[Effect of chronic mild and moderate iodine excess on thyroid anti-oxidative ability of iodine deficiency and non-iodine deficiency Wistar rats].

OBJECTIVE

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.

METHODS

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.

RESULTS

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).

CONCLUSION

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.