Loading…
Sepsis Induces Diaphragm Electron Transport Chain Dysfunction and Protein Depletion
Sepsis significantly alters skeletal muscle mitochondrial function, but the mechanisms responsible for this abnormality are unknown. We postulated that endotoxin elicits specific changes in electron transport chain proteins that produce derangements in mitochondrial function. To examine this issue,...
Saved in:
| Published in: | American journal of respiratory and critical care medicine 2005-10, Vol.172 (7), p.861-868 |
|---|---|
| Main Authors: | , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Citations: | Items that this one cites Items that cite this one |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | cdi_FETCH-LOGICAL-c392t-f94b9922c3e4d3559f77bab3bade50a2dcb49617f4ab7fcf217ae10e6a857d223 |
|---|---|
| cites | cdi_FETCH-LOGICAL-c392t-f94b9922c3e4d3559f77bab3bade50a2dcb49617f4ab7fcf217ae10e6a857d223 |
| container_end_page | 868 |
| container_issue | 7 |
| container_start_page | 861 |
| container_title | American journal of respiratory and critical care medicine |
| container_volume | 172 |
| creator | Callahan, Leigh A Supinski, Gerald S |
| description | Sepsis significantly alters skeletal muscle mitochondrial function, but the mechanisms responsible for this abnormality are unknown.
We postulated that endotoxin elicits specific changes in electron transport chain proteins that produce derangements in mitochondrial function. To examine this issue, we compared the effects of endotoxin-induced sepsis on mitochondrial ATP (adenosine triphosphate) formation and electron transport chain protein composition.
Diaphragm mitochondrial oxygen consumption and mitochondrial nicotinamide adenine dinucleotide, reduced form, oxidase assays were measured in control rats (n=13) and rats given endotoxin (8 mg/kg/d) for 12 (n=14), 24 (n=14), 36 (n=14), and 48 h (n=13). Electron transport chain subunits from Complexes I, III, IV, and V were isolated using Blue Native polyacrylamide gel electrophoresis techniques.
Endotoxin administration: 1) elicited large reductions in mitochondrial oxygen consumption (e.g., 201+/-3.9 SE natoms O/min/mg for controls and 101+/-4.5 SE natoms O/minutes/mg after 48 h endotoxin, p |
| doi_str_mv | 10.1164/rccm.200410-1344OC |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_68619680</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>68619680</sourcerecordid><originalsourceid>FETCH-LOGICAL-c392t-f94b9922c3e4d3559f77bab3bade50a2dcb49617f4ab7fcf217ae10e6a857d223</originalsourceid><addsrcrecordid>eNpdkE1r3DAQhkVpaD7aP9BDMYUWenCqkWRpdQybpAkEEkgKvYmxLGW1-KuSTcm_r4wXAjlJjJ55Z_QQ8hnoOYAUP6O13TmjVAAtgQtxv31HTqDiVSm0ou_znSpeCqH_HJPTlPaUAtsA_UCOodJaCMlOyOOjG1NIxW3fzNal4jLguIv43BVXrbNTHPriKWKfxiFOxXaHoS8uX5KfezuF_IZ9UzzEYXJL3Y2tW6ofyZHHNrlPh_OM_L6-etrelHf3v263F3el5ZpNpdei1poxy51oeFVpr1SNNa-xcRVF1thaaAnKC6yVt56BQgfUSdxUqmGMn5Hva-4Yh7-zS5PpQrKubbF3w5yM3EjQckMz-PUNuB_m2OfdDGhdKQ1SZoitkI1DStF5M8bQYXwxQM3i2yy-zerbrL5z05dD8lx3rnltOQjOwLcDgMli67NLG9Irp0DkDUXmfqzcLjzv_oXoTOqwbXMsGNwvk0Exo0z-Ev8Pj8uYKA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>199579166</pqid></control><display><type>article</type><title>Sepsis Induces Diaphragm Electron Transport Chain Dysfunction and Protein Depletion</title><source>Freely Accessible Science Journals</source><source>EZB Free E-Journals</source><creator>Callahan, Leigh A ; Supinski, Gerald S</creator><creatorcontrib>Callahan, Leigh A ; Supinski, Gerald S</creatorcontrib><description>Sepsis significantly alters skeletal muscle mitochondrial function, but the mechanisms responsible for this abnormality are unknown.
We postulated that endotoxin elicits specific changes in electron transport chain proteins that produce derangements in mitochondrial function. To examine this issue, we compared the effects of endotoxin-induced sepsis on mitochondrial ATP (adenosine triphosphate) formation and electron transport chain protein composition.
Diaphragm mitochondrial oxygen consumption and mitochondrial nicotinamide adenine dinucleotide, reduced form, oxidase assays were measured in control rats (n=13) and rats given endotoxin (8 mg/kg/d) for 12 (n=14), 24 (n=14), 36 (n=14), and 48 h (n=13). Electron transport chain subunits from Complexes I, III, IV, and V were isolated using Blue Native polyacrylamide gel electrophoresis techniques.
Endotoxin administration: 1) elicited large reductions in mitochondrial oxygen consumption (e.g., 201+/-3.9 SE natoms O/min/mg for controls and 101+/-4.5 SE natoms O/minutes/mg after 48 h endotoxin, p<0.001), in nicotinamide adenine dinucleotide, reduced form, oxidase activity (p<0.002), and in uncoupled respiration (p<0.001) and 2) induced selective reductions in two subunits of Complex I, three subunits of Complex III, one subunit of Complex IV, and one subunit of Complex V. The time course of depletion of protein subunits mirrored alterations in oxygen consumption.
Our data indicate that endotoxin selectively depletes critical components of the electron transport chain that diminishes electron flow, reduces proton pumping and decreases ATP formation.</description><identifier>ISSN: 1073-449X</identifier><identifier>EISSN: 1535-4970</identifier><identifier>DOI: 10.1164/rccm.200410-1344OC</identifier><identifier>PMID: 15994462</identifier><language>eng</language><publisher>New York, NY: Am Thoracic Soc</publisher><subject>Abdomen ; Adenosine triphosphate ; Adenosine Triphosphate - biosynthesis ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Biological and medical sciences ; Diaphragm - metabolism ; Electron Transport Chain Complex Proteins - physiology ; Electrophoresis, Polyacrylamide Gel ; Emergency and intensive care: infection, septic shock ; Emergency and intensive care: techniques, logistics ; Hypotheses ; Intensive care medicine ; Intensive care unit. Emergency transport systems. Emergency, hospital ward ; Male ; Medical sciences ; Mitochondria ; Mitochondria, Muscle - physiology ; Mitochondrial Diseases - physiopathology ; Multienzyme Complexes - analysis ; Musculoskeletal system ; NADH, NADPH Oxidoreductases - analysis ; Oxygen Consumption ; Proteins ; Protons ; Rats ; Rats, Inbred Strains ; Respiration ; Sepsis ; Sepsis - physiopathology</subject><ispartof>American journal of respiratory and critical care medicine, 2005-10, Vol.172 (7), p.861-868</ispartof><rights>2005 INIST-CNRS</rights><rights>Copyright American Thoracic Society Oct 1, 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-f94b9922c3e4d3559f77bab3bade50a2dcb49617f4ab7fcf217ae10e6a857d223</citedby><cites>FETCH-LOGICAL-c392t-f94b9922c3e4d3559f77bab3bade50a2dcb49617f4ab7fcf217ae10e6a857d223</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17146804$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15994462$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Callahan, Leigh A</creatorcontrib><creatorcontrib>Supinski, Gerald S</creatorcontrib><title>Sepsis Induces Diaphragm Electron Transport Chain Dysfunction and Protein Depletion</title><title>American journal of respiratory and critical care medicine</title><addtitle>Am J Respir Crit Care Med</addtitle><description>Sepsis significantly alters skeletal muscle mitochondrial function, but the mechanisms responsible for this abnormality are unknown.
We postulated that endotoxin elicits specific changes in electron transport chain proteins that produce derangements in mitochondrial function. To examine this issue, we compared the effects of endotoxin-induced sepsis on mitochondrial ATP (adenosine triphosphate) formation and electron transport chain protein composition.
Diaphragm mitochondrial oxygen consumption and mitochondrial nicotinamide adenine dinucleotide, reduced form, oxidase assays were measured in control rats (n=13) and rats given endotoxin (8 mg/kg/d) for 12 (n=14), 24 (n=14), 36 (n=14), and 48 h (n=13). Electron transport chain subunits from Complexes I, III, IV, and V were isolated using Blue Native polyacrylamide gel electrophoresis techniques.
Endotoxin administration: 1) elicited large reductions in mitochondrial oxygen consumption (e.g., 201+/-3.9 SE natoms O/min/mg for controls and 101+/-4.5 SE natoms O/minutes/mg after 48 h endotoxin, p<0.001), in nicotinamide adenine dinucleotide, reduced form, oxidase activity (p<0.002), and in uncoupled respiration (p<0.001) and 2) induced selective reductions in two subunits of Complex I, three subunits of Complex III, one subunit of Complex IV, and one subunit of Complex V. The time course of depletion of protein subunits mirrored alterations in oxygen consumption.
Our data indicate that endotoxin selectively depletes critical components of the electron transport chain that diminishes electron flow, reduces proton pumping and decreases ATP formation.</description><subject>Abdomen</subject><subject>Adenosine triphosphate</subject><subject>Adenosine Triphosphate - biosynthesis</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Diaphragm - metabolism</subject><subject>Electron Transport Chain Complex Proteins - physiology</subject><subject>Electrophoresis, Polyacrylamide Gel</subject><subject>Emergency and intensive care: infection, septic shock</subject><subject>Emergency and intensive care: techniques, logistics</subject><subject>Hypotheses</subject><subject>Intensive care medicine</subject><subject>Intensive care unit. Emergency transport systems. Emergency, hospital ward</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mitochondria</subject><subject>Mitochondria, Muscle - physiology</subject><subject>Mitochondrial Diseases - physiopathology</subject><subject>Multienzyme Complexes - analysis</subject><subject>Musculoskeletal system</subject><subject>NADH, NADPH Oxidoreductases - analysis</subject><subject>Oxygen Consumption</subject><subject>Proteins</subject><subject>Protons</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Respiration</subject><subject>Sepsis</subject><subject>Sepsis - physiopathology</subject><issn>1073-449X</issn><issn>1535-4970</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNpdkE1r3DAQhkVpaD7aP9BDMYUWenCqkWRpdQybpAkEEkgKvYmxLGW1-KuSTcm_r4wXAjlJjJ55Z_QQ8hnoOYAUP6O13TmjVAAtgQtxv31HTqDiVSm0ou_znSpeCqH_HJPTlPaUAtsA_UCOodJaCMlOyOOjG1NIxW3fzNal4jLguIv43BVXrbNTHPriKWKfxiFOxXaHoS8uX5KfezuF_IZ9UzzEYXJL3Y2tW6ofyZHHNrlPh_OM_L6-etrelHf3v263F3el5ZpNpdei1poxy51oeFVpr1SNNa-xcRVF1thaaAnKC6yVt56BQgfUSdxUqmGMn5Hva-4Yh7-zS5PpQrKubbF3w5yM3EjQckMz-PUNuB_m2OfdDGhdKQ1SZoitkI1DStF5M8bQYXwxQM3i2yy-zerbrL5z05dD8lx3rnltOQjOwLcDgMli67NLG9Irp0DkDUXmfqzcLjzv_oXoTOqwbXMsGNwvk0Exo0z-Ev8Pj8uYKA</recordid><startdate>20051001</startdate><enddate>20051001</enddate><creator>Callahan, Leigh A</creator><creator>Supinski, Gerald S</creator><general>Am Thoracic Soc</general><general>American Lung Association</general><general>American Thoracic Society</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20051001</creationdate><title>Sepsis Induces Diaphragm Electron Transport Chain Dysfunction and Protein Depletion</title><author>Callahan, Leigh A ; Supinski, Gerald S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c392t-f94b9922c3e4d3559f77bab3bade50a2dcb49617f4ab7fcf217ae10e6a857d223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Abdomen</topic><topic>Adenosine triphosphate</topic><topic>Adenosine Triphosphate - biosynthesis</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Diaphragm - metabolism</topic><topic>Electron Transport Chain Complex Proteins - physiology</topic><topic>Electrophoresis, Polyacrylamide Gel</topic><topic>Emergency and intensive care: infection, septic shock</topic><topic>Emergency and intensive care: techniques, logistics</topic><topic>Hypotheses</topic><topic>Intensive care medicine</topic><topic>Intensive care unit. Emergency transport systems. Emergency, hospital ward</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mitochondria</topic><topic>Mitochondria, Muscle - physiology</topic><topic>Mitochondrial Diseases - physiopathology</topic><topic>Multienzyme Complexes - analysis</topic><topic>Musculoskeletal system</topic><topic>NADH, NADPH Oxidoreductases - analysis</topic><topic>Oxygen Consumption</topic><topic>Proteins</topic><topic>Protons</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Respiration</topic><topic>Sepsis</topic><topic>Sepsis - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Callahan, Leigh A</creatorcontrib><creatorcontrib>Supinski, Gerald S</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of respiratory and critical care medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Callahan, Leigh A</au><au>Supinski, Gerald S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sepsis Induces Diaphragm Electron Transport Chain Dysfunction and Protein Depletion</atitle><jtitle>American journal of respiratory and critical care medicine</jtitle><addtitle>Am J Respir Crit Care Med</addtitle><date>2005-10-01</date><risdate>2005</risdate><volume>172</volume><issue>7</issue><spage>861</spage><epage>868</epage><pages>861-868</pages><issn>1073-449X</issn><eissn>1535-4970</eissn><abstract>Sepsis significantly alters skeletal muscle mitochondrial function, but the mechanisms responsible for this abnormality are unknown.
We postulated that endotoxin elicits specific changes in electron transport chain proteins that produce derangements in mitochondrial function. To examine this issue, we compared the effects of endotoxin-induced sepsis on mitochondrial ATP (adenosine triphosphate) formation and electron transport chain protein composition.
Diaphragm mitochondrial oxygen consumption and mitochondrial nicotinamide adenine dinucleotide, reduced form, oxidase assays were measured in control rats (n=13) and rats given endotoxin (8 mg/kg/d) for 12 (n=14), 24 (n=14), 36 (n=14), and 48 h (n=13). Electron transport chain subunits from Complexes I, III, IV, and V were isolated using Blue Native polyacrylamide gel electrophoresis techniques.
Endotoxin administration: 1) elicited large reductions in mitochondrial oxygen consumption (e.g., 201+/-3.9 SE natoms O/min/mg for controls and 101+/-4.5 SE natoms O/minutes/mg after 48 h endotoxin, p<0.001), in nicotinamide adenine dinucleotide, reduced form, oxidase activity (p<0.002), and in uncoupled respiration (p<0.001) and 2) induced selective reductions in two subunits of Complex I, three subunits of Complex III, one subunit of Complex IV, and one subunit of Complex V. The time course of depletion of protein subunits mirrored alterations in oxygen consumption.
Our data indicate that endotoxin selectively depletes critical components of the electron transport chain that diminishes electron flow, reduces proton pumping and decreases ATP formation.</abstract><cop>New York, NY</cop><pub>Am Thoracic Soc</pub><pmid>15994462</pmid><doi>10.1164/rccm.200410-1344OC</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1073-449X |
| ispartof | American journal of respiratory and critical care medicine, 2005-10, Vol.172 (7), p.861-868 |
| issn | 1073-449X 1535-4970 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_68619680 |
| source | Freely Accessible Science Journals; EZB Free E-Journals |
| subjects | Abdomen Adenosine triphosphate Adenosine Triphosphate - biosynthesis Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Biological and medical sciences Diaphragm - metabolism Electron Transport Chain Complex Proteins - physiology Electrophoresis, Polyacrylamide Gel Emergency and intensive care: infection, septic shock Emergency and intensive care: techniques, logistics Hypotheses Intensive care medicine Intensive care unit. Emergency transport systems. Emergency, hospital ward Male Medical sciences Mitochondria Mitochondria, Muscle - physiology Mitochondrial Diseases - physiopathology Multienzyme Complexes - analysis Musculoskeletal system NADH, NADPH Oxidoreductases - analysis Oxygen Consumption Proteins Protons Rats Rats, Inbred Strains Respiration Sepsis Sepsis - physiopathology |
| title | Sepsis Induces Diaphragm Electron Transport Chain Dysfunction and Protein Depletion |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-04T01%3A48%3A43IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Sepsis%20Induces%20Diaphragm%20Electron%20Transport%20Chain%20Dysfunction%20and%20Protein%20Depletion&rft.jtitle=American%20journal%20of%20respiratory%20and%20critical%20care%20medicine&rft.au=Callahan,%20Leigh%20A&rft.date=2005-10-01&rft.volume=172&rft.issue=7&rft.spage=861&rft.epage=868&rft.pages=861-868&rft.issn=1073-449X&rft.eissn=1535-4970&rft_id=info:doi/10.1164/rccm.200410-1344OC&rft_dat=%3Cproquest_cross%3E68619680%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c392t-f94b9922c3e4d3559f77bab3bade50a2dcb49617f4ab7fcf217ae10e6a857d223%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=199579166&rft_id=info:pmid/15994462&rfr_iscdi=true |