High dietary consumption of iodine induced thyroid cytotoxicity in diabetic intoxicated rats and oxidonitrergic stress in non-diabetic rats

This study aimed to investigate the role of iodine intake in thyroid function ofdiabetic rats. Twenty-four (24) male Wistar rats were placed into four groups (n=6): Group (non-diabetic without iodine), Group 2 (non-diabetic + iodine), Group 3 (diabetic without iodine) and Group 4 (diabetic + iodine). 10mg/kg bw of iodine were mixed with the feeds. Serum triodothyronine (T3), thyroxine (T4), Thyroid Stimulating Hormone (TSH), thyroglobulin and thyroperoxidase antibodies were assessed using ELISA. Serum MDA, SOD, and NO levels were assessed with spectrophotometry. In the diabetic rats, lower mean serum T4 and TSH concentrations were observed (T4: 13.16±0.55 Vs 11.75±0.21 mg/dL, TSH: 2.62±0.11 Vs 2.28±0.08 IU/mL). Iodine treatment further reduced T4 and increased TSH concentrations (T4: 11.75±0.21 vs 6.75±0.22 mg/dL, TSH: 2.28±0.08 Vs 3.08±0.15 IU/mL). Thyroglobulin and thyroperoxidase antibodies were absent in all the rats. It was also observed that iodine intake caused an increase in oxidative stress in both diabetic and non-diabetic treated rats (MDA; 18.4±1.3 Vs 22.2±2.7 μmol/l X 10-5, NO; 14.08±0.38 Vs 13.24±0.07μm/l) and increased SOD levels in diabetic rats (44.44±2.94 Vs 68.94±0.91 mg/ml); this increase could be due to the increased TSH. Consumption of excess iodine suppressed thyroid function in diabetic rats and induced oxidative stress in both diabetic and non-diabetic treated rats.