A potential risk of plastic and plasticizer pollution: a molecular toxicological study on DIDP-exacerbated autism-like behaviors in juvenile mice.

Abstract

Plastic pollution and childhood health are two significant public health issues worldwide. However, there is a lack of corresponding toxicological studies to confirm this association, and the molecular pathological mechanism behind it remains unknown. Here, we utilized DIDP as a proxy to examine the association. A mouse model of autism-like behaviors was successfully constructed using the early social deprivation (ESD) approach. Social deficits were evaluated through the three-chamber social preference test, while cognitive impairments were assessed using the Morris water maze test. Various metrics, including oxidative stress (ROS, GSH, MDA, and 8-OHdG), inflammatory response (IL-6/TNF-α), and pathological impairments in brain tissue, were examined. Additionally, we explored the mediation of oxidative stress signaling pathways as molecular pathological mechanisms and investigated the preventive and therapeutic effects of vitamin E (VitE) on social disorders. The results indicate that mice exposed to the plasticizer DIDP exhibited oxidative stress, pathological damage, and inflammatory responses in the hippocampal region of the brain. Additionally, behavioral tests revealed that these mice displayed social deficits and cognitive impairments. However, upon administration of VitE, the mice exhibited significant improvement in social deficits and cognition impairments. The study finds that exposure to the plasticizer DIDP exacerbates autism in mice, possibly through the molecular pathological mechanisms of oxidative stress and inflammation in brain tissue. Furthermore, VitE is found to have a noteworthy protective effect against the worsening of autism caused by exposure to the plasticizer DIDP.