碘过量对人甲状腺细胞的损伤作用及机制研究

Effect of Iodide Excess on Human Thyroid Cells(Nthy-ori 3-1) Apoptosis

目的探讨碘过量对人正常甲状腺细胞(Nthy-ori 3-1)的损伤作用及机制。方法用0(对照)、1、10、50mmol/L的碘化钾(KI)作用于体外培养的Nthy-ori 3-1细胞24 h后,分别采用噻唑蓝(MTT)法、乳酸脱氢酶(LDH)比色法检测细胞存活率和LDH漏出率,利用流式细胞术检测活性氧(ROS)水平、细胞周期构成比及凋亡率。结果与对照组相比,50 mmol/L碘染毒组细胞存活率明显下降(P<0.05),LDH漏出率明显上升(P<0.05)。各剂量组之间ROS产生水平差异无统计学意义。50 mmol/L碘染毒组G0/G1期细胞百分比明显增多(P<0.05),但S期百分比明显减少(P<0.05),且细胞凋亡率明显上升(P<0.05)。结论一定剂量的碘能降低甲状腺细胞存活率,增加LDH漏出率,细胞G0/G1期阻滞和诱导细胞凋亡,碘对甲状腺的损伤作用可能与碘对细胞周期的影响有关。

Objective To explore the damage effect of iodide excess on the human thyroid cells （Nthy--ori 3-1） and the mechanism. Methods Nthy-ori 3-1 cells were treated with different concentrations of potassium iodide （KI） in vitro. After 24 hours of culture, the MTF assay and lactate dehydrogenase （LDH） assay were used to measure the cell viabilities and the LDH leakage rate. The reactive oxygen species （ROS） level, the constituent ratio of the cell cycle and the apoptosis rate were measured by using flow cytometry. Results Compared with the control group, the cell viabilities in 50 mmol/L iodide-treated group decreased （P〈0.05） and LDH leakage rate increased significantly （P〈0.05）. No significant difference was seen for ROS level among four groups （P〉0.05）. The percentage of GdGl phase cells in 50 mmol/L iodide-treated group was higher than the control group and the percentage of apoptosis was significantly increased in 50 mmol/L iodide-treated group （P〈0.05）. Conclusion Iodide excess can decrease the cell viabilities, increase the LDH leakage rate, block the cells in G0/Gl phase and induce cell apoptosis. These results indicate that cell cycle arrest may be related to the thyroid cells damage induced by iodide excess.