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Effects of Pm2.5 and Gases Exposure During Prenatal and Early-Life on Autism-Like Phenotypes in Male Rat Offspring Publisher Pubmed



Emam B1 ; Shahsavani A1, 2 ; Khodagholi F3 ; Zarandi SM1 ; Hopke PK4, 5 ; Hadei M6, 7 ; Behbahani H3 ; Yarahmadi M8
Authors
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Authors Affiliations
  1. 1. Department of Environmental Health Engineering, School of Public Health and Safety, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  2. 2. Environmental and Occupational Hazards Control Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  3. 3. Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  4. 4. Department of Public Health Sciences, University of Rochester School of Medicine and Dentistry, Rochester, 14642, NY, United States
  5. 5. Center for Air Resources Engineering and Science, Clarkson University, Potsdam, 13699, NY, United States
  6. 6. Department of Environmental Health Engineering, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
  7. 7. Stud. Scientific Research Center (SSRC), Tehran University of Medical Sciences, Tehran, Iran
  8. 8. Center of Environmental and Occupational Health, Ministry of Health and Medical Education, Tehran, Iran

Source: Particle and Fibre Toxicology Published:2020


Abstract

Background: Epidemiological studies have reported associations between elevated air pollution and autism spectrum disorders (ASD). However, we hypothesized that exposure to air pollution that mimics real world scenarios, is a potential contributor to ASD. The exact etiology and molecular mechanisms underlying ASD are not well understood. Thus, we assessed whether changes in OXTR levels may be part of the mechanism linking PM2.5/gaseous pollutant exposure and ASD. The current in-vivo study investigated the effect of exposure to fine particulate matter (PM2.5) and gaseous pollutants on ASD using behavioral and molecular experiments. Four exposure groups of Wistar rats were included in this study: 1) particulate matter and gaseous pollutants exposed (PGE), 2) gaseous pollutants only exposed (GE), 3) autism-like model (ALM) with VPA induction, and 4) clean air exposed (CAE) as the control. Pregnant dams and male pups were exposed to air pollutants from embryonic day (E0) to postnatal day (PND21). Results: The average ± SD concentrations of air pollutants were: PM2.5: 43.8 ± 21.1 μg/m3, CO: 13.5 ± 2.5 ppm, NO2: 0.341 ± 0.100 ppm, SO2: 0.275 ± 0.07 ppm, and O3: 0.135 ± 0.01 ppm. The OXTR protein level, catalase activity (CAT), and GSH concentrations in the ALM, PGE, and GE rats were lower than those in control group (CAE). However, the decrements in the GE rats were smaller than other groups. Also in behavioral assessments, the ALM, PGE, and GE rats demonstrated a repetitive /restricted behavior and poor social interaction, but the GE rats had weaker responses compared to other groups of rats. The PGE and GE rats showed similar trends in these tests compared to the VPA rats. Conclusions: This study suggested that exposure to ambient air pollution contributed to ASD and that OXTR protein may serve as part of the mechanism linking them. © 2020 The Author(s).
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