Lung development is controlled by various hormones, including thyroid hormone. The herbicide 2,4-dichlorophenyl-p-nitrophenyl ether (Nitrofen) induces lung hypoplasia in fetal rats, when administered to the mother during gestation. Nitrofen might be teratogenic by an anti-thyroid activity. The present study shows that Nitrofen decreases the binding of T3 to the alpha 1 and beta 1 form of the thyroid hormone receptor in a non-competitive way. Consequently, rat lung hypoplasia might result from the decreased binding of T3 to its receptor, via exposure to Nitrofen during fetal development.

Additional Metadata
Keywords Nitrofen, T3 receptor, Development, Hypoplasia, Triodothyronine, (Human lung)
Persistent URL dx.doi.org/10.1016/0304-4165(94)90050-7, hdl.handle.net/1765/100486
Journal Biochimica et Biophysica Acta: international journal of biochemistry and biophysics
Citation
Brandsma, A.E, Tibboel, D, Vulto, I.M, de Vijlder, J.J.M, ten Have-Opbroek, A.A.W, & Wiersinga, W.M. (1994). Inhibition of T3-receptor binding by Nitrofen. Biochimica et Biophysica Acta: international journal of biochemistry and biophysics, 1201(2), 266–336. doi:10.1016/0304-4165(94)90050-7