Exposure of BALB/c Mice to Diesel Engine Exhaust Origin Secondary Organic Aerosol (DE-SOA) during the Developmental Stages Impairs the Social Behavior in Adult Life of the Males

Win-Shwe, Tin-Tin; Kyi-Tha-Thu, Chaw; Moe, Yadanar; Fujitani, Yuji; Tsukahara, Shinji; Hirano, Seishiro

doi:10.3389/fnins.2015.00524

Cited by 21 publications

(18 citation statements)

References 55 publications

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“…Several studies examined the effects of diesel exhaust inhalational exposures on mRNA levels of glutamatergic receptors. In a study of diesel exhaust exposure of mice from GD14 to PND21, glutamate concentrations in hypothalamus were increased to the same extent by diesel exhaust alone and in conjunction with secondary organic aerosols (85). In a study of diesel injected subcutaneously at GD 6, 9, 12, 15 and 18, a slight reduction was found in NR2A receptor mRNA in hippocampus in offspring at 10 weeks of age (52).…”

Section: Potential Mechanisms Of Cognitive Impairmentmentioning

confidence: 99%

Cognitive Effects of Air Pollution Exposures and Potential Mechanistic Underpinnings

Allen

Klocke

Morris‐Schaffer

et al. 2017

Curr Envir Health Rpt

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Purpose of review This review sought to address the potential for air pollutants to impair cognition and mechanisms by which that might occur. Recent findings Air pollution has been associated with deficits in cognitive functions across a wide range of epidemiological studies, both with developmental and adult exposures. Studies in animal models are significantly more limited in number, with somewhat inconsistent findings to date for measures of learning, but show more consistent impairments for short term memory. Potential contributory mechanisms include oxidative stress/inflammation, altered levels of dopamine and/or glutamate and changes in synaptic plasticity/structure. Summary Epidemiological studies are consistent with adverse effects of air pollutants on cognition, but additional studies and better phenotypic characterization are needed for animal models, including more precise delineation of specific components of cognition that are affected, as well as definitions of critical exposure periods for such effects and the components of air pollution responsible. This would permit development of more circumscribed hypotheses as to potential behavioral and neurobiological mechanisms.

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Section: Potential Mechanisms Of Cognitive Impairmentmentioning

confidence: 99%

Cognitive Effects of Air Pollution Exposures and Potential Mechanistic Underpinnings

Allen

Klocke

Morris‐Schaffer

et al. 2017

Curr Envir Health Rpt

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“…In that study we have showed that GAD67 de ciency may be associated with glutamate/GABA imbalance in autistic brain. We have also reported that early life exposure of BALB/c mice to DE-SOA may affect their late-onset hypothalamic expression of social behavior related genes (ERα and oxytocin receptor) and induced impaired social behavior [27]. Taken together, environmental factors such as maternal infection, nutrition, antenatal care, education, drug usage and exposure to chemicals or pollutants during pregnancy are risk factors for ASD.…”

Section: Discussionmentioning

confidence: 83%

“…We have also established the neonatal animal model for early detection of environmental pollutant-induced learning disability and reported that DE-SOA impairs olfactory-based spatial learning activity in preweaning mice [26]. In addition, we have showed that early life exposure to DE-SOA impaired social behavior and alteration in social behavior related gene expression in the hypothalamus of adult male BALB/c mice [27]. Recently, we have developed valproic acid (VPA)-induced autism model rats and showed that reduction of gamma amino butyric acid (GABA) synthetic enzyme glutamic acid decarboxylase (GAD) 67 protein in both male and female VPA-exposed rats resulting in imbalance of glutamate/GABA was the possible mechanism for ASD [28].…”

Section: Introductionmentioning

confidence: 99%

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

Shwe

Thu

Fujitani

et al. 2020

Preprint

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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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“…Nanoparticles, a systemic inflammation mediator, and cytokines are linked to a lesion of cerebral tissue and results in neurological damage, which has been proposed in the literature (Harris et al, ). After previous studies have illustrated that particles have adverse cardiopulmonary effects, research about the CNS effect was reported recently (Liu et al, ; Win‐Shwe et al, ).…”

Section: Particles‐induced Detrimental Effects On Cnsmentioning

confidence: 99%

“…Animal experimental data illustrated that PM can cause a neurodevelopmental disorder. When male mice where exposured to SOAs during the neurodevelopmental stage, male adult mice were weak in social behavior including social novelty preference and social interaction (Win‐Shwe et al, ). In utero exposure to high‐concentrated DEP affects spatial learning and the memory of male offspring, with a reduced NMDAR expression in the hippocampus.…”

Section: Particles‐induced Detrimental Effects On Cnsmentioning

confidence: 99%

Toxicity of inhaled particulate matter on the central nervous system: neuroinflammation, neuropsychological effects and neurodegenerative disease

2017

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Particulate matter (PM) combined with meteorological factors cause the haze, which brings inconvenience to people's daily life and deeply endanger people's health. Accumulating literature, to date, reported that PM are closely related to cardiopulmonary disease. Outpatient visits and admissions as a result of asthma and heart attacks gradually increase with an elevated concentration of PM. Owing to its special physicochemical property, the brain could be a potential target beyond the cardiopulmonary system. Possible routes of PM to the brain via a direct route or stimulation of pro-inflammatory cytokines have been reported in several documents concerning toxicity of engineered nanoparticles in rodents. Recent studies have demonstrated that PM have implications in oxidative stress, inflammation, dysfunction of cellular organelles, as well as the disturbance of protein homeostasis, promoting neuron loss and exaggerating the burden of central nervous system (CNS). Moreover, the smallest particles (nano-sized particles), which were involved in inflammation, reactive oxygen species (ROS), microglial activation and neuron loss, may accelerate the process of the neurodevelopmental disorder and neurodegenerative disease. Potential or other undiscovered mechanisms are not mutually exclusive but complementary aspects of each other. Epidemiology studies have shown that exposure to PM could bring about neurotoxicity and play a significant role in the etiology of CNS disease, which has been gradually corroborated by in vivo and in vitro studies. This review highlights research advances on the health effects of PM with an emphasis on neurotoxicity. With the hope of enhancing awareness in the public and calling for prevention and protective measures, it is a critical topic that requires proceeding exploration. Copyright © 2017 John Wiley & Sons, Ltd.

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Exposure of BALB/c Mice to Diesel Engine Exhaust Origin Secondary Organic Aerosol (DE-SOA) during the Developmental Stages Impairs the Social Behavior in Adult Life of the Males

Cited by 21 publications

References 55 publications

Cognitive Effects of Air Pollution Exposures and Potential Mechanistic Underpinnings

Cognitive Effects of Air Pollution Exposures and Potential Mechanistic Underpinnings

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

Toxicity of inhaled particulate matter on the central nervous system: neuroinflammation, neuropsychological effects and neurodegenerative disease

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