甲状腺损伤中的作用

Role of Oxidative Stress in High Iodide and/or High Fluoride Induced Thyroid Damage

  • 摘要: 目的

    探讨氧化应激在高碘和(或)高氟致甲状腺损伤中的作用。

    方法

    建立50 mmol/L KI(高碘)、1 mmol/L NaF(高氟)、50 mmol/L KI+1 mmol/L NaF(高碘高氟)暴露的甲状腺细胞模型和含1.685 mg/L KIO3自来水(高碘)、含20 mg/L NaF自来水(高氟)、含1.685 mg/L KIO3+20 mg/L NaF自来水(高碘高氟)暴露的Wistar大鼠模型并开展人群流行病学调查,采用噻唑蓝(MTT)法、流式细胞术、分光光度法、电极法、比色法、放射法等检测细胞活性、活性氧(ROS)水平,大鼠尿碘、尿氟、血液丙二醛(MDA)、超氧化物歧化酶(SOD)水平,人血清ROS及三碘甲状腺素(T3)、甲状腺素(T4)和促甲状腺激素(TSH)水平。

    结果

    对照组细胞的活力为(100.00±0.00)%,而高碘、高氟及高碘高氟组下降为(73.54±8.37)%、(84.54±7.55)%和(72.62±7.15)%(P < 0.05),且高碘和(或)高氟组均可改变细胞形态;相对于对照组细胞的ROS荧光度(1 409.50±208.46),高氟及高碘高氟组的ROS荧光度上升,分别为2 304.15±390.47和2 669.24±646.80(P < 0.05)。高碘及高碘高氟联合均明显升高大鼠尿碘水平(P < 0.05);高氟及高碘高氟联合明显升高大鼠尿氟水平(P < 0.05);高碘和(或)高氟可改变大鼠甲状腺滤泡形状;雄性对照组大鼠MDA水平为(3.00±0.33)μmol/L,高氟组大鼠MDA水平上升为(4.27±0.82)μmol/L(P < 0.05),同时雄性对照组大鼠SOD水平为(300.92±36.02)×103 U/L,而高氟组下降为(226.33±41.21)×103 U/L(P < 0.05)。儿童高碘高氟组T4浓度明显上升(P < 0.05);高氟及高碘高氟组儿童血清ROS水平由对照组的(72.83±13.70)×103 IU/L上升为(76.65±125.45)×103 IU/L及(89.95±63.85)×103 IU/L(P < 0.05)。

    结论

    高碘和(或)高氟可造成甲状腺损伤,未发现高碘可致机体氧化应激,但氧化应激参与了高氟及高碘高氟致甲状腺损伤的过程。

     

    Abstract: Objective

    To investigate the role of oxidative stress in high iodide and/or high fluoride induced thyroid damage.

    Methods

    Models of thyroid cells were exposed to 50 mmol/L KI (high iodide), 1 mmol/L NaF (high fluoride), and 50 mmol/L KI+1 mmol/L NaF (high iodide and high fluoride); models of Wistar rats were exposed to water containing 1.685 mg/L KIO3 (high iodide), 20 mg/L NaF (high fluoride), and 1.685 mg/L KIO3+20 mg/L NaF (high iodide and high fluoride); and an epidemiological survey was carried out. Cell viabilities and reactive oxygen species (ROS) levels, rat urinary iodide and fluoride levels, blood malondialdehyde (MDA) and superoxide dismutase (SOD) levels, as well as human blood ROS, triiodothyronine (T3), thyroxine (T4), and thyrotropin (TSH) levels were detected by methyl thiazolyl tetrazolium (MTT) assay, flow cytometry, spectrophotometry, electrode, colorimetry, and radioimmunoassay.

    Results

    The cell viability of the control group was (100.00±0.00)%, and the cell viabilities of the high iodide, high fluoride, and combined groups were reduced to (73.54±8.37)%, (84.54±7.55)%, and (72.62±7.15)% (P < 0.05), respectively. Morphological changes were observed in the cells of the high iodide groups and/or high fluoride groups. The fluorescence intensity of ROS in the control group was 1 409.50±208.46, and the high fluoride groups and the combined groups induced intracellular ROS fluorescence intensity to 2 304.15±390.47 and 2 669.24±646.80 respectively (P < 0.05). The high iodide and the combined treatments increased the levels of urinary iodide in rats (P < 0.05). The high fluoride and the combined groups increased the levels of urinary fluoride in rats (P < 0.05). Morphological changes in rat thyroid follicles were observed in the high iodide and/or high fluoride treated groups. The MDA and SOD levels in the male control rat group were (3.00±0.33) μmol/mL and (300.92±36.02)×103 U/L, and those in the high fluoride group were (4.27±0.82) μmol/mL (P < 0.05) and (226.33±41.21)×103 U/L (P < 0.05) respectively. The children's T4 was elevated in the combined group (P < 0.05); the serum ROS levels were elevated in the high fluoride and the combined groups from (72.83±13.70)×103 IU/L in the control group to (76.65±125.45)×103 IU/mL and (89.95±63.85)×103 IU/mL respectively (P < 0.05).

    Conclusion

    High iodide and/or high fluoride could cause thyroid damage and there is no evidence indicating oxidative stress induced by high iodide, but oxidative stress is involved in the process of thyroid damage induced by high fluoride and the combination of high iodide and high fluoride.

     

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