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Abstract
Previous animal experiments have implied that organophosphate esters (OPEs) have a
disruption effect on the thyroid endocrine system. However, knowledge of the toxicological
mechanism remains limited. In this study, the activities of four OPEs have been characterized
against the thyroid hormone (TH) nuclear receptor (TR) using two in vitro models,
with the aim of evaluating their toxicity mechanisms towards the TR. The results of
a TH-dependent cell proliferation assay showed that tris(2-chloro-1-(chloromethyl)ethyl)phosphate
(TDCPP) could induce cell growth, while the other three OPEs had no effect. The results
of a luciferase reporter gene assay revealed that all four of the OPEs tested in the
current study showed agonistic activity towards TRβ, with TDCPP being the most potent
one. Moreover, molecular docking revealed that all the tested OPEs could fit into
the ligand binding pocket of TRβ, with TDCPP binding more effectively than the other
three OPEs. Taken together, these data suggest that OPEs might disrupt the thyroid
endocrine system via a mechanism involving the activation of TR.