Hydrogen sulfide donor NaHS causes bronchitis with enhanced respiratory secretion in rats

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  • Unuma Kana
    Department of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University
  • Aki Toshihiko
    Department of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University
  • Yamashita Ayaka
    Department of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University Yamaguchi University School of Medicine
  • Yoshikawa Ayaka
    Department of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University
  • Uemura Koichi
    Department of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University

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<p>Inhalation of toxic gases is dangerous to humans; experiments using toxic gases themselves are also hazardous to researchers. Gas-releasing molecules are widely used as alternatives to toxic gases, but their impacts on the whole body remain to be examined. To investigate responses during hydrogen sulfide (H2S) poisoning, rats (Sprague-Dawley, male, 8-week-old) were intraperitoneally (i.p.) administered H2S donor, NaHS, and sacrificed 24 hr after the administration. The main histopathological finding commonly observed in NaHS-administered rat heart, liver, brain, and lung was congestion. In addition, inflammation and accumulation of mucopolysaccharides were observed in bronchioles of the lung. Immunoblot analysis indicated increasing trend of NF-κB activation, and real-time PCR analysis showed increasing tendency of TNFα and IL-1β, as well as MUC1 and 5B, in NaHS-administered rat lung. Immunohistochemistry by use of anti-MUC1 and 5B antibodies confirmed enhanced mucosal secretion from bronchial epithelium. Moreover, administration of TNFα or IL-1β to A549 lung epithelial cells resulted with enhanced expressions of MUC1 and 5B. This report shows bronchitis and respiratory mucosal secretion in animal model of H2S intoxication, which is created by i.p. administration of a H2S donor, through NF-κB-TNFα/IL-1β-ΜUC1/5B pathway.</p>

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