Lung development is controlled by various hormones, including thyroid
hormone. The herbicide 2,4-dichlorophenyl-p-nitrophenyl ether (Nitrofe
n) induces lung hypoplasia in fetal rats, when administered to the mot
her during gestation. Nitrofen might be teratogenic by an anti-thyroid
activity. The present study shows that Nitrofen decreases the binding
of T-3 to the alpha(1) and beta(1) form of the thyroid hormone recept
or in a non-competitive way. Consequently, rat lung hypoplasia might r
esult from the decreased binding of T-3 to its receptor, via exposure
to Nitrofen during fetal development.