Enhancing effects of trichloroethylene and tetrachloroethylene on type I allergic responses in mice

  • Seo Makoto
    Laboratory of Hygienic Chemistry and Molecular Toxicology, Gifu Pharmaceutical University Department of Biochemistry, Faculty of Medicine, Saitama Medical University
  • Kobayashi Ryo
    Laboratory of Hygienic Chemistry and Molecular Toxicology, Gifu Pharmaceutical University
  • Okamura Tetsunori
    Laboratory of Hygienic Chemistry and Molecular Toxicology, Gifu Pharmaceutical University
  • Ikeda Koji
    Laboratory of Hygienic Chemistry and Molecular Toxicology, Gifu Pharmaceutical University
  • Satoh Masahiko
    Laboratory of Hygienic Chemistry and Molecular Toxicology, Gifu Pharmaceutical University Laboratory of Pharmaceutical Health Sciences, School of Pharmacy, Aichi Gakuin University
  • Inagaki Naoki
    Laboratory of Pharmacology, Gifu Pharmaceutical University
  • Nagai Hiroichi
    Laboratory of Pharmacology, Gifu Pharmaceutical University
  • Nagase Hisamitsu
    Laboratory of Hygienic Chemistry and Molecular Toxicology, Gifu Pharmaceutical University

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Trichloroethylene (TCE) and tetrachloroethylene (perchloroethylene; PCE) are commonly identified as environmental contaminants of groundwater. Previously, we investigated the enhancing effects of TCE and PCE on antigen-induced histamine release and inflammatory mediator production in rat mast cells. In this study, to examine the potential effect of TCE and PCE on antigen-induced histamine release from mouse mast cells, mouse bone marrow-derived mast cells (BMMC) were sensitized with anti-dinitrophenol (DNP) monoclonal IgE antibody and then stimulated with DNP-BSA containing with TCE or PCE. Both TCE and PCE significantly enhanced antigen-induced histamine release from BMMC. Next we investigated the effects of TCE and PCE on the passive cutaneous anaphylaxis (PCA) reaction in vivo using ICR mice. TCE and PCE significantly enhanced the PCA reaction in a dose-dependent manner. In addition, we examined the enhancing effects of ingesting small amount of TCE and PCE in drinking water on antigen-stimulated allergic responses. After the ICR mice had ingested TCE or PCE in their drinking water for 2 or 4 weeks, we performed the PCA reaction. Both TCE and PCE ingestion enhanced the PCA reaction in a dose-dependent manner for 4 weeks. These results suggest that exposure to TCE and PCE leads to the augmentation of type I allergic responses in many species.

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