Year-end Sale % OFF 
Abstract
Secondary organic aerosol (SOA) is a component of particulate matter (PM) 2.5 and formed in the atmosphere by oxidation of volatile organic compounds. Recently, we have reported that inhalation exposure to diesel engine exhaust (DE) originated SOA (DE-SOA) affect novel object recognition ability and impair maternal behavior in adult mice. However, it is not clear whether early life exposure to SOA during the developmental stages affect social behavior in adult life or not. In the present study, to investigate the effects of early life exposure to DE-SOA during the gestational and lactation stages on the social behavior in the adult life, BALB/c mice were exposed to clean air (control), DE, DE-SOA and gas without any PM in the inhalation chambers from gestational day 14 to postnatal day 21 for 5 h a day and 5 days per week. Then adult mice were examined for changes in their social behavior at the age of 13 week by a sociability and social novelty preference, social interaction with a juvenile mouse and light-dark transition test, hypothalamic mRNA expression levels of social behavior-related genes, estrogen receptor-alpha and oxytocin receptor as well as of the oxidative stress marker gene, heme oxygenase (HO)-1 by real-time RT-PCR method. In addition, hypothalamic level of neuronal excitatory marker, glutamate was determined by ELISA method. We observed that sociability and social novelty preference as well as social interaction were remarkably impaired, expression levels of estrogen receptor-alpha, oxytocin receptor mRNAs were significantly decreased, expression levels of HO-1 mRNAs and glutamate levels were significantly increased in adult male mice exposed to DE-SOA compared to the control ones. Findings of this study indicate early life exposure of BALB/c mice to DE-SOA may affect their late-onset hypothalamic expression of social behavior related genes, trigger neurotoxicity and impair social behavior in the males.
Highlights
Current epidemiological studies have indicated that inhalation of high levels of particulate matter (PM) is associated with damage to the central nervous system (Block and CalderónGarcidueñas, 2009; Win-Shwe and Fujimaki, 2011; Block et al, 2012; Genc et al, 2012; Weisskopf et al, 2015)
To understand the mechanism underlying the inflammatory response in the hypothalamus of mice exposed to diesel engine exhaust (DE)-Secondary organic aerosol (SOA), we examined the expression of the oxidative stress marker HO1 and found that HO1 mRNA was significantly upregulated in the derived secondary organic aerosol (DE-SOA)-exposed group compared with the control group (Figure 3B, ∗P < 0.05)
The major findings in the present study indicate that exposure to DE-SOA during brain developmental period may impair some social behaviors in adult male BALB/c mice accompanied with modulation of expression of ERα and oxytocin receptor (OTR), inflammatory mediator COX2 and oxidative stress marker HO1 in the hypothalamus
Summary
Current epidemiological studies have indicated that inhalation of high levels of particulate matter (PM) is associated with damage to the central nervous system (Block and CalderónGarcidueñas, 2009; Win-Shwe and Fujimaki, 2011; Block et al, 2012; Genc et al, 2012; Weisskopf et al, 2015). Ambient PM consists of primary particles emitted directly from sources, and secondary particles formed by photo-oxidation reactions of volatile organic compounds and gases in the atmosphere, which are known as secondary organic aerosols (SOAs) (Robinson et al, 2007). The importance of SOA formation in urban areas is well-recognized, in the atmosphere and in indoor environments (Wang et al, 2012; Youssefi and Waring, 2012). It has been reported that exposure to SOA emitted from coal-fired power plants may be associated with an increased risk of heart disease in susceptible animals (Wellenius et al, 2011). Data showing the effects of SOA on central nervous system and neurobehavioral functions are very limited
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
