Effects of 3,5-Diiodotyrosine and Potassium Iodide on Thyroid Function and Oxidative Stress in Iodine-Excess Wistar Rats

Abstract

The objective of this study was to investigate the effects of organic iodine (3,5-diiodotyrosine, DIT) and inorganic iodine (potassium iodine, KI) on thyroid function and oxidative stress in iodine-excess Wistar rats. Seventy-two Wistar rats were randomly divided into eight groups: normal control (NC), thyroid tablet-induced hyperthyroidism model (HM), low DIT (L-DIT), medium DIT (M-DIT), high DIT (H-DIT), low KI (L-KI), medium KI (M-KI), and high KI (H-KI). All rats were fed ad libitum for 30 days. Morphological changes in the thyroid, absolute and relative weights of the thyroid, thyroid function markers free triiodothyronine (FT3) and free thyroxine (FT4), urinary iodine level, and oxidative stress indicators were measured. Compared to the HM groups, the FT3 and FT4 levels decreased in the L-DIT groups; the thyroid weight and thyroid weight/body weight values decreased markedly in the L-DIT and M-DIT groups; serum superoxide dismutase/malondialdehyde increased markedly; glutathione peroxidase activity increased markedly in the L-DIT groups; and malondialdehyde levels decreased significantly in the M-DIT groups. However, the FT3 and FT4 levels decreased and glutathione peroxidase levels increased significantly in the DIT groups compared to their corresponding KI groups. Additionally, urinary iodine levels increased significantly in both DIT and KI groups, while the highest urinary iodine excretion was showed in the DIT groups among groups. When the addition of iodine with the same doses in iodine-excess rats, although neither DIT nor KI normalized iodine levels in the iodine-excess rats, the DIT did less damage than did KI to thyroid follicular cells. Therefore, DIT rather than KI had a protective effect by balancing the antioxidant system when exposed to supraphysiological iodine. These suggest that DIT may be used as a new alternative iodized salt in the universal salt iodization to avoid the potential damage of surplus KI.

Propylthiouracil, Perchlorate, and Thyroid-Stimulating Hormone Modulate High Concentrations of Iodide Instigated Mitochondrial Superoxide Production in the Thyroids of Metallothionein I/II Knockout Mice

“…In regard to MTs expression during states of excess iodide, since iodide excess increases oxidative stress [ 52 53 ], similar degrees of MT expression may be observed in various types of cells, especially thyroid cells, during oxidative stress. Previous studies have exhibited the link between excess iodide exposure and its role in increasing oxidative stress in the rat model [ 52 ].…”

“…In regard to MTs expression during states of excess iodide, since iodide excess increases oxidative stress [ 52 53 ], similar degrees of MT expression may be observed in various types of cells, especially thyroid cells, during oxidative stress. Previous studies have exhibited the link between excess iodide exposure and its role in increasing oxidative stress in the rat model [ 52 ]. Specifically, high concentrations of KI damaged rat thyroid follicular cells and increased oxidative stress indicators, which demonstrated the effects of oxidative damage caused by varying concentrations of KI [ 52 ].…”

“…Previous studies have exhibited the link between excess iodide exposure and its role in increasing oxidative stress in the rat model [ 52 ]. Specifically, high concentrations of KI damaged rat thyroid follicular cells and increased oxidative stress indicators, which demonstrated the effects of oxidative damage caused by varying concentrations of KI [ 52 ]. In mice, the MT-I and MT-II genes are highly upregulated in response to oxidative stress [ 54 ].…”

Detection of some hormonal and enzymatic disorders associated to experimentally iodine induced hyperthyrodism.

“…Table (6) showed some affected serum parameters associated with the excess of KI administration. Significant increasing levels were observed in case of random glucose that were accompanied with significant decreasing levels in total antioxidant capacity (TOAC) in the KI injected group compared to control.…”

“…Iodine is obtained mainly from sea food, plants and animal products in addition to fortified food, salt and many drugs [4,5]. It can display a powerful antioxidant role in the body if it is accurately monitored and directed for serving the cells compartments [6]. Both high and low iodine ingestion was reported to cause thyroid dysfunction in vertebrates leading to abnormal thyroid hormones (THs) level in serum [7,8,9].…”