Abstract
In pregnant women, the lungs, skin and placenta are exposed daily to endocrine-disrupting chemicals (EDCs). EDCs induce multiple adverse effects, not only on endocrine organs, but also on non-endocrine organs, with the P2X7 cell death receptor being potentially the common key element. Our objective was first to investigate mechanisms of EDCs toxicity in both endocrine and non-endocrine cells through P2X7 receptor activation, and second, to compare the level of activation in lung, skin and placental cells. In addition, apoptosis in placental cells was studied because the placenta is the most exposed organ to EDCs and has essential endocrine functions. A total of nine EDCs were evaluated on three human cell models. We observed that the P2X7 receptor was not activated by EDCs in lung non-endocrine cells but was activated in skin and placenta cells, with the highest activation in placenta cells. P2X7 receptor activation and apoptosis are pathways shared by all tested EDCs in endocrine placental cells. P2X7 receptor activation along with apoptosis induction could be key elements in understanding endocrine placental and skin disorders induced by EDCs.
Highlights
Endocrine-disrupting chemicals (EDCs) are defined by the World Health Organization as exogenous substances or mixtures that alter function(s) of the endocrine system and cause adverse health effects in an intact organism, or its progeny, orpopulations [1]
We previously showed that P2X7 receptor activation plays a pivotal role in toxicity induced by both known EDCs such as bisphenols [25] and suspected EDCs such as benzo[a]pyrene [26]
A one-way analysis of variance for repeated measures followed by a Dunnett’s test with risk α set at 5% was performed to compare EDCs incubation with control (p-value expressed as follows: *) and a t-test was used to compare results in the presence of Brilliant Blue G (BBG) with results in its absence
Summary
Endocrine-disrupting chemicals (EDCs) are defined by the World Health Organization as exogenous substances or mixtures that alter function(s) of the endocrine system and cause adverse health effects in an intact organism, or its progeny, or (sub)populations [1]. Pregnant women and children are the most vulnerable populations to be affected by EDCs exposure, and the effects of exposure to EDCs may not become evident until later in life. Chronic exposure to EDCs can occur through breathed air, food and daily life products such as cosmetics; inhalation, ingestion and skin contact are the main routes of exposure. The lungs, skin and placenta (through blood circulation) are continuously exposed to EDCs that have been reported to induce multiple adverse effects including asthma [2], urticaria, allergic contact dermatitis and skin aging [3], preterm birth and the worst case scenario of preeclampsia [4,5,6,7,8,9,10]. It is obvious that EDCs act in endocrine organs and in non-endocrine organs, and exert pleiotropic effects
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