Inhibition of T3-receptor binding by Nitrofen
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.
|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|
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