Effects of diesel exhaust derived secondary organic aerosol (DE-SOA) exposure during developmental period on anxiety and depression in mice

Abstract Background: Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social communication, poor social interactions and repetitive behaviors. The exact cause and mechanism of autism remains unknown. Both genetic and environmental factors may involve in ASD. In this study, we used diesel exhaust (DE) origin secondary organic aerosol (DE-SOA) as environmental pollutants. DE-SOA was generated by oxidative reaction of mixing DE with ozone. The aim of present study is to examine autism-like behaviors and related gene expressions in rats exposed to DE-SOA perinatally. Sprague-Dawley pregnant rats were exposed to clean air (control), DE and DE-SOA in the exposure chamber for 5 h per day (from 10:00 pm to 3:00 am), 5 days a week excluding weekends from gestational day 14 to postnatal day 21 with their pups. At postnatal day 21, the male and female offspring rats were allocated into three different groups as follows: 1) rats exposed to clean filtered air; 2) rats exposed to DE; 3) rats exposed to DE-SOA. Social behaviors were investigated at 10~13-weeks-old rats using a 3-chambered social behavior test, social dominance tube test and marble burying test. Prefrontal cortex was collected to examine neurological and immunological markers, and glutamate concentration, using real-time RT-PCR and ELISA methods. Results: DE-SOA-exposed male and female rats showed poor sociability and social novelty preference, socially dominant behavior and increased repetitive behavior compared with the control rats. The mRNA expression levels of serotonin receptor (5-HT(5B)) and brain-derived neurotrophic factor (BDNF) were down-regulated whereas interleukin 1 b　(IL-b), and heme oxygenase 1 (HO-1) were upregulated in the prefrontal cortex of male and female rats exposed to DE-SOA compared to the control rats. Glutamate concentration was increased significantly in the prefrontal cortex of both male and female rats exposed to DE-SOA.Conclusion: Our results indicate that perinatal exposure to DE-SOA may induce autism-like behavior in rats by modulating neurological and immunological markers in the prefrontal cortex.

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Perinatal exposure to diesel exhaust origin secondary organic aerosol induces autism-like behavior in rats

10.21203/rs.3.rs-41390/v1 ◽

2020 ◽

Author(s):

Tin Tin Win Shwe ◽

Chaw Kyi Tha Thu ◽

Yuji Fujitani ◽

Shinji Tsukahara ◽

Seishiro Hirano

Keyword(s):

Prefrontal Cortex ◽

Diesel Exhaust ◽

Secondary Organic Aerosol ◽

Organic Aerosol ◽

Female Rats ◽

Perinatal Exposure ◽

Male And Female ◽

Glutamate Concentration ◽

Immunological Markers ◽

Male And Female Rats

Abstract Background Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social communication, social interactions and repetitive behaviors. The etiology of autism remains unknown and its molecular basis is not well understood. Both genetic and environmental factors may contribute ASD. In this study, we used diesel exhaust origin secondary organic aerosol (DE-SOA) as environmental pollutants. The aim of present study is to examine autism-like behaviors and related gene expressions in rats exposed to DE-SOA perinatally. Sprague-Dawley pregnant rats were exposed to clean air (control), diesel exhaust (DE) and DE-SOA in the exposure chamber for 5 h per day, 5days a week from gestational day 8 to postnatal day 21. At postnatal day 21, the male and female offspring rats were allocated into three different groups as follows: 1) rats exposed to clean filtered air; 2) rats exposed to DE; 3) rats exposed to DE-SOA. Social behaviors were investigated at 10 ~ 13-weeks-old rats using a 3-chambered social behavior test, social dominance tube test and marble burying test. Prefrontal cortex was collected under deep anesthesia to examine neurological and immunological markers, glutamate concentration, mast cell and microglia activation using real-time RT-PCR method, ELISA method and immunohistochemical analysis. Results DE-SOA-exposed male and female rats showed poor sociability and social novelty preference, socially dominant behavior and increased repetitive behavior compared with the control rats. The mRNA expression levels of serotonin receptor (5-HT(5B)) and brain-derived neurotrophic factor (BDNF) were down-regulated whereas interleukin 1 β (IL-β), and heme oxygenase 1 (HO-1) were upregulated in the prefrontal cortex of male and female rats exposed to DE-SOA compared to the control rats. In addition, the expression of mast cells and microglia marker ionized calcium-binding adapter molecule (Iba)1 were increased in the prefrontal cortex of male and female rats exposed to DE-SOA. Glutamate concentration was increased significantly in the prefrontal cortex of both male and female rats exposed to DE-SOA. Conclusion Our results indicate that perinatal exposure to DE-SOA may induce autism-like behavior in rats by modulating neurological and immunological markers in the prefrontal cortex.

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Supplementary material to "Modeling the Formation and Composition of Secondary Organic Aerosol from Diesel Exhaust Using Parameterized and Semi-Explicit Chemistry and Thermodynamic Models"

10.5194/acp-2017-1060-supplement ◽

2017 ◽

Cited By ~ 1

Author(s):

Sailaja Eluri ◽

Christopher D. Cappa ◽

Beth Friedman ◽

Delphine K. Farmer ◽

Shantanu H. Jathar

Keyword(s):

Diesel Exhaust ◽

Secondary Organic Aerosol ◽

Organic Aerosol ◽

Thermodynamic Models ◽

Supplementary Material

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Perinatal exposure to diesel exhaust origin secondary organic aerosol induces autism-like behavior in rats

10.21203/rs.3.rs-41390/v2 ◽

2020 ◽

Author(s):

Tin Tin Win Shwe ◽

Chaw Kyi Tha Thu ◽

Yuji Fujitani ◽

Shinji Tsukahara ◽

Seishiro Hirano

Keyword(s):

Prefrontal Cortex ◽

Diesel Exhaust ◽

Secondary Organic Aerosol ◽

Organic Aerosol ◽

Female Rats ◽

Perinatal Exposure ◽

Male And Female ◽

Glutamate Concentration ◽

Immunological Markers ◽

Male And Female Rats

Abstract Background: Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social communication, poor social interactions and repetitive behaviors. The exact cause and mechanism of autism remains unknown. Both genetic and environmental factors may involve in ASD. In this study, we used diesel exhaust origin secondary organic aerosol (DE-SOA) as environmental pollutants. The aim of present study is to examine autism-like behaviors and related gene expressions in rats exposed to DE-SOA perinatally. Sprague-Dawley pregnant rats were exposed to clean air (control), diesel exhaust (DE) and DE-SOA in the exposure chamber for 5 h per day, 5days a week from gestational day 8 to postnatal day 21. At postnatal day 21, the male and female offspring rats were allocated into three different groups as follows: 1) rats exposed to clean filtered air; 2) rats exposed to DE; 3) rats exposed to DE-SOA. Social behaviors were investigated at 10~13-weeks-old rats using a 3-chambered social behavior test, social dominance tube test and marble burying test. Prefrontal cortex was collected under deep anesthesia to examine neurological and immunological markers, glutamate concentration, mast cell and microglia activation using real-time RT-PCR method, ELISA method and immunohistochemical analysis. Results: DE-SOA-exposed male and female rats showed poor sociability and social novelty preference, socially dominant behavior and increased repetitive behavior compared with the control rats. The mRNA expression levels of serotonin receptor (5-HT(5B)) and brain-derived neurotrophic factor (BDNF) were down-regulated whereas interleukin 1 b　(IL-b), and heme oxygenase 1 (HO-1) were upregulated in the prefrontal cortex of male and female rats exposed to DE-SOA compared to the control rats. In addition, the expression of mast cells and microglia marker ionized calcium-binding adapter molecule (Iba)1 were increased in the prefrontal cortex of male and female rats exposed to DE-SOA. Glutamate concentration was increased significantly in the prefrontal cortex of both male and female rats exposed to DE-SOA. Conclusion: Our results indicate that perinatal exposure to DE-SOA may induce autism-like behavior in rats by modulating neurological and immunological markers in the prefrontal cortex.

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Establishment of an olfactory-based spatial learning test for preweaning mice and the effects of early exposure to diesel exhaust origin secondary organic aerosol

Toxicology Letters ◽

10.1016/j.toxlet.2015.08.754 ◽

2015 ◽

Vol 238 (2) ◽

pp. S261

Author(s):

T.-T. Win-Shwe ◽

C. Kyi-Tha-Thu ◽

Y. Moe ◽

Y. Fujitani ◽

S. Tsukahara ◽

...

Keyword(s):

Spatial Learning ◽

Diesel Exhaust ◽

Secondary Organic Aerosol ◽

Organic Aerosol ◽

Early Exposure ◽

Learning Test

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Perinatal Exposure to Diesel Exhaust-Origin Secondary Organic Aerosol Induces Autism-Like Behavior in Rats

International Journal of Molecular Sciences ◽

10.3390/ijms22020538 ◽

2021 ◽

Vol 22 (2) ◽

pp. 538

Author(s):

Tin-Tin Win-Shwe ◽

Chaw Kyi-Tha-Thu ◽

Yuji Fujitani ◽

Shinji Tsukahara ◽

Seishiro Hirano

Keyword(s):

Prefrontal Cortex ◽

Diesel Exhaust ◽

Secondary Organic Aerosol ◽

Organic Aerosol ◽

Female Rats ◽

Perinatal Exposure ◽

Male And Female ◽

Glutamate Concentration ◽

Immunological Markers ◽

Male And Female Rats

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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