Effect of chronic excess iodine intake on thyroid function and oxidative stress in hypothyroid rats

Author:

Hussein Abd El-Aziz M.1,Abbas Amr M.1,El Wakil Gehan A.1,Elsamanoudy Ayman Z.2,El Aziz Azza Abd3

Affiliation:

1. Department of Medical Physiology, Faculty of Medicine, Mansoura University, Egypt.

2. Department of Medical Biochemistry, Faculty of Medicine, Mansoura University, Egypt.

3. Department of Pathology, Faculty of Medicine, Mansoura University, Egypt.

Abstract

Our objective was to investigate the effects of chronic excess iodine intake on thyroid functions and thyroid oxidative stress state in hypothyroid rats. Sixty rats were divided into euthyroid and hypothyroid (thiocyanate-induced) groups with or without administration of excess iodine (3000 or 6000 μg/L) for 8 weeks. Serum thyroxine (T4), triiodothyronine (T3), thyroid-stimulating hormone (TSH), thyroid antioxidants (catalase, superoxide dismutase enzymes, and total antioxidants), and lipid peroxide (malondialdehyde; MDA) were measured. Reverse transcription – PCR gene expression for thyroidal Na+/I symporter (NIS), D1 deiodinase, and thyroid peroxidase (TPO) were performed. Thiocyanate significantly decreased thyroid hormones (T3, T4), increased lipid peroxides and antioxidants, and increased gene expression of NIS, D1 deiodinase, and TPO. Excess iodine intake in hypothyroid rats increased T3 and T4. Also, high iodine intake by hypothyroid rats significantly decreased NIS, D1 deiodinase, and TPO genes expression. Excess iodine significantly increased MDA and antioxidants in euthyroid and hypothyroid rats. In conclusion, thiocyanate-hypothyroidism increases gene expression of NIS, TPO, and TPO and induces oxidative stress. High iodine intake decreases NIS and D1 deiodinase gene expression in hypothyroid rats. Moreover, excess iodine increase thyroid hormones, lipid peroxides, and antioxidants in hypothyroid rats.

Publisher

Canadian Science Publishing

Subject

Physiology (medical),Pharmacology,General Medicine,Physiology

Reference19 articles.

1. Bastomsky, C.H. 1974. Thyroid iodide transport. In Handbook of Physiology. Vol. 3. Edited by S.R. Geiger. American Physiological Society, Washington D.C. p. 81 (Sect. 7).

2. Beckers, C., Delange, F., Gaintan, E., Suzuki, H., Koutras, D.A., and Medeiros-Neto, G.A. 1980. Etiology of endemic goiter. In Endemic goiter and endemic cretinism: iodine nutrition in health and disease. Edited by J.B. Stanbury, and B.S. Heztel. John Wiley & Sons, New York. pp. 237–53.

3. A simple method for direct cloning and sequencing cDNA by the use of a single specific oligonucleotide and oligo(dT) in a polymerase chain reaction (PCR)

4. Carrasco, N., Taurog, A.M., Pisarev, M.A., and Gatner, R. 2000. Thyroid hormone synthesis. In Werner and Ingbar’s the thyroid: a fundamental and clinical text. Edited by L.E. Braverman, and R.D. Utiger. Lippincott Williams & Wilkins, Philadelphia, Pa. pp. 52–104.

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