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  2. 市原 佐保子

市原 佐保子

イチハラ サホコ  (Sahoko Ichihara)

基本情報

所属
自治医科大学 医学部　環境予防医学講座 教授
学位
医学博士(名古屋大学)
J-GLOBAL ID
200901089139977563
researchmap会員ID
5000079149
外部リンク

研究キーワード

 6

研究分野

 3

経歴

 3

学歴

 2

論文

 160
  • Jidapa Hanvoravongchai, Methasit Laochindawat, Yusuke Kimura, Nathan Mise, Sahoko Ichihara
    Chemosphere 368 143745-143745 2024年11月  
  • Yuji Fujitani, Akihiko Ikegami, Kouta Morikawa, Jun Kumoi, Takeo Yano, Atsushi Watanabe, Ai Shiono, Chuichi Watanabe, Norio Teramae, Gaku Ichihara, Sahoko Ichihara
    Journal of hazardous materials 467 133679-133679 2024年4月5日  
    Focusing on the relatively unexplored presence of micro- and nano-plastic aerosol particles, this study quantitatively assessed the emission of nano-plastic particles during the machining of carbon fiber reinforced plastic (CFRP) in the working environment. Measurements of aerosol particles smaller than 1 µm in size were performed by aerosol mass spectrometry. The findings revealed that concentrations of carbonous aerosol particles (organic aerosol and refractory black carbon (rBC)) were higher during working hours than during non-working hours. Positive matrix factorization identified CFRP particles as a significant source, contributing an average of approximately 30% of concentration of carbonous aerosol particles during working hours. This source apportionment was corroborated by the presence of bisphenol A and F fragments, principal components of the epoxy resins used in CFRP, and was corroborated by similarities to the carbon cluster ion distribution observed in rBC during CFRP pipe-cutting operations. Further, the particle size distribution suggested the existence of plastic aerosol particles smaller than 100 nm. This study established the method to quantitatively distinguish nano-plastic aerosol particles from other aerosol particles in high temporal resolution and these techniques are useful for accurately assessing exposure to nano-plastic aerosol particles in working environments.
  • Ryoya Takizawa, Akihiko Ikegami, Cai Zong, Syun Nemoto, Yuki Kitamura, Nathan Mise, Gaku Ichihara, Sahoko Ichihara
    Fundamental Toxicological Sciences 11(3) 109-121 2024年  
  • Alzahraa Fergany, Cai Zong, Frederick Adams Ekuban, Bin Wu, Satoshi Ueha, Shigeyuki Shichino, Kouji Matsushima, Yoichiro Iwakura, Sahoko Ichihara, Gaku Ichihara
    Archives of toxicology 2023年11月16日  
    Acrylamide is an environmental electrophile that has been produced in large amounts for many years. There is concern about the adverse health effects of acrylamide exposure due to its widespread industrial use and also presence in commonly consumed foods and others. IL-1β is a key cytokine that protects the brain from inflammatory insults, but its role in acrylamide-induced neurotoxicity remains unknown. We reported recently that deletion of IL-1β gene exacerbates ACR-induced neurotoxicity in mice. The aim of this study was to identify genes or signaling pathway(s) involved in enhancement of ACR-induced neurotoxicity by IL-1β gene deletion or ACR-induced neurotoxicity to generate a hypothesis mechanism explaining ACR-induced neurotoxicity. C57BL/6 J wild-type and IL-1β KO mice were exposed to ACR at 0, 12.5, 25 mg/kg by oral gavage for 7 days/week for 4 weeks, followed by extraction of mRNA from mice cerebral cortex for RNA sequence analysis. IL-1β deletion altered the expression of genes involved in extracellular region, including upregulation of PFN1 gene related to amyotrophic lateral sclerosis and increased the expression of the opposite strand of IL-1β. Acrylamide exposure enhanced mitochondria oxidative phosphorylation, synapse and ribosome pathways, and activated various pathways of different neurodegenerative diseases, such as Alzheimer disease, Parkinson disease, Huntington disease, and prion disease. Protein network analysis suggested the involvement of different proteins in related to learning and cognitive function, such as Egr1, Egr2, Fos, Nr4a1, and Btg2. Our results identified possible pathways involved in IL-1β deletion-potentiated and ACR-induced neurotoxicity in mice.
  • Walaa Slouma Hamouda Abd El Naby, Cai Zong, Alzahraa Fergany, Frederick Adams Ekuban, Saleh Ahmed, Yousra Reda, Harue Sato, Sahoko Ichihara, Natsuko Kubota, Shinya Yanagita, Gaku Ichihara
    International journal of molecular sciences 24(12) 2023年6月8日  
    Epidemiological studies showed the association between air pollution and dementia. A soluble fraction of particulate matters including polycyclic aromatic hydrocarbons (PAHs) is suspected to be involved with the adverse effects of air pollution on the central nervous system of humans. It is also reported that exposure to benzopyrene (B[a]P), which is one of the PAHs, caused deterioration of neurobehavioral performance in workers. The present study investigated the effect of B[a]P on noradrenergic and serotonergic axons in mouse brains. In total, 48 wild-type male mice (10 weeks of age) were allocated into 4 groups and exposed to B[a]P at 0, 2.88, 8.67 or 26.00 µg/mice, which is approximately equivalent to 0.12, 0.37 and 1.12 mg/kg bw, respectively, by pharyngeal aspiration once/week for 4 weeks. The density of noradrenergic and serotonergic axons was evaluated by immunohistochemistry in the hippocampal CA1 and CA3 areas. Exposure to B[a]P at 2.88 µg/mice or more decreased the density of noradrenergic or serotonergic axons in the CA1 area and the density of noradrenergic axons in the CA3 area in the hippocampus of mice. Furthermore, exposure to B[a]P dose-dependently upregulated Tnfα at 8.67 µg/mice or more, as well as upregulating Il-1β at 26 µg/mice, Il-18 at 2.88 and 26 µg/mice and Nlrp3 at 2.88 µg/mice. The results demonstrate that exposure to B[a]P induces degeneration of noradrenergic or serotonergic axons and suggest the involvement of proinflammatory or inflammation-related genes with B[a]P-induced neurodegeneration.
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MISC

 91

所属学協会

 6
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共同研究・競争的資金等の研究課題

 33
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