Neonatal hypothyroidism caused by maternal nicotine exposure is reversed by higher T3 transfer by milk after nicotine withdraw

Maternal nicotine exposure leads to neonatal hypothyroidism that can be returned to euthyroidism after nicotine withdrawal. Here, we examined the transfer of iodine through milk, deiodinase activities (D1 and D2), and serum T3, T4 and TSH in rat offspring after maternal exposure to nicotine. One day after birth, a minipump was implanted to dams releasing nicotine (NIC), 6 mg/kg/day for 13 days or vehicle saline. Animals were killed at the day 15 and 21 of lactation. At day 15, NIC-treated dams showed decreased T4 and mammary 2 h-radioiodine uptake (RAIU) and increase of TSH, thyroid 2 h-RAIU, liver D1 and mammary D2. At the cessation of NIC-exposure, pups displayed decreased T3, T4 and thyroid 2 h-RAIU and increased TSH. At weaning (21-postnatal day), NIC-treated dams recovered their T4 and TSH, but increased deiodinase level in the liver and mammary gland. Milk T3 content in NIC-treated dams was higher at both day 15 and 21, and thyroid function was recovered at the day 21. Thus, thyroid function was affected by nicotine in both mothers and pups, suggesting a primary hypothyroidism. After nicotine withdrawal, pups recovered thyroid function probably due to the increased lactational transfer of T3 in relation with increased mammary gland deiodinase activities.