Zhang Nuo, Tong Ya-jie, Shan Zhong-yan, Teng Wei-ping
Department of Endocrinology, First Affiliated Hospital, China Medical University, Shenyang 110001, China.
Zhonghua Yi Xue Za Zhi. 2006 May 16;86(18):1274-8.
To investigate the effects of chronic mild and moderate iodine excess on thyroid oxidative injury and anti-oxidative ability of iodine deficiency and non-iodine deficiency Wistar rats.
Four-week-old Wistar rats were fed with iodine deficient diet for three months to make iodine deficient goiter models, then divided randomly into three groups: iodine deficient control group (Group IDC) fed with double distilled water, iodine-supplement group I (Group IS I) fed with potassium iodate solutions with the iodine concentrations of 100 microg/L, and iodine-supplement group II (Group IS II), fed with potassium iodate solution with the iodine concentrations of 330 microg/L. Another four-week-old Wistar rats were fed with normal diet for three months, and then divided randomly into three groups: normal control group (NC) fed with double distilled water, iodine-excess group I (IEI) fed with potassium iodate solution with the iodine concentration of 300 microg/L, and iodine-excess group II (Group IEII), fed with potassium iodate solution with the iodine concentration of 660 microg/L. 1, 2, 4, 8, and 24 weeks after treatment samples of urine were collected to detect the median urine iodine (MUI), samples of plasma were collected from the hearts of 8-14 rats from each group and then rats were killed. Their thyroid glands were taken out to measure the wet weight and made into homogenate. Biochemical method was used to measure the activities of glutathione-peroxidase (GSH-P(X)) and superoxide dismutase (SOD) as well as the contents of malonyldialdehyde (MDA) and H2O2 in the homogenates of thyroid glands.
The GSH-P(X) activity 2 weeks after treatment of Group IS II was significantly lower than that of Group IDC (P < 0.05), and the GSH-P(X) activity 4 weeks after treatment of Group IS I was significantly lower than that of Group IDC (P < 0.001). The activities of GSH-P(X) 4, 8, and 24 weeks after treatment of Groups IS I and IS II were all lower than those of Group C at the same time points significantly (P < 0.001, < 0.01, and < 0.05 respectively). The activities of SOD were decreased gradually in Groups IS I and IS II and were significantly lower than those of Group IDC since 8 weeks after treatment (P < 0.001 or < 0.05). The SOD activities in thyroid glands of Groups IEI and IEII since 8 weeks after treatment decreased significantly in comparison with Group NC (all P < 0.01 or < 0.001). The contents of H2O2 in thyroid glands of Groups IS I and IS II were significantly lower than those of Group IDC at different time points (P < 0.001, < 0.01, or < 0.05), and were significantly lower than those of Group NC 8 and 24 weeks after treatment (P < 0.001 or < 0.01). The contents of MDA in thyroid glands since 2 weeks after treatment of Group IEI were all significantly lower than those of Group IDC at the same time points (all P < 0.05), and the content of MDA in thyroid glands since 1 week after treatment of Groups IS II were all significantly lower than those of Group IDC at the same time points (all P < 0.05).
Supplementation of 100 microg/L and 330 microg/L iodine on iodine deficiency Wistar rats may alleviate the oxidative injury but weaken the anti-oxidative protection of thyroid. The anti-oxidative protection of thyroid glands of non-iodine deficiency Wistar rats may also be weakened by supplementation of 300 microg/L and 660 microg/L iodine.
探讨慢性轻度和中度碘过量对碘缺乏及非碘缺乏Wistar大鼠甲状腺氧化损伤和抗氧化能力的影响。
将4周龄Wistar大鼠给予缺碘饲料喂养3个月制成碘缺乏性甲状腺肿模型，然后随机分为3组：缺碘对照组（IDC组）给予双蒸水，补碘组I（ISI组）给予碘浓度为100μg/L的碘酸钾溶液，补碘组II（ISII组）给予碘浓度为330μg/L的碘酸钾溶液。另取4周龄Wistar大鼠给予正常饲料喂养3个月，然后随机分为3组：正常对照组（NC组）给予双蒸水，碘过量组I（IEI组）给予碘浓度为300μg/L的碘酸钾溶液，碘过量组II（IEII组）给予碘浓度为660μg/L的碘酸钾溶液。处理后1、2、4、8和24周收集尿液样本检测尿碘中位数（MUI），从每组8 - 14只大鼠心脏采集血浆样本后处死大鼠，取出甲状腺测量湿重并制成匀浆。采用生化方法检测甲状腺匀浆中谷胱甘肽过氧化物酶（GSH-P(X)）、超氧化物歧化酶（SOD）活性以及丙二醛（MDA）和H2O2含量。
ISII组处理后2周GSH-P(X)活性显著低于IDC组（P < 0.05），ISI组处理后4周GSH-P(X)活性显著低于IDC组（P < 0.001）。ISI组和ISII组处理后4、8和24周GSH-P(X)活性均显著低于同期C组（分别为P < 0.001、< 0.01和< 0.05）。ISI组和ISII组SOD活性逐渐降低，处理后8周起显著低于IDC组（P < 0.001或< 0.05）。IEI组和IEII组处理后8周起甲状腺SOD活性与NC组相比显著降低（均P < 0.01或< 0.001）。ISI组和ISII组甲状腺不同时间点H2O2含量显著低于IDC组（P < 0.001、< 0.01或< 0.05），处理后8周和24周显著低于NC组（P < 0.001或< 0.01）。IEI组处理后2周起甲状腺MDA含量在各时间点均显著低于IDC组（均P < 0.05），ISII组处理后1周起甲状腺MDA含量在各时间点均显著低于IDC组（均P < 0.05）。
对碘缺乏Wistar大鼠补充100μg/L和330μg/L碘可减轻氧化损伤，但会削弱甲状腺的抗氧化保护作用。对非碘缺乏Wistar大鼠补充300μg/L和660μg/L碘也可能削弱甲状腺的抗氧化保护作用。
