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Exposure to organophosphate flame retardants and phthalates alters neuronal activity and network development
In our latest article, we studied the neurotoxic effects of acute and chronic exposure to organophosphate flame retardants (OPFRs) and phthalates on neuronal activity and network development. Specifically, we studied the effects of triphenyl phosphate (TPhP), diethyl phthalate (DEP), dibutyl phthalate (DBP), benzyl butyl phthalate (BBzP), bis(2-ethylhexyl) phthalate (DEHP), and their metabolites using micro-electrode array (MEA) recordings. Our findings indicate that acute exposure to TPhP, DEP, DBP, and BBzP inhibits neuronal activity, while chronic exposure to TPhP and DEP induces a hyperexcitation. Chronic exposure to DBP, DEHP, and its metabolite mono-2-ethylhexyl phthalate (MEHP) inhibited neuronal network development. Interestingly, exposure to BBzP and DEHP affected neuronal function at human-relevant concentrations. Acute and chronic exposure to the metabolites of TPhP, DEP, DBP, and BBzP did not affect neuronal activity and network development. Since both OPFRs and phthalates are known endocrine-disrupting compounds (EDCs), we also analyzed whether modulation of the retinoic acid, retinoic X, liver X, and prostaglandin E2 receptor could affect neuronal activity and network development. While (ant)agonists of the retinoic acid, retinoic X, and liver X receptor had no clear effects, a clear hyperexcitation was observed after exposure to prostaglandin E2. Since an antagonist of the prostaglandin E2 receptor is not available, further research is needed to elucidate if the effects of OPFRs and phthalates are endocrine-mediated. Taken together, these results add to the evidence that TPhP and various phthalates illicit neurotoxic effects, some at low, human-relevant concentrations. These novel results should be considered in the risk assessment of these chemicals.
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