Effects of exposure to nanoparticle-rich diesel exhaust on 8-OHdG synthesis in the mouse asthmatic lung

Tanaka,Michitaka; Takano,Hirohisa; Fujitani,Yuji; Hirano,Seishiro; Ichinose,Takamichi; Shimada,Akinori; Inoue,Ken-Ichiro

doi:10.3892/etm.2013.1198

Effects of exposure to nanoparticle-rich diesel exhaust on 8-OHdG synthesis in the mouse asthmatic lung

Authors:
- Michitaka Tanaka
- Hirohisa Takano
- Yuji Fujitani
- Seishiro Hirano
- Takamichi Ichinose
- Akinori Shimada
- Ken-Ichiro Inoue
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Affiliations: Center for Medical Science, International University of Health and Welfare, Ohtawara, Tochigi 324-8501, Japan, Department of Environmental Engineering, Graduate School of Engineering, Kyoto University, Nishikyo-ku, Kyoto 615-8540, Japan, Research Center for Environmental Risk, National Institute for Environmental Studies, Tsukuba, Ibaraki 305‑8506, Japan, Department of Health Science, Oita University of Nursing and Health Science, Oita 871‑1201, Japan, Department of Veterinary Pathology, Tottori University, Tottori 680-8553, Japan
Published online on: July 2, 2013 https://doi.org/10.3892/etm.2013.1198
Pages: 703-706

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Abstract

It has been demonstrated that exposure to diesel exhaust (DE) is associated with the induction and exacerbation of respiratory disorders; however, the impacts of DE containing mainly nanoparticles have been less studied. We have previously demonstrated that inhalation exposure to nanoparticle-rich DE (NR-DE) exacerbated allergic pulmonary inflammation, in the context of enhanced local expression of proinflammatory molecules. However, the underlying mechanisms have not been fully elucidated. 8-Hydroxydeoxyguanosine (8-OHdG) is a marker of oxidative damage, particularly in DNA. This study examined the effects of NR-DE on 8-OHdG synthesis in the lung in the presence or absence of an allergen. Institute for Cancer Research (ICR) mice were exposed by inhalation to four different gas compositions (control air, low-concentration DE, high-concentration DE and high-concentration DE without particulate matter) for 8 weeks, in the presence or absence of repetitive intratracheal administration of ovalbumin (OVA). Thereafter, we assessed the levels of 8-OHdG synthesis and expression in the lungs by means of enzyme immunoassay (EIA) and immunohistochemistry. The EIA revealed that the level of 8-OHdG was significantly higher in the high-concentration NR-DE-exposed and allergen-sensitized/stimulated group compared with that in the control air-exposed and allergen-treated group. The immunohistochemistry results demonstrated that the level of immunoreactive 8-OHdG was higher in the NR-DE-exposed and allergen-treated lungs compared with that in the corresponding control air-exposed lungs. The results suggested that NR-DE exposure enhanced 8-OHdG formation in asthmatic lungs. This, at least in part, is involved in the NR-DE-mediated exacerbation of the allergic pathophysiology that was identified in our previous study.

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