title: Hydrogen sulfide inhibits oxidative stress in lungs from allergic mice in vivo.
abstract: Recent studies show that endogenous hydrogen sulfide (H(2)S) plays an anti-inflammatory role in the pathogenesis of airway inflammation. This study investigated whether exogenous H(2)S may counteract oxidative stress-mediated lung damage in allergic mice. Female BALB/c mice previously sensitized with ovalbumin (OVA) were treated with sodium hydrosulfide (NaHS) 30 min before OVA challenge. Forty eight hours after antigen-challenge, the mice were killed and leukocyte counting as well as nitrite plus nitrate concentrations were determined in the bronchoalveolar lavage fluid, and lung tissue was analysed for nitric oxide synthase (NOS) activity, iNOS expression, superoxide dismutase (SOD), catalase, glutathione reductase (GR) and glutathione peroxidase (GPx) activities, thiobarbituric acid reactive species and 3-nitrotyrosine containing proteins (3-NT). Pre-treatment of OVA-sensitized mice with NaHS resulted in significant reduction of both eosinophil and neutrophil migration to the lungs, and prevented the elevation of iNOS expression and activity observed in the lungs from the untreated allergic mice, although it did not affect 3-NT. NaHS treatment also abolished the increased lipid peroxidation present in the allergic mouse lungs and increased SOD, GPx and GR enzyme activities. These results show, for the first time, that the beneficial in vivo effects of the H(2)S-donor NaHS on allergic airway inflammation involve its inhibitory action on leukocyte recruitment and the prevention of lung damage by increasing endogenous antioxidant defenses. Thus, exogenous administration of H(2)S donors may be beneficial in reducing the deleterius impact of allergic pulmonary disease, and might represent an additional class of pharmacological agents for treatment of chronic pulmonary diseases.
authors.affiliation: Laboratory of Inflammation Research, São Francisco University, Bragança Paulista, São Paulo 12 916 900, Brazil.
authors.forename: Leticia R
authors.initials: LR
authors.lastname: Benetti
authors.forename: Daiana
authors.initials: D
authors.lastname: Campos
authors.forename: Sonia A
authors.initials: SA
authors.lastname: Gurgueira
authors.forename: Anibal E
authors.initials: AE
authors.lastname: Vercesi
authors.forename: Cristiane E V
authors.initials: CE
authors.lastname: Guedes
authors.forename: Kleber L
authors.initials: KL
authors.lastname: Santos
authors.forename: John L
authors.initials: JL
authors.lastname: Wallace
authors.forename: Simone A
authors.initials: SA
authors.lastname: Teixeira
authors.forename: Juliana
authors.initials: J
authors.lastname: Florenzano
authors.forename: Soraia K P
authors.initials: SK
authors.lastname: Costa
authors.forename: Marcelo N
authors.initials: MN
authors.lastname: Muscará
authors.forename: Heloisa H A
authors.initials: HH
authors.lastname: Ferreira
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D006967:Hypersensitivity / Q000201:enzymology / Q000276:immunology / Q000378:metabolism*; D007962:Leukocytes / Q000187:drug effects / Q000276:immunology; D008168:Lung / Q000187:drug effects* / Q000201:enzymology / Q000276:immunology / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D019001:Nitric Oxide Synthase / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D013440:Sulfides / Q000494:pharmacology; D013482:Superoxide Dismutase / Q000378:metabolism; D013858:Thiobarbiturates / Q000378:metabolism; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism
chemical_list: D013440:Sulfides; D013858:Thiobarbiturates; C002744:3-nitrotyrosine; D014443:Tyrosine; D002374:Catalase; D005979:Glutathione Peroxidase; D019001:Nitric Oxide Synthase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; C025451:sodium bisulfide; C029684:thiobarbituric acid; D006862:Hydrogen Sulfide