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 |
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| creator | Tokuda, Kentaro Kida, Kotaro Marutani, Eizo Crimi, Ettore Bougaki, Masahiko Khatri, Ashok Kimura, Hideo Ichinose, Fumito |
| description | 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 |
| doi_str_mv | 10.1089/ars.2011.4363 |
| format | Article |
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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<0.05). H(2)S breathing attenuated LPS-induced increase of plasma ALT activity and NOx levels and lung MPO activity. Inhaled H(2)S suppressed LPS-induced upregulation of inflammatory cytokines, while it markedly induced anti-inflammatory interleukin (IL)-10 in the liver. Beneficial effects of H(2)S inhalation after LPS challenge were associated with restored sulfide levels and markedly increased thiosulfate levels in plasma. Increased thiosulfate levels after LPS challenge were associated with upregulation of rhodanese, but not cystathionine-γ-lyase (CSE), in the liver. Administration of sodium thiosulfate dose-dependently improved survival after LPS challenge in mice.
By measuring changes in plasma levels of sulfide and sulfide metabolites using an advanced analytical method, this study revealed a critical role of thiosulfate in the protective effects of H(2)S breathing during endotoxemia.
These observations suggest that H(2)S breathing prevents inflammation and improves survival after LPS challenge by altering sulfide metabolism in mice.</description><identifier>ISSN: 1523-0864</identifier><identifier>EISSN: 1557-7716</identifier><identifier>DOI: 10.1089/ars.2011.4363</identifier><identifier>PMID: 22221071</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Administration, Inhalation ; Alanine transaminase ; Animals ; Anti-Inflammatory Agents - administration & dosage ; Anti-Inflammatory Agents - therapeutic use ; Antioxidants ; Endotoxemia ; Endotoxins ; Endotoxins - toxicity ; Forum Original Research Communications ; Hydrogen sulfide ; Hydrogen Sulfide - administration & dosage ; Hydrogen Sulfide - therapeutic use ; Inflammation ; Inflammation - chemically induced ; Inflammation - metabolism ; Inflammation - prevention & control ; Interleukins ; Lipopolysaccharides ; Liver ; Lung ; Male ; Metabolites ; Mice ; Mice, Inbred BALB C ; Nitrate ; Peroxidase ; Plasma levels ; Respiration ; sodium thiosulfate ; Sulfide ; Sulfides - metabolism ; Survival ; thiosulfate</subject><ispartof>Antioxidants & redox signaling, 2012-07, Vol.17 (1), p.11-21</ispartof><rights>Copyright 2012, Mary Ann Liebert, Inc. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22221071$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tokuda, Kentaro</creatorcontrib><creatorcontrib>Kida, Kotaro</creatorcontrib><creatorcontrib>Marutani, Eizo</creatorcontrib><creatorcontrib>Crimi, Ettore</creatorcontrib><creatorcontrib>Bougaki, Masahiko</creatorcontrib><creatorcontrib>Khatri, Ashok</creatorcontrib><creatorcontrib>Kimura, Hideo</creatorcontrib><creatorcontrib>Ichinose, Fumito</creatorcontrib><title>Inhaled hydrogen sulfide prevents endotoxin-induced systemic inflammation and improves survival by altering sulfide metabolism in mice</title><title>Antioxidants & redox signaling</title><addtitle>Antioxid Redox Signal</addtitle><description>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<0.05). H(2)S breathing attenuated LPS-induced increase of plasma ALT activity and NOx levels and lung MPO activity. Inhaled H(2)S suppressed LPS-induced upregulation of inflammatory cytokines, while it markedly induced anti-inflammatory interleukin (IL)-10 in the liver. Beneficial effects of H(2)S inhalation after LPS challenge were associated with restored sulfide levels and markedly increased thiosulfate levels in plasma. Increased thiosulfate levels after LPS challenge were associated with upregulation of rhodanese, but not cystathionine-γ-lyase (CSE), in the liver. Administration of sodium thiosulfate dose-dependently improved survival after LPS challenge in mice.
By measuring changes in plasma levels of sulfide and sulfide metabolites using an advanced analytical method, this study revealed a critical role of thiosulfate in the protective effects of H(2)S breathing during endotoxemia.
These observations suggest that H(2)S breathing prevents inflammation and improves survival after LPS challenge by altering sulfide metabolism in mice.</description><subject>Administration, Inhalation</subject><subject>Alanine transaminase</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - administration & dosage</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Antioxidants</subject><subject>Endotoxemia</subject><subject>Endotoxins</subject><subject>Endotoxins - toxicity</subject><subject>Forum Original Research Communications</subject><subject>Hydrogen sulfide</subject><subject>Hydrogen Sulfide - administration & dosage</subject><subject>Hydrogen Sulfide - therapeutic use</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - prevention & control</subject><subject>Interleukins</subject><subject>Lipopolysaccharides</subject><subject>Liver</subject><subject>Lung</subject><subject>Male</subject><subject>Metabolites</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Nitrate</subject><subject>Peroxidase</subject><subject>Plasma levels</subject><subject>Respiration</subject><subject>sodium thiosulfate</subject><subject>Sulfide</subject><subject>Sulfides - metabolism</subject><subject>Survival</subject><subject>thiosulfate</subject><issn>1523-0864</issn><issn>1557-7716</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkElrHDEQRkVwiJfkmGvQ0Zcea2ktczEEk8QGQy7JuZFaNTMKWtpSd5P5A_ndUYht7LpUQT3eRxVCHynZUKK3V6bUDSOUbnou-Rt0RoVQnVJUnvybGe-Ilv0pOq_1FyGEUUreoVPWihJFz9Cfu3QwARw-HF3Je0i4LmHnHeCpwApprhiSy3P-7VPnk1vGxtZjnSH6Efu0CyZGM_ucsEkO-ziVvEJtlrL61QRsj9iEGYpP-2d1hNnYHHyNzYCbCN6jtzsTKnx47Bfo59cvP25uu_vv3-5uPt93E2PbudNmlP1oiQHonZKylwS0VZxqqglQRbUiVlCuuHJqa50g0jFnlRMWxJYyfoGu_3unxUZwYzuwmDBMxUdTjkM2fni9Sf4w7PM6cN4zIUUTXD4KSn5YoM5D9HWEEEyCvNSBMi2I1o1u6KeXWc8hT8_nfwH9g4r_</recordid><startdate>20120701</startdate><enddate>20120701</enddate><creator>Tokuda, Kentaro</creator><creator>Kida, Kotaro</creator><creator>Marutani, Eizo</creator><creator>Crimi, Ettore</creator><creator>Bougaki, Masahiko</creator><creator>Khatri, Ashok</creator><creator>Kimura, Hideo</creator><creator>Ichinose, Fumito</creator><general>Mary Ann Liebert, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7T7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>5PM</scope></search><sort><creationdate>20120701</creationdate><title>Inhaled hydrogen sulfide prevents endotoxin-induced systemic inflammation and improves survival by altering sulfide metabolism in mice</title><author>Tokuda, Kentaro ; Kida, Kotaro ; Marutani, Eizo ; Crimi, Ettore ; Bougaki, Masahiko ; Khatri, Ashok ; Kimura, Hideo ; Ichinose, Fumito</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p229t-8ac64cb0aee4d766460e8b7318180e171870b513737d79bd506d2db7d5be59123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Administration, Inhalation</topic><topic>Alanine transaminase</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - administration & dosage</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Antioxidants</topic><topic>Endotoxemia</topic><topic>Endotoxins</topic><topic>Endotoxins - toxicity</topic><topic>Forum Original Research Communications</topic><topic>Hydrogen sulfide</topic><topic>Hydrogen Sulfide - administration & dosage</topic><topic>Hydrogen Sulfide - therapeutic use</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - prevention & control</topic><topic>Interleukins</topic><topic>Lipopolysaccharides</topic><topic>Liver</topic><topic>Lung</topic><topic>Male</topic><topic>Metabolites</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Nitrate</topic><topic>Peroxidase</topic><topic>Plasma levels</topic><topic>Respiration</topic><topic>sodium thiosulfate</topic><topic>Sulfide</topic><topic>Sulfides - metabolism</topic><topic>Survival</topic><topic>thiosulfate</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tokuda, Kentaro</creatorcontrib><creatorcontrib>Kida, Kotaro</creatorcontrib><creatorcontrib>Marutani, Eizo</creatorcontrib><creatorcontrib>Crimi, Ettore</creatorcontrib><creatorcontrib>Bougaki, Masahiko</creatorcontrib><creatorcontrib>Khatri, Ashok</creatorcontrib><creatorcontrib>Kimura, Hideo</creatorcontrib><creatorcontrib>Ichinose, Fumito</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Antioxidants & redox signaling</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tokuda, Kentaro</au><au>Kida, Kotaro</au><au>Marutani, Eizo</au><au>Crimi, Ettore</au><au>Bougaki, Masahiko</au><au>Khatri, Ashok</au><au>Kimura, Hideo</au><au>Ichinose, Fumito</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhaled hydrogen sulfide prevents endotoxin-induced systemic inflammation and improves survival by altering sulfide metabolism in mice</atitle><jtitle>Antioxidants & redox signaling</jtitle><addtitle>Antioxid Redox Signal</addtitle><date>2012-07-01</date><risdate>2012</risdate><volume>17</volume><issue>1</issue><spage>11</spage><epage>21</epage><pages>11-21</pages><issn>1523-0864</issn><eissn>1557-7716</eissn><abstract>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<0.05). H(2)S breathing attenuated LPS-induced increase of plasma ALT activity and NOx levels and lung MPO activity. Inhaled H(2)S suppressed LPS-induced upregulation of inflammatory cytokines, while it markedly induced anti-inflammatory interleukin (IL)-10 in the liver. Beneficial effects of H(2)S inhalation after LPS challenge were associated with restored sulfide levels and markedly increased thiosulfate levels in plasma. Increased thiosulfate levels after LPS challenge were associated with upregulation of rhodanese, but not cystathionine-γ-lyase (CSE), in the liver. Administration of sodium thiosulfate dose-dependently improved survival after LPS challenge in mice.
By measuring changes in plasma levels of sulfide and sulfide metabolites using an advanced analytical method, this study revealed a critical role of thiosulfate in the protective effects of H(2)S breathing during endotoxemia.
These observations suggest that H(2)S breathing prevents inflammation and improves survival after LPS challenge by altering sulfide metabolism in mice.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>22221071</pmid><doi>10.1089/ars.2011.4363</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Administration, Inhalation Alanine transaminase Animals Anti-Inflammatory Agents - administration & dosage Anti-Inflammatory Agents - therapeutic use Antioxidants Endotoxemia Endotoxins Endotoxins - toxicity Forum Original Research Communications Hydrogen sulfide Hydrogen Sulfide - administration & dosage Hydrogen Sulfide - therapeutic use Inflammation Inflammation - chemically induced Inflammation - metabolism Inflammation - prevention & control Interleukins Lipopolysaccharides Liver Lung Male Metabolites Mice Mice, Inbred BALB C Nitrate Peroxidase Plasma levels Respiration sodium thiosulfate Sulfide Sulfides - metabolism Survival thiosulfate |
| title | Inhaled hydrogen sulfide prevents endotoxin-induced systemic inflammation and improves survival by altering sulfide metabolism in mice |
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