碘过量对大鼠甲状腺细胞线粒体超氧化物生成和膜电位的影响

目的 探讨碘过量对Fisher大鼠甲状腺细胞(FRTL)线粒体超氧化物生成和膜电位(△ψ)的影响.方法 FRTL细胞分别以10-4mol/L碘化钾(KI)、10 U/L促甲状腺素(TSH)、10-4mol/L KI+10 U/L TSH 处理24 h,利用甲基噻唑基四唑(MTT)比色法检测FRTL细胞增殖情况,利用MitoSOX探针通过活细胞影像法检测线粒体超氧化物生成,利用罗丹明123(rh123)通过荧光分光光度计检测△ψ的变化.结果 细胞增殖情况,KI组(0.794±0.144)明显低于对照组(1.000±0.183,P<0.05),TSH组(1.215±0.156)明显高于对照组(P<0.05),KI+TSH组(1.025±0.254)与对照组比较差异无统计学意义(P>0.05),但明显高于KI组(P<0.05);细胞MitoSOX平均荧光强度(MFI),KI组和KI+TSH组(18.16±6.57、13.33±2.92)明显高于对照组(9.74±3.24,P均<0.05),TSH组(6.64±2.15)明显低于对照组(P<0.05),但KI+TSH组明显低于KI组(P<0.05);细胞rh123 MFI,KI组和KI+TSH组(210 593±31 328、295 525±34 243)明显低于对照组(407 824±37 198,P均<0.05),而KI+TSH组明显高于KI组(P<0.05),TSH组(411 187±72 852)与对照组比较差异无统计学意义(P>0.05).结论 碘过量(10-4mol/L KI)能造成FRTL细胞线粒体过氧化损伤,抑制细胞增殖,10 U/L TSH能够促进FRTL细胞增殖,减轻碘过量对FRTL细胞线粒体的过氧化损伤.

Effects of iodine excess on mitochondrial superoxide production and mitochondrial membrane potential in rat thyroid cell line cells

Objective To investigate the effects of iodine excess on mitochondrial superoxide production and mitoehondrial membrane potential(△ψ)changes in Fisher rat thyroid cell line(FRTL)cells.Methods FRTL cells were treated with 10-4mol/L potassium iodine(KI),10 U/L thyrotropin(TSH),10-4 mol/L KI+10 U/L TSH respectively for 24 h.Effects on cell proliferation were assayed by methyl thiazolyl tetrazolium(MTT)colorimetric method.Changes of mitochondrial superoxide production and △ψ were measured by live cell imaging and spectrofluorometer using MitoSOX and rhodamine 123(rh123)respectively.Results Absorbance(A)in the KI group (0.794±0.144)showed a significant decline compared to the control group(1.000 ±0.183,P<0.05),whereas a significant elevation was observed in the TSH group(1.215±0.156,P<0.05).No significant differences was found between the KI+TSH group(1.025±0.254)and the control group(P>0.05),but the former was marked higher than the KI group(P<0.05).Compared to the control group(9.74±3.24).MitoSOX mean fluorescence intensity (MFI)in the KI and KI+TSH groups(18.16±6.57,13.33±2.92)were significantly increased(all P<0.05),which was a significant decline in the TSH group(6.64±2.15,P<0.05).MitoSOX MFI in the KI+TSH group was lower than the KI group(P<0.05).Rh123 MFI in the KI and KI+TSH groups(210 593±31 328,295 525±34 243)showed significant decline than the control group(407 824±37 198,all P<0.05).Compared with the KI group.the KI+TSH group pronouncedly attenuated the reduction of Rh 123 MFI(P<0.05).No significant differences of Rh 123 MFI were found between the TSH group(411 187 ± 72 852) and the control group(P > 0.05). Conclusion Iodine excess (10-4 mol/L KI) may lead to peroxide damage on the mitochondria of FRTL cells, and cell proliferation is inhibited. Combining treatment with 10 U/L TSH may attenuate mitochondrial peroxide damage and inhibition of cell proliferation caused by iodine excess.