Early-life exposure to PM2.5 leads to ASD-like phenotype in male offspring rats through activation of PI3K-AKT signaling pathway.

Previous studies have shown that early-life exposure to fine particulate matter (PM2.5) is associated with an increasing risk of autism spectrum disorder (ASD), however, the specific sensitive period of ASD is unknown. Here, a model of dynamic whole-body concentrated PM2.5 exposure in pre- and early-postnatal male offspring rats (MORs) was established. And we found that early postnatal PM2.5 exposed rats showed more typical ASD behavioral characteristics than maternal pregnancy exposure rats, including poor social interaction, novelty avoidance and anxiety disorder. And more severe oxidative stress and inflammatory responses were observed in early postnatal PM2.5 exposed rats. Moreover, the expression level of phosphatase and tensin homolog deleted on chromosome ten (PTEN) was down-regulated and the ratios of p-PI3K/PI3K and p-AKT/AKT were up-regulated in early postnatal PM2.5 exposed rats. This study suggests that early postnatal exposure to PM2.5 is more susceptible to ASD-like phenotype in offspring than maternal pregnancy exposure and the activation of PI3K-AKT signaling pathway may represent underlying mechanisms.

Molecular mechanisms underlying mitochondrial damage, endoplasmic reticulum stress, and oxidative stress induced by environmental pollutants.

Mitochondria and endoplasmic reticulum (ER) are essential organelles playing pivotal roles in the regulation of cellular metabolism, energy production, and protein synthesis. In addition, these organelles are important targets susceptible to external stimuli, such as environmental pollutants. Exposure to environmental pollutants can cause the mitochondrial damage, endoplasmic reticulum stress (ERS), and oxidative stress, leading to cellular dysfunction and death. Therefore, understanding the toxic effects and molecular mechanisms of environmental pollution underlying these processes is crucial for developing effective strategies to mitigate the adverse effects of environmental pollutants on human health. In the present study, we summarized and reviewed the toxic effects and molecular mechanisms of mitochondrial damage, ERS, and oxidative stress caused by exposure to environmental pollutants as well as interactions inducing the cell apoptosis and the roles in exposure to environmental pollutants.