Abstract
The UV absorber benzophenone-3 (BP-3) is the most extensively used chemical substance in various personal care products. Despite that BP-3 exposure is widespread, knowledge about the impact of BP-3 on the brain development is negligible. The present study aimed to explore the mechanisms of prenatal exposure to BP-3 in neuronal cells, with particular emphasis on autophagy and nuclear receptors signaling as well as the epigenetic and post-translational modifications occurring in response to BP-3. To observe the impact of prenatal exposure to BP-3, we administered BP-3 to pregnant mice, and next, we isolated brain tissue from pretreated embryos for primary cell neocortical culture. Our study revealed that prenatal exposure to BP-3 (used in environmentally relevant doses) impairs autophagy in terms of BECLIN-1, MAP1LC3B, autophagosomes, and autophagy-related factors; disrupts the levels of retinoid X receptors (RXRs) and peroxisome proliferator-activated receptor gamma (PPARγ); alters epigenetic status (i.e., attenuates HDAC and sirtuin activities); inhibits post-translational modifications in terms of global sumoylation; and dysregulates expression of neurogenesis- and neurotransmitter-related genes as well as miRNAs involved in pathologies of the nervous system. Our study also showed that BP-3 has good permeability through the BBB. We strongly suggest that BP-3-evoked effects may substantiate a fetal basis of the adult onset of neurological diseases, particularly schizophrenia and Alzheimer’s disease.
Highlights
The ultraviolet (UV) absorber benzophenone-3 (2-hydroxy-4methoxybenzophenone, oxybenzone, 2OH-4 MeO-BP, or BP3) is the most extensively used chemical substance as a UV filter, especially in various personal care products [1]
Our previous study demonstrated that prenatal exposure to BP-3 causes severe apoptosis and neurotoxicity, evokes global DNA hypomethylation, alters methylation status of apoptosis-related and estrogen receptors genes, and disrupts estrogen receptors expression [25]. Taking these data into account, we strongly suggest that BP-3 can significantly affect the neural development, which may be the fetal basis of the adult onset of nervous system disease
Our study revealed that prenatal exposure to BP-3 used in environmentally relevant doses impaired autophagy in terms of BECLIN-1, MAP1LC3B, autophagosomes formation, and autophagy-related factors, disrupted the levels of retinoid X receptors (RXRs) and
Summary
The ultraviolet (UV) absorber benzophenone-3 (2-hydroxy-4methoxybenzophenone, oxybenzone, 2OH-4 MeO-BP, or BP3) is the most extensively used chemical substance as a UV filter, especially (but ) in various personal care products [1]. It is a plastic and textile ingredient as Prenatal and early postnatal exposures to BP-3 seem to be undeniable. Current data provide evidence that BP-3 crosses through the placental barrier since it has been observed in amniotic fluid, placental tissue, cord blood, and fetal blood in research studies with human participants [5,6,7]. Despite the fact that BP-3 exposure is extremely widespread and affects prenatal features, knowledge of the impact of BP-3 on the development of the nervous system is negligible
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