Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social communication, poor social interactions, and repetitive behaviors. We aimed to examine autism-like behaviors and related gene expressions in rats exposed to diesel exhaust (DE)-origin secondary organic aerosol (DE-SOA) perinatally. Sprague–Dawley pregnant rats were exposed to clean air (control), DE, and DE-SOA in the exposure chamber from gestational day 14 to postnatal day 21. Behavioral phenotypes of ASD were investigated in 10~13-week-old offspring using a three-chambered social behavior test, social dominance tube test, and marble burying test. Prefrontal cortex was collected to examine molecular analyses including neurological and immunological markers and glutamate concentration, using RT-PCR and ELISA methods. DE-SOA-exposed male and female rats showed poor sociability and social novelty preference, socially dominant behavior, and increased repetitive behavior. Serotonin receptor (5-HT(5B)) and brain-derived neurotrophic factor (BDNF) mRNAs were downregulated whereas interleukin 1 β (IL-β) and heme oxygenase 1 (HO-1) mRNAs were upregulated in the prefrontal cortex of male and female rats exposed to DE-SOA. Glutamate concentration was also increased significantly in DE-SOA-exposed male and female rats. Our results indicate that perinatal exposure to DE-SOA may induce autism-like behavior by modulating molecules such as neurological and immunological markers in rats.
Highlights
Exposure to air pollutants may trigger neurodevelopmental and neurodegenerative disorders like autism spectrum disorder (ASD) and Alzheimer’s disease [1,2,3,4]
We showed that developmental period exposure to diesel exhaust (DE)-secondary organic aerosol (SOA) induced impaired social behavior in mouse models [23], we need to compare autism-like behaviors in valproic acid (VPA)-induced autism model rats [24]
We showed that developmental exposure to diesel exhaust-origin secondary organic aerosol (DE-SOA) impaired sociability and social novelty preference and the hypothalamic expression of social behaviorrelated genes estrogen receptor alpha and oxytocin receptor in male mice [23]
Summary
Exposure to air pollutants may trigger neurodevelopmental and neurodegenerative disorders like autism spectrum disorder (ASD) and Alzheimer’s disease [1,2,3,4]. According to the Centers for Disease Control and Prevention (CDC), USA, recent ASD prevalence in the US is 1 in 59 children and it represents a public health issue and a large burden for education, social service, and economy [10]. Both genetic and environmental factors are considerable for ASD [11]. In this study, using diesel exhaust (DE)origin secondary organic aerosol (SOA) as a model of air pollutants, we aimed to examine the effects of early life exposure to DE-SOA on autism-like behavior and neuroimmune responses including neurological and immunological biomarkers in rats
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