Chlorotriazines Do Not Activate the Aryl Hydrocarbon Receptor, the Oestrogen Receptor or the Thyroid Receptor in In Vitro

///Chlorotriazines Do Not Activate the Aryl Hydrocarbon Receptor, the Oestrogen Receptor or the Thyroid Receptor in In Vitro

Chlorotriazines Do Not Activate the Aryl Hydrocarbon Receptor, the Oestrogen Receptor or the Thyroid Receptor in In Vitro

Irene de la Casa-Resino, José M. Navas and María L. Fernández-Cruz

Atrazine, prometryn, propazine and simazine are chlorotriazines that are commonly
employed as herbicides. However, their use is a major cause of concern, due to their reported endocrine disrupting effects in different taxa. Data from studies on the molecular and cellular processes underlying the hormonal action of these substances are contradictory. The ability of these chlorotriazines and the  atrazine metabolites, desethyl-s-chlorotriazine and desisopropyl-s-chlorotriazine, to trigger responses mediated by the oestrogen receptor (ER), aryl hydrocarbon receptor (AhR) and thyroid receptor (TR), was studied by using in vitro approaches. Transcriptional activation assays were applied to observe the activation  of ER and TR. The induction of ethoxyresorufin-O-deethylase (EROD) activity in the RTG-2 cell line served as an indicator of AhR activation. No responses were found in any of the assays, with any of the six chlorotriazines tested. Our observations indicate that the chlorotriazines tested are unlikely to cause their endocrine effects via these receptors.
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