Abstract

Very recently, it has been reported that subclinical hypothyroidism is more severe and peripheral markers of hypothyroidism are more pronounced in women with subclinical or overt hypothyroidism who smoke. Increased concentrations of the known goitrogen thiocyanate, generated from cigarette smoke, have been the major explanation for the decreased thyroid function in these women but do not explain the reported increased peripheral markers of hypothyroidism. There are no data on the effect of the other major product of cigarettes, nicotine, on thyroid function in vivo. The present studies were therefore performed to determine the effects of large doses of nicotine infused for 7 days on thyroid function, outer-ring 5′ deiodinase activity (5′D-I), and hepatic malic enzyme activity (a measure of thyroid hormone action) in euthyroid, subclinically hypothyroid (hemithyroidectomized), and l-thyroxine (L-T 4)—treated thyroidectomized rats. Nicotine infusion had no effect on serum T 4, triiodothyronine (T 3), thyrotropin (TSH), and cholesterol concentrations, intrathyroidal metabolism of 125I, liver and kidney 5′D-I activity, and hepatic malic enzyme activity in euthyroid and subclinically hypothyroid rats. Nicotine administration also did not affect serum T 3, TSH, or cholesterol concentrations, liver and kidney 5′D-I activity, and hepatic malic enzyme activity in L-T 4—treated thyroidectomized rats. These studies provide strong evidence that nicotine is not responsible for the observed adverse effects of smoking on the thyroid in humans.

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