Inhaled hydrogen sulfide prevents endotoxin-induced systemic inflammation and improves survival by altering sulfide metabolism in mice

The role of hydrogen sulfide (H(2)S) in endotoxin (lipopolysaccharide [LPS])-induced inflammation is incompletely understood. We examined the impact of H(2)S breathing on LPS-induced changes in sulfide metabolism, systemic inflammation, and survival in mice. Mice that breathed air alone exhibited de...

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Veröffentlicht in:Antioxidants & redox signaling 2012-07, Vol.17 (1), p.11-21
Hauptverfasser: Tokuda, Kentaro, Kida, Kotaro, Marutani, Eizo, Crimi, Ettore, Bougaki, Masahiko, Khatri, Ashok, Kimura, Hideo, Ichinose, Fumito
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Sprache:eng
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Zusammenfassung:The role of hydrogen sulfide (H(2)S) in endotoxin (lipopolysaccharide [LPS])-induced inflammation is incompletely understood. We examined the impact of H(2)S breathing on LPS-induced changes in sulfide metabolism, systemic inflammation, and survival in mice. Mice that breathed air alone exhibited decreased plasma sulfide levels and poor survival rate at 72 h after LPS challenge. Endotoxemia markedly increased alanine aminotransferase (ALT) activity and nitrite/nitrate (NOx) levels in plasma and lung myeloperoxidase (MPO) activity in mice that breathed air. In contrast, breathing air supplemented with 80 ppm of H(2)S for 6 h after LPS challenge markedly improved survival rate compared to mice that breathed air alone (p
ISSN:1523-0864
1557-7716
DOI:10.1089/ars.2011.4363