Chronic Ambient Ozone Exposure Aggravates Autism-Like Symptoms in a Susceptible Mouse Model

Although there is evidence that exposure to groundlevel ozone (O3) may cause an increased risk of neurological disorders (e.g., autistic spectrum disorder), low-dose chronic ozone exposure and its adverse effects on the nervous system have not been fully understood. Here, we evaluated the potential neurotoxic effects of long-term exposure to environmentally relevant O-3 concentration (200 mu g/m(3) via a whole-body inhalation system, 12 h/day for 5 days/week) using a susceptible mouse model of autism induced by valproic acid. Various indicators of oxidative stress, mitochondria, and synapse in the brain tissues were then measured to determine the overall damage of O-3 to the mouse brain. The results showed an aggravated risk of autism in mice offspring, which was embodied in decreased antioxidant contents, disturbed energy generation in mitochondria, as well as reduced expressions of protein kinase M. (PKM.) and synaptic proteins [e.g., Synapsin 1 (SYN 1), postsynaptic density protein-95 (PSD-95)]. Overall, our study indicates that prenatal exposure to environmentally relevant O-3 may exacerbate the symptoms of autism, shedding light on possible molecular mechanisms and providing valuable insights into the pathogenesis of autism, especially concerning low-dose levels of those pollutants.

Automated summary

This study evaluated the potential neurotoxic effects of long-term exposure to low-dose ozone on a mouse model of autism. The results showed that prenatal exposure to environmentally relevant ozone may exacerbate the symptoms of autism and lead to oxidative stress, impaired mitochondrial function, and reduced expression of synaptic proteins.