碘化钾、碘酸钾对低碘大鼠脑组织抗氧化能力影响的实验研究
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摘要
目的：复制低碘Wistar大鼠动物模型，分别补充碘化钾及碘酸钾，观察两种不同碘制剂对低碘大鼠24小时尿碘含量、甲状腺吸碘率、血清甲状腺激素水平及脑组织抗氧化能力的影响
方法：选用Wistar大鼠，分为低碘组和适碘组，两组动物均用低碘饲料喂养，低碘组饮去离子水，喂养至3个月时取其中20只大鼠记录尿量，测定尿碘，然后腹腔分别注射Na~(131)I和Na~(131)IO_3，6小时后股动脉放血处死，记录甲状腺重量，用γ-放射免疫分析仪分别测定甲状腺吸碘率，及采用放免法测定血清T_3、T_4含量，证明低碘动物复制成功后，再把剩余的其它低碘组动物分为3组，一组为持续低碘组(LI—LI组)，继续饮用去离子水，第二组给予碘化钾治疗(LI—I)，饮水中碘化钾浓度为0.3μg／ml，第三组给予碘酸钾治疗(LI—O)饮水中碘酸钾浓度为0.4μg／ml，在上述条件下继续喂养3个月后重复测定尿碘、甲状腺重量、血清T_3、T_4，并检测脑组织匀浆中SOD、GSH—Px及MDA水平；适碘组从实验开始便在饮水中加入适量碘作为对照，分为两组，一组给予碘化钾水(NI组)，另一组给予碘酸钾水(NO组)，剂量分别为0.3μg／ml和0.4μg／ml。实验阶段为6个月，6个月后同低碘组一样，测定尿碘、甲状腺重量、血清T_3、T_4，及脑组织匀浆中SOD、GSH—Px和MDA的水平。
结果：低碘组大鼠3个月时甲状腺重量增加，血清T_4水平下降，尿碘含量降低，甲状腺吸碘率升高。证明低碘大鼠模型复制成功。持续低碘组
天津医科大学硕士研究生学位论文
甲状腺重量、尿碘、血清T;都明显低于补碘治疗组(LI一I、LI一O)，而补
充碘化钾的LI一I组和补充碘酸钾的LI一O组间甲状腺重量、血清T4水平、
尿碘含量间均无显著差别;适碘组的Nl和NO间上述指标也无显著性变化。
持续低碘组(LI一LI)大鼠与各组相比，SOD略有下降的趋势，但仅与LI
一I相比P<0.05，与其他各组间无显著性差异;Ll一Ll组GSH一Px明显低于
其他三组，P<0.01;同时MDA水平明显高于其他各组，尸<0.01。LI一I和
Ll一O组相比，GSH一Px、SOD、MDA等指标间均无显著性差异，P>0.05，
而且补碘3个月后，与正常对照组(Nl)相比，GSH一Px、SOn、MDA之
间均无显著性差别，P>O.05。
结论:
1.各组大鼠尿碘水平与饮水中碘含量相平行。2.低碘大鼠甲状腺组织对碘
化钠和碘酸钠的吸收率没有明显差别。3.适碘大鼠甲状腺组织对碘化钠和
碘酸钠的吸收率没有明显差别。4.适量补充碘化钾及碘酸钾，对碘缺乏病
均有良好的治疗作用。甲肿消退的速度以及甲状腺功能的恢复情况无明显
差别。5.低碘大鼠脑组织谷肤甘肤过氧化物酶活性降低，MDA含量增多，
说明在长期低碘状态下大鼠脑组织存在自由基的过氧化损伤。6.低碘大鼠
给予碘化钾及碘酸钾治疗，对脑组织SOD、GSH一Px及MDA的影响没有
显著性差异，而且经过3个月的补碘治疗，无论是碘化钾还是碘酸钾均可
使低碘大鼠脑组织的抗氧化酶活性及MDA含量恢复到接近适碘组的水
平。
Object: The Wistar rat model of iodine deficiency was made successfully.
Following that, the potassium iodide and potassium iodated were given to the rat model with different groups respectively. Before and after feeding the compounds, the rate of iodine metabolic in rats and the 131I-uptake rate
of thyroid gland were examined, the level of T3 and T4 in serum were measured and the variation of antioxidative capability of brain were observed.
Methods: 90 Wistar rats were divided into two groups - low iodine group
(LI) and normal iodine group (NI). The LI rats were fed with low iodine food and deionized water. Three months later, 20 LI rats were chosen from LI group randomly, and then the volume of urine and content of urinary
iodine in 24 h were measured for each rat. Following that, Na I and
Na 103 were injected into rat abdomen for testing 131I-uptake rate. Finally, the rats were killed by bloodletting from femoral artery after 6 hours after
injection. The thyroid glands were weighted, I-uptake rate examined
and the level of T3 and T4 in serum determined for each rats. All of data of 20 rats were shown that the rat model of iodine deficiency was made successfully.
The other deficiency iodine rats in LI group were divided into three groups: (1) LI-LI, fed with deionized water and low iodine food continually; (2) Ll-I, fed with 0.3ug/ml potassium iodide and low iodine food; (3) L1-O, fed with 0.4ug/ml potassium iodated water and low iodine food for another three months. The data including the weight of thyroid gland, 131I-uptake
rate of thyroid gland, the level of urinary iodine and TS and T4 in serum, and the content of SOD, GSH-Px and MDA in brain were observed for each rat as well.
In the other hand, the NI rats of two groups were fed low iodine food in same time; but One of them was fed the water containing 0.3ug/ml KI and
another were fed the water containing 0.4ug/ml KIO3 for 6 months totally.
All items tested were same as that in LI group observed.
Results: In this experiment, It was shown that thyroid weight in rats
were increased, the level of T4 in serum decreased and the excretion of urinary iodine were declined in LI group since The rats had been fed low dietary for three months. So it was demonstrated that the deficiency iodine rat had been established well. In the other hand, all of data including the weights of thyroid glands, the level of urinary iodine and serum T4 in LI rats were lower than that in LI-I and LI-O respectively, but they were not significant different between LI-I and LI-O group, and neither in NI and NO group. The activity of SOD in LI-LI group was lower than in LI-I group (P<0.05), but not different significantly compared with other groups (LI-O and NI); the content of GSH-Px in LI-LI was less than that in other three groups (P<0.01), meanwhile, the content of Malondialdehyde (MDA) of brain in LI-LI was higher striking than that in others (P <0.01). In another hand, each of GSH-Px, SOD and MDA was not different between LI-I and LI-O rats (P>0.05) when the rats were fed with low iodine dietary. In first three months; neither were they when each of group was compared with NI rats after giving iodized salt.
Cone I us i ons : l.The level of excretion of urinary iodine is varied with the content of iodine in drinking water.2.There was no significant difference between intake- rate of potassium iodine and intake-rate of potassium iodate in thyroid gland for low iodine rats.3.There was no significant difference between uptake - rate of potassium iodine and potassium iodate in thyroid gland for normal iodine rats.4.It is effective for LI rat to treat with a reasonable dosage of potassium iodide or potassium iodate.5.The decreasing of content of GSH-Px and increasing of MDA of brain in low iodine rats suggest that the damage of rat brain may come from oxidizing of free radical.6.There were no variation of antioxidative capability of brain between two group rats which were treated potassium iodine and potassium iodate respectively; and the
方法：选用Wistar大鼠，分为低碘组和适碘组，两组动物均用低碘饲料喂养，低碘组饮去离子水，喂养至3个月时取其中20只大鼠记录尿量，测定尿碘，然后腹腔分别注射Na~(131)I和Na~(131)IO_3，6小时后股动脉放血处死，记录甲状腺重量，用γ-放射免疫分析仪分别测定甲状腺吸碘率，及采用放免法测定血清T_3、T_4含量，证明低碘动物复制成功后，再把剩余的其它低碘组动物分为3组，一组为持续低碘组(LI—LI组)，继续饮用去离子水，第二组给予碘化钾治疗(LI—I)，饮水中碘化钾浓度为0.3μg／ml，第三组给予碘酸钾治疗(LI—O)饮水中碘酸钾浓度为0.4μg／ml，在上述条件下继续喂养3个月后重复测定尿碘、甲状腺重量、血清T_3、T_4，并检测脑组织匀浆中SOD、GSH—Px及MDA水平；适碘组从实验开始便在饮水中加入适量碘作为对照，分为两组，一组给予碘化钾水(NI组)，另一组给予碘酸钾水(NO组)，剂量分别为0.3μg／ml和0.4μg／ml。实验阶段为6个月，6个月后同低碘组一样，测定尿碘、甲状腺重量、血清T_3、T_4，及脑组织匀浆中SOD、GSH—Px和MDA的水平。
结果：低碘组大鼠3个月时甲状腺重量增加，血清T_4水平下降，尿碘含量降低，甲状腺吸碘率升高。证明低碘大鼠模型复制成功。持续低碘组
天津医科大学硕士研究生学位论文
甲状腺重量、尿碘、血清T;都明显低于补碘治疗组(LI一I、LI一O)，而补
充碘化钾的LI一I组和补充碘酸钾的LI一O组间甲状腺重量、血清T4水平、
尿碘含量间均无显著差别;适碘组的Nl和NO间上述指标也无显著性变化。
持续低碘组(LI一LI)大鼠与各组相比，SOD略有下降的趋势，但仅与LI
一I相比P<0.05，与其他各组间无显著性差异;Ll一Ll组GSH一Px明显低于
其他三组，P<0.01;同时MDA水平明显高于其他各组，尸<0.01。LI一I和
Ll一O组相比，GSH一Px、SOD、MDA等指标间均无显著性差异，P>0.05，
而且补碘3个月后，与正常对照组(Nl)相比，GSH一Px、SOn、MDA之
间均无显著性差别，P>O.05。
结论:
1.各组大鼠尿碘水平与饮水中碘含量相平行。2.低碘大鼠甲状腺组织对碘
化钠和碘酸钠的吸收率没有明显差别。3.适碘大鼠甲状腺组织对碘化钠和
碘酸钠的吸收率没有明显差别。4.适量补充碘化钾及碘酸钾，对碘缺乏病
均有良好的治疗作用。甲肿消退的速度以及甲状腺功能的恢复情况无明显
差别。5.低碘大鼠脑组织谷肤甘肤过氧化物酶活性降低，MDA含量增多，
说明在长期低碘状态下大鼠脑组织存在自由基的过氧化损伤。6.低碘大鼠
给予碘化钾及碘酸钾治疗，对脑组织SOD、GSH一Px及MDA的影响没有
显著性差异，而且经过3个月的补碘治疗，无论是碘化钾还是碘酸钾均可
使低碘大鼠脑组织的抗氧化酶活性及MDA含量恢复到接近适碘组的水
平。
Object: The Wistar rat model of iodine deficiency was made successfully.
Following that, the potassium iodide and potassium iodated were given to the rat model with different groups respectively. Before and after feeding the compounds, the rate of iodine metabolic in rats and the 131I-uptake rate
of thyroid gland were examined, the level of T3 and T4 in serum were measured and the variation of antioxidative capability of brain were observed.
Methods: 90 Wistar rats were divided into two groups - low iodine group
(LI) and normal iodine group (NI). The LI rats were fed with low iodine food and deionized water. Three months later, 20 LI rats were chosen from LI group randomly, and then the volume of urine and content of urinary
iodine in 24 h were measured for each rat. Following that, Na I and
Na 103 were injected into rat abdomen for testing 131I-uptake rate. Finally, the rats were killed by bloodletting from femoral artery after 6 hours after
injection. The thyroid glands were weighted, I-uptake rate examined
and the level of T3 and T4 in serum determined for each rats. All of data of 20 rats were shown that the rat model of iodine deficiency was made successfully.
The other deficiency iodine rats in LI group were divided into three groups: (1) LI-LI, fed with deionized water and low iodine food continually; (2) Ll-I, fed with 0.3ug/ml potassium iodide and low iodine food; (3) L1-O, fed with 0.4ug/ml potassium iodated water and low iodine food for another three months. The data including the weight of thyroid gland, 131I-uptake
rate of thyroid gland, the level of urinary iodine and TS and T4 in serum, and the content of SOD, GSH-Px and MDA in brain were observed for each rat as well.
In the other hand, the NI rats of two groups were fed low iodine food in same time; but One of them was fed the water containing 0.3ug/ml KI and
another were fed the water containing 0.4ug/ml KIO3 for 6 months totally.
All items tested were same as that in LI group observed.
Results: In this experiment, It was shown that thyroid weight in rats
were increased, the level of T4 in serum decreased and the excretion of urinary iodine were declined in LI group since The rats had been fed low dietary for three months. So it was demonstrated that the deficiency iodine rat had been established well. In the other hand, all of data including the weights of thyroid glands, the level of urinary iodine and serum T4 in LI rats were lower than that in LI-I and LI-O respectively, but they were not significant different between LI-I and LI-O group, and neither in NI and NO group. The activity of SOD in LI-LI group was lower than in LI-I group (P<0.05), but not different significantly compared with other groups (LI-O and NI); the content of GSH-Px in LI-LI was less than that in other three groups (P<0.01), meanwhile, the content of Malondialdehyde (MDA) of brain in LI-LI was higher striking than that in others (P <0.01). In another hand, each of GSH-Px, SOD and MDA was not different between LI-I and LI-O rats (P>0.05) when the rats were fed with low iodine dietary. In first three months; neither were they when each of group was compared with NI rats after giving iodized salt.
Cone I us i ons : l.The level of excretion of urinary iodine is varied with the content of iodine in drinking water.2.There was no significant difference between intake- rate of potassium iodine and intake-rate of potassium iodate in thyroid gland for low iodine rats.3.There was no significant difference between uptake - rate of potassium iodine and potassium iodate in thyroid gland for normal iodine rats.4.It is effective for LI rat to treat with a reasonable dosage of potassium iodide or potassium iodate.5.The decreasing of content of GSH-Px and increasing of MDA of brain in low iodine rats suggest that the damage of rat brain may come from oxidizing of free radical.6.There were no variation of antioxidative capability of brain between two group rats which were treated potassium iodine and potassium iodate respectively; and the
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