Dual role of endogenous nitric oxide in tumor necrosis factor shock: induced NO tempers oxidative stress
Tumor necrosis factor (TNF) is involved in pathologies like septic shock, inflammatory bowel disease and rheumatoid arthritis. TNF and lipopolysaccharide can incite lethal shock, in which cardiovascular collapse is centrally orchestrated by the vasodilating free radical nitric oxide (NO). However, N...
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| Veröffentlicht in: | Cellular and molecular life sciences : CMLS 2005-07, Vol.62 (14), p.1632-1640 |
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| description | Tumor necrosis factor (TNF) is involved in pathologies like septic shock, inflammatory bowel disease and rheumatoid arthritis. TNF and lipopolysaccharide can incite lethal shock, in which cardiovascular collapse is centrally orchestrated by the vasodilating free radical nitric oxide (NO). However, NO synthase (NOS) inhibition causes increased morbidity and/or mortality, suggesting a dual role for NO. To investigate the potential protective role of NO during TNF shock, we treated mice with TNF with or without NOS inhibition. Experiments in endothelial- NOS- and inducible NOS-deficient mice identified inducible NOS as the source of protective NO. Distinctive TNF-induced lipid peroxidation, especially in liver and kidney, was aggravated by NOS inhibition. In addition, various antioxidant treatments and a phospholipase A2 (PLA2) inhibitor prevented sensitization by NOS inhibition. Together, these in vivo results indicate that induced NO not only causes hemodynamic collapse, but is also essential for curbing TNF-induced oxidative stress, which appears to hinge on PLA2-dependent mechanisms. |
| doi_str_mv | 10.1007/s00018-005-5142-z |
| format | Article |
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TNF and lipopolysaccharide can incite lethal shock, in which cardiovascular collapse is centrally orchestrated by the vasodilating free radical nitric oxide (NO). However, NO synthase (NOS) inhibition causes increased morbidity and/or mortality, suggesting a dual role for NO. To investigate the potential protective role of NO during TNF shock, we treated mice with TNF with or without NOS inhibition. Experiments in endothelial- NOS- and inducible NOS-deficient mice identified inducible NOS as the source of protective NO. Distinctive TNF-induced lipid peroxidation, especially in liver and kidney, was aggravated by NOS inhibition. In addition, various antioxidant treatments and a phospholipase A2 (PLA2) inhibitor prevented sensitization by NOS inhibition. Together, these in vivo results indicate that induced NO not only causes hemodynamic collapse, but is also essential for curbing TNF-induced oxidative stress, which appears to hinge on PLA2-dependent mechanisms.</description><identifier>ISSN: 1420-682X</identifier><identifier>EISSN: 1420-9071</identifier><identifier>DOI: 10.1007/s00018-005-5142-z</identifier><identifier>PMID: 15990956</identifier><language>eng</language><publisher>Switzerland: Springer Nature B.V</publisher><subject>Aldehydes - analysis ; Animals ; Antioxidants - pharmacology ; Butylated Hydroxyanisole - pharmacology ; Catalase - pharmacology ; Cyclic N-Oxides - pharmacology ; Enzyme Inhibitors - pharmacology ; Female ; Immunohistochemistry ; Inflammatory bowel disease ; Injections, Intravenous ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide - physiology ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitric Oxide Synthase - genetics ; Nitric Oxide Synthase - metabolism ; Oxidative Stress ; Peroxidation ; Phospholipases A - antagonists & inhibitors ; Phospholipases A2 ; Reactive Oxygen Species - metabolism ; Rheumatoid arthritis ; Rodents ; Shock - etiology ; Shock - metabolism ; Shock - mortality ; Spin Labels ; Superoxide Dismutase - pharmacology ; Survival Rate ; Tumor Necrosis Factors - pharmacology ; Tumor Necrosis Factors - toxicity</subject><ispartof>Cellular and molecular life sciences : CMLS, 2005-07, Vol.62 (14), p.1632-1640</ispartof><rights>Birkhäuser Verlag, Basel 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c425t-d02def30b266f5f5c96e1ff64bb34a504be823b811a220a0cdfe5fd00d80cec3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11139077/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11139077/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,729,782,786,887,27931,27932,53798,53800</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15990956$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cauwels, A</creatorcontrib><creatorcontrib>Bultinck, J</creatorcontrib><creatorcontrib>Brouckaert, P</creatorcontrib><title>Dual role of endogenous nitric oxide in tumor necrosis factor shock: induced NO tempers oxidative stress</title><title>Cellular and molecular life sciences : CMLS</title><addtitle>Cell Mol Life Sci</addtitle><description>Tumor necrosis factor (TNF) is involved in pathologies like septic shock, inflammatory bowel disease and rheumatoid arthritis. TNF and lipopolysaccharide can incite lethal shock, in which cardiovascular collapse is centrally orchestrated by the vasodilating free radical nitric oxide (NO). However, NO synthase (NOS) inhibition causes increased morbidity and/or mortality, suggesting a dual role for NO. To investigate the potential protective role of NO during TNF shock, we treated mice with TNF with or without NOS inhibition. Experiments in endothelial- NOS- and inducible NOS-deficient mice identified inducible NOS as the source of protective NO. Distinctive TNF-induced lipid peroxidation, especially in liver and kidney, was aggravated by NOS inhibition. In addition, various antioxidant treatments and a phospholipase A2 (PLA2) inhibitor prevented sensitization by NOS inhibition. Together, these in vivo results indicate that induced NO not only causes hemodynamic collapse, but is also essential for curbing TNF-induced oxidative stress, which appears to hinge on PLA2-dependent mechanisms.</description><subject>Aldehydes - analysis</subject><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Butylated Hydroxyanisole - pharmacology</subject><subject>Catalase - pharmacology</subject><subject>Cyclic N-Oxides - pharmacology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Female</subject><subject>Immunohistochemistry</subject><subject>Inflammatory bowel disease</subject><subject>Injections, Intravenous</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Oxidative Stress</subject><subject>Peroxidation</subject><subject>Phospholipases A - antagonists & inhibitors</subject><subject>Phospholipases A2</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Rheumatoid arthritis</subject><subject>Rodents</subject><subject>Shock - etiology</subject><subject>Shock - metabolism</subject><subject>Shock - mortality</subject><subject>Spin Labels</subject><subject>Superoxide Dismutase - pharmacology</subject><subject>Survival Rate</subject><subject>Tumor Necrosis Factors - pharmacology</subject><subject>Tumor Necrosis Factors - toxicity</subject><issn>1420-682X</issn><issn>1420-9071</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdUctuFDEQtBCIPOADuCCLA7chbc_YO8MFRSGBSBG55MDN8tjtrMOMvdieCPL18bIrXqfuVleVuqsIecXgHQNYnWQAYH0DIBrBOt48PCGHtUIzwIo93fey518PyFHOdxUsei6fkwMmhgEGIQ_J-uOiJ5rihDQ6isHGWwxxyTT4kryh8Ye3SH2gZZljogFNitln6rQpdc7raL69r3u7GLT0yzUtOG8w5V9EXfw90lwS5vyCPHN6yvhyX4_JzcX5zdnn5ur60-XZ6VVjOi5KY4FbdC2MXEonnDCDROac7Max7bSAbsSet2PPmOYcNBjrUDgLYHswaNpj8mEnu1nGGa3BUJKe1Cb5WaefKmqv_t0Ev1a38V4xxtpq26oqvN0rpPh9wVzU7LPBadIBqzFK9iCqp0MFvvkPeBeXFOpzqu1kv-K826qxHWjrW07ofp_CQG1DVLsQVQ1RbUNUD5Xz-u8f_jD2qbWPGDSbHA</recordid><startdate>20050701</startdate><enddate>20050701</enddate><creator>Cauwels, A</creator><creator>Bultinck, J</creator><creator>Brouckaert, P</creator><general>Springer Nature B.V</general><general>Birkhäuser-Verlag</general><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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20050701</creationdate><title>Dual role of endogenous nitric oxide in tumor necrosis factor shock: induced NO tempers oxidative stress</title><author>Cauwels, A ; Bultinck, J ; Brouckaert, P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c425t-d02def30b266f5f5c96e1ff64bb34a504be823b811a220a0cdfe5fd00d80cec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Aldehydes - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cellular and molecular life sciences : CMLS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cauwels, A</au><au>Bultinck, J</au><au>Brouckaert, P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dual role of endogenous nitric oxide in tumor necrosis factor shock: induced NO tempers oxidative stress</atitle><jtitle>Cellular and molecular life sciences : CMLS</jtitle><addtitle>Cell Mol Life Sci</addtitle><date>2005-07-01</date><risdate>2005</risdate><volume>62</volume><issue>14</issue><spage>1632</spage><epage>1640</epage><pages>1632-1640</pages><issn>1420-682X</issn><eissn>1420-9071</eissn><abstract>Tumor necrosis factor (TNF) is involved in pathologies like septic shock, inflammatory bowel disease and rheumatoid arthritis. TNF and lipopolysaccharide can incite lethal shock, in which cardiovascular collapse is centrally orchestrated by the vasodilating free radical nitric oxide (NO). However, NO synthase (NOS) inhibition causes increased morbidity and/or mortality, suggesting a dual role for NO. To investigate the potential protective role of NO during TNF shock, we treated mice with TNF with or without NOS inhibition. Experiments in endothelial- NOS- and inducible NOS-deficient mice identified inducible NOS as the source of protective NO. Distinctive TNF-induced lipid peroxidation, especially in liver and kidney, was aggravated by NOS inhibition. In addition, various antioxidant treatments and a phospholipase A2 (PLA2) inhibitor prevented sensitization by NOS inhibition. Together, these in vivo results indicate that induced NO not only causes hemodynamic collapse, but is also essential for curbing TNF-induced oxidative stress, which appears to hinge on PLA2-dependent mechanisms.</abstract><cop>Switzerland</cop><pub>Springer Nature B.V</pub><pmid>15990956</pmid><doi>10.1007/s00018-005-5142-z</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cellular and molecular life sciences : CMLS, 2005-07, Vol.62 (14), p.1632-1640 |
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| subjects | Aldehydes - analysis Animals Antioxidants - pharmacology Butylated Hydroxyanisole - pharmacology Catalase - pharmacology Cyclic N-Oxides - pharmacology Enzyme Inhibitors - pharmacology Female Immunohistochemistry Inflammatory bowel disease Injections, Intravenous Mice Mice, Inbred C57BL Mice, Knockout NG-Nitroarginine Methyl Ester - pharmacology Nitric oxide Nitric Oxide - metabolism Nitric Oxide - physiology Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase - genetics Nitric Oxide Synthase - metabolism Oxidative Stress Peroxidation Phospholipases A - antagonists & inhibitors Phospholipases A2 Reactive Oxygen Species - metabolism Rheumatoid arthritis Rodents Shock - etiology Shock - metabolism Shock - mortality Spin Labels Superoxide Dismutase - pharmacology Survival Rate Tumor Necrosis Factors - pharmacology Tumor Necrosis Factors - toxicity |
| title | Dual role of endogenous nitric oxide in tumor necrosis factor shock: induced NO tempers oxidative stress |
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