Perinatal Exposure to Diesel Exhaust-Origin Secondary Organic Aerosol Induces Autism-Like Behavior in Rats.
Tin-Tin Win-Shwe, Chaw Kyi-Tha-Thu, Yuji Fujitani, Shinji Tsukahara, Seishiro Hirano
Author Information
Tin-Tin Win-Shwe: Center for Health and Environmental Risk Research, National Institute for Environmental Studies, Tsukuba 305-8506, Japan.
Chaw Kyi-Tha-Thu: Division of Life Science, Graduate School of Science and Engineering, Saitama University, Saitama City 338-8570, Japan.
Yuji Fujitani: Center for Health and Environmental Risk Research, National Institute for Environmental Studies, Tsukuba 305-8506, Japan. ORCID
Shinji Tsukahara: Division of Life Science, Graduate School of Science and Engineering, Saitama University, Saitama City 338-8570, Japan.
Seishiro Hirano: Center for Health and Environmental Risk Research, National Institute for Environmental Studies, Tsukuba 305-8506, Japan.
中文译文
English
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.
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JP19K12361/Grant-in-Aid for Scientific Research (C) JSPS KAKENHI
1620AA041/a research fund from the National Institute for Environmental Studies, Japan
Aerosols
Air Pollutants
Animals
Autism Spectrum Disorder
Brain-Derived Neurotrophic Factor
Female
Gene Expression Regulation
Heme Oxygenase-1
Humans
Interleukin-1beta
Male
Pregnancy
Prenatal Exposure Delayed Effects
Rats
Rats, Sprague-Dawley
Receptors, Serotonin
Vehicle Emissions
Aerosols
Air Pollutants
Bdnf protein, rat
Brain-Derived Neurotrophic Factor
Interleukin-1beta
Receptors, Serotonin
Vehicle Emissions
Heme Oxygenase-1