Background and aim of work: The aim of the current study was to investigate the
effects of long term excessive iodine intake on gene expression of thyroidal sodium
iodide symporter (NIS), D1 deiodinase and thyroid peroxidase (TPO), thyroid
hormones, oxidative injury and anti-oxidative ability of euthyroid and hypothyroid
Sprague Dawley rats. Materials and Methods: Ninety rats were divided into
euthyroid and hypothyroid (thiocyanate induced) groups with or without
administration of excess iodine (3000 or 6000 μg/l) for 4 weeks. Serum thyroxine (T4),
triiodothyronine (T3), TSH, thyroid antioxidants ((glutathione S transferase, catalase,
superoxide dismutase enzymes, nitric oxide and total antioxidants), lipid peroxide
(malondialdehyde, MDA) were measured. RT-PCR gene expression for thyroidal NIS,
D1 deiodinase and TPO were performed. Results: Thiocyanate significantly
decreased thyroid hormones (T3, T4), increased lipid peroxides and antioxidants,
increased gene expression of NIS, D1 deiodinase, TPO. High iodine intake to
hypothyroid rats significantly decreased NIS, D1 deiodinase and TPO genes
expression. Excess iodine significantly increased MDA and antioxidants in euthyroid
and hypothyroid rats. Despite the increase in T4 in euthyroid rats administered excess
iodine, T3 decreased whereas in hypothyroid rats, both of them were increased. NIS,
and D1 deiodinase genes expression in euthyroid rats administered excess iodine
were decreased but TPO was non-significantly increased. Conclusion:
Hypothyroidism increased gene expression of NIS, TPO, and induces an oxidative
stress. High iodine intake decreased NIS and D1 deiodinase gene expression in
euthyroid and hypothyroid rats. Moreover, excess iodine increase thyroid hormones,
lipid peroxides and antioxidants in cases of euthyroid and hypothyroid rats.
Therefore, screening of thyroid function and assessment of prooxidant/antioxidant
status in subjects treated with drugs containing iodine and after investigations with
contrast media are recommended.