Stoffwechsel und Analyse von Leukotrienen in vivo
Identifieur interne : 000F87 ( Main/Corpus ); précédent : 000F86; suivant : 000F88Stoffwechsel und Analyse von Leukotrienen in vivo
Auteurs : D. KepplerSource :
- Klinische Wochenschrift [ 0023-2173 ] ; 1988-10-01.
Abstract
Summary: Leukotrienes are potent mediators of inflammatory and allergic reactions involved, among others, in endotoxin action and shock, tissue trauma, acute liver injury, hepatorenal syndrome, inflammatory bowel disease, acute pancreatitis, and asthma. Studies on metabolism and analysis of these arachidonate metabolites in vivo are a prerequisite for an improved understanding of their role under physiological and pathophysiological conditions and for the development of inhibitors of leukotriene synthesis and of receptor antagonists. Leukotriene C4 and its metabolites, collectively termed the cysteinyl leukotrienes, are predominantly inactivated by the liver. Rapid hepatocellular uptake is followed by partial metabolic inactivation, comprising ω-oxidation and N-acetylation of leukotriene E4, and excretion into bile. A minor portion of the cysteinyl leukotrienes undergoes enterohepatic circulation. In all species investigated so far, hepatobiliary elimination of cysteinyl leukotrienes predominates over renal excretion. Analysis of the systemic production of cysteinyl leukotrienes in vivo has been accomplished by radioimmunological determination of species-characteristic index metabolites in bile after their separation by high-performance liquid chromatography. The mercapturate N-acetyl-leukotriene E4 is the index metabolite of choice in the rat. In man, leukotriene E4 is the predominant endogenous cysteinyl leukotriene in both bile and urine. The amounts of cysteinyl leukotrienes detected under various pathophysiological conditions may be sufficient to induce known phenomena associated with the respective disease. As shown under experimental conditions, inhibition of leukotriene synthesis or receptor antagonism can serve as therapeutic approaches.
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DOI: 10.1007/BF01733441
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Keppler</name><affiliation><mods:affiliation>Deutsches Krebsforschungszentrum, Abteilung Tumorbiochemie, Heidelberg</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:4010E799B631240493F7ABC3C70791AF6458B8FB</idno><date when="1988" year="1988">1988</date><idno type="doi">10.1007/BF01733441</idno><idno type="url">https://api.istex.fr/document/4010E799B631240493F7ABC3C70791AF6458B8FB/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000F87</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="de">Stoffwechsel und Analyse von Leukotrienen in vivo</title><author><name sortKey="Keppler, D" sort="Keppler, D" uniqKey="Keppler D" first="D." last="Keppler">D. Keppler</name><affiliation><mods:affiliation>Deutsches Krebsforschungszentrum, Abteilung Tumorbiochemie, Heidelberg</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Klinische Wochenschrift</title><title level="j" type="abbrev">Klin Wochenschr</title><idno type="ISSN">0023-2173</idno><idno type="eISSN">1432-1440</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1988-10-01">1988-10-01</date><biblScope unit="volume">66</biblScope><biblScope unit="issue">20</biblScope><biblScope unit="page" from="997">997</biblScope><biblScope unit="page" to="1004">1004</biblScope></imprint><idno type="ISSN">0023-2173</idno></series><idno type="istex">4010E799B631240493F7ABC3C70791AF6458B8FB</idno><idno type="DOI">10.1007/BF01733441</idno><idno type="ArticleID">Art1</idno><idno type="ArticleID">BF01733441</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0023-2173</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="de">de</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Leukotrienes are potent mediators of inflammatory and allergic reactions involved, among others, in endotoxin action and shock, tissue trauma, acute liver injury, hepatorenal syndrome, inflammatory bowel disease, acute pancreatitis, and asthma. Studies on metabolism and analysis of these arachidonate metabolites in vivo are a prerequisite for an improved understanding of their role under physiological and pathophysiological conditions and for the development of inhibitors of leukotriene synthesis and of receptor antagonists. Leukotriene C4 and its metabolites, collectively termed the cysteinyl leukotrienes, are predominantly inactivated by the liver. Rapid hepatocellular uptake is followed by partial metabolic inactivation, comprising ω-oxidation and N-acetylation of leukotriene E4, and excretion into bile. A minor portion of the cysteinyl leukotrienes undergoes enterohepatic circulation. In all species investigated so far, hepatobiliary elimination of cysteinyl leukotrienes predominates over renal excretion. Analysis of the systemic production of cysteinyl leukotrienes in vivo has been accomplished by radioimmunological determination of species-characteristic index metabolites in bile after their separation by high-performance liquid chromatography. The mercapturate N-acetyl-leukotriene E4 is the index metabolite of choice in the rat. In man, leukotriene E4 is the predominant endogenous cysteinyl leukotriene in both bile and urine. The amounts of cysteinyl leukotrienes detected under various pathophysiological conditions may be sufficient to induce known phenomena associated with the respective disease. As shown under experimental conditions, inhibition of leukotriene synthesis or receptor antagonism can serve as therapeutic approaches.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>D. Keppler</name><affiliations><json:string>Deutsches Krebsforschungszentrum, Abteilung Tumorbiochemie, Heidelberg</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>deu</json:string></lang><value>Cysteinyl leukotrienes</value></json:item><json:item><lang><json:string>deu</json:string></lang><value>Hepatobiliary elimination</value></json:item><json:item><lang><json:string>deu</json:string></lang><value>Hepatorenal syndrome</value></json:item><json:item><lang><json:string>deu</json:string></lang><value>Leukotriene metabolism</value></json:item><json:item><lang><json:string>deu</json:string></lang><value>Leukotriene analysis</value></json:item><json:item><lang><json:string>deu</json:string></lang><value>ω-Oxidation of leukotrienes</value></json:item><json:item><lang><json:string>deu</json:string></lang><value>Pancreatitis</value></json:item><json:item><lang><json:string>deu</json:string></lang><value>HPLC : High-performance liquid chromatography, Hochleistungsflüssigkeitschromatographie</value></json:item><json:item><lang><json:string>deu</json:string></lang><value>LT : Leukotrien</value></json:item><json:item><lang><json:string>deu</json:string></lang><value>LTC4 : (S)5-Hydroxy-(R)-6-S-glutathionyl-7,9-trans-11,14-cis-eikosatetraenoat</value></json:item><json:item><lang><json:string>deu</json:string></lang><value>LTD4 : (S)5-Hydroxy-(R)-6-S-cysteinylglycyl-7,9-trans-11,14-cis-eikosatetraenoat</value></json:item><json:item><lang><json:string>deu</json:string></lang><value>LTE4 : (S)5-Hydroxy-(R)-6-S-cysteinyl-7,9-trans-11,14-cis-eikosatetraenoat</value></json:item><json:item><lang><json:string>deu</json:string></lang><value>LTE4NAc : N-Acetyl-LTE4</value></json:item></subject><language><json:string>deu</json:string></language><abstract>Summary: Leukotrienes are potent mediators of inflammatory and allergic reactions involved, among others, in endotoxin action and shock, tissue trauma, acute liver injury, hepatorenal syndrome, inflammatory bowel disease, acute pancreatitis, and asthma. Studies on metabolism and analysis of these arachidonate metabolites in vivo are a prerequisite for an improved understanding of their role under physiological and pathophysiological conditions and for the development of inhibitors of leukotriene synthesis and of receptor antagonists. Leukotriene C4 and its metabolites, collectively termed the cysteinyl leukotrienes, are predominantly inactivated by the liver. Rapid hepatocellular uptake is followed by partial metabolic inactivation, comprising ω-oxidation and N-acetylation of leukotriene E4, and excretion into bile. A minor portion of the cysteinyl leukotrienes undergoes enterohepatic circulation. In all species investigated so far, hepatobiliary elimination of cysteinyl leukotrienes predominates over renal excretion. Analysis of the systemic production of cysteinyl leukotrienes in vivo has been accomplished by radioimmunological determination of species-characteristic index metabolites in bile after their separation by high-performance liquid chromatography. The mercapturate N-acetyl-leukotriene E4 is the index metabolite of choice in the rat. In man, leukotriene E4 is the predominant endogenous cysteinyl leukotriene in both bile and urine. The amounts of cysteinyl leukotrienes detected under various pathophysiological conditions may be sufficient to induce known phenomena associated with the respective disease. As shown under experimental conditions, inhibition of leukotriene synthesis or receptor antagonism can serve as therapeutic approaches.</abstract><qualityIndicators><score>6.811</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>13</keywordCount><abstractCharCount>1776</abstractCharCount><pdfWordCount>4075</pdfWordCount><pdfCharCount>30555</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>228</abstractWordCount></qualityIndicators><title>Stoffwechsel und Analyse von Leukotrienen in vivo</title><genre><json:string>research-article</json:string></genre><host><volume>66</volume><pages><last>1004</last><first>997</first></pages><issn><json:string>0023-2173</json:string></issn><issue>20</issue><subject><json:item><value>Molecular Medicine</value></json:item><json:item><value>Internal Medicine</value></json:item></subject><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1432-1440</json:string></eissn><title>Klinische Wochenschrift</title><publicationDate>1988</publicationDate><copyrightDate>1988</copyrightDate></host><publicationDate>1988</publicationDate><copyrightDate>1988</copyrightDate><doi><json:string>10.1007/BF01733441</json:string></doi><id>4010E799B631240493F7ABC3C70791AF6458B8FB</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/4010E799B631240493F7ABC3C70791AF6458B8FB/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/4010E799B631240493F7ABC3C70791AF6458B8FB/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/4010E799B631240493F7ABC3C70791AF6458B8FB/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="de">Stoffwechsel und Analyse von Leukotrienen in vivo</title><title level="a" type="alt" xml:lang="en">Metabolism and analysis of leukotrienes in vivo</title><respStmt xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><availability><p>SPRINGER</p></availability><date>1988-07-05</date></publicationStmt><notesStmt><note>Heinrich-Wieland-Preis-Vorlesung</note><note>Vortrag anläßlich der Preis-Verleihung am 30. Oktober 1987</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="de">Stoffwechsel und Analyse von Leukotrienen in vivo</title><title level="a" type="alt" xml:lang="en">Metabolism and analysis of leukotrienes in vivo</title><author><persName><forename type="first">D.</forename><surname>Keppler</surname></persName><affiliation>Deutsches Krebsforschungszentrum, Abteilung Tumorbiochemie, Heidelberg</affiliation></author></analytic><monogr><title level="j">Klinische Wochenschrift</title><title level="j" type="abbrev">Klin Wochenschr</title><idno type="JournalID">109</idno><idno type="pISSN">0023-2173</idno><idno type="eISSN">1432-1440</idno><idno type="IssueArticleCount">20</idno><idno type="VolumeIssueCount">24</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1988-10-01"></date><biblScope unit="volume">66</biblScope><biblScope unit="issue">20</biblScope><biblScope unit="page" from="997">997</biblScope><biblScope unit="page" to="1004">1004</biblScope></imprint></monogr><idno type="istex">4010E799B631240493F7ABC3C70791AF6458B8FB</idno><idno type="DOI">10.1007/BF01733441</idno><idno type="ArticleID">Art1</idno><idno type="ArticleID">BF01733441</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1988-07-05</date></creation><langUsage><language ident="de">de</language></langUsage><abstract xml:lang="en"><p>Summary: Leukotrienes are potent mediators of inflammatory and allergic reactions involved, among others, in endotoxin action and shock, tissue trauma, acute liver injury, hepatorenal syndrome, inflammatory bowel disease, acute pancreatitis, and asthma. Studies on metabolism and analysis of these arachidonate metabolites in vivo are a prerequisite for an improved understanding of their role under physiological and pathophysiological conditions and for the development of inhibitors of leukotriene synthesis and of receptor antagonists. Leukotriene C4 and its metabolites, collectively termed the cysteinyl leukotrienes, are predominantly inactivated by the liver. Rapid hepatocellular uptake is followed by partial metabolic inactivation, comprising ω-oxidation and N-acetylation of leukotriene E4, and excretion into bile. A minor portion of the cysteinyl leukotrienes undergoes enterohepatic circulation. In all species investigated so far, hepatobiliary elimination of cysteinyl leukotrienes predominates over renal excretion. Analysis of the systemic production of cysteinyl leukotrienes in vivo has been accomplished by radioimmunological determination of species-characteristic index metabolites in bile after their separation by high-performance liquid chromatography. The mercapturate N-acetyl-leukotriene E4 is the index metabolite of choice in the rat. In man, leukotriene E4 is the predominant endogenous cysteinyl leukotriene in both bile and urine. The amounts of cysteinyl leukotrienes detected under various pathophysiological conditions may be sufficient to induce known phenomena associated with the respective disease. As shown under experimental conditions, inhibition of leukotriene synthesis or receptor antagonism can serve as therapeutic approaches.</p></abstract><textClass><keywords scheme="keyword"><list><head>Abkürzungen</head><item><term>HPLC</term><term>High-performance liquid chromatography, Hochleistungsflüssigkeitschromatographie</term></item><item><term>LT</term><term>Leukotrien</term></item><item><term>LTC4</term><term>(S)5-Hydroxy-(R)-6-S-glutathionyl-7,9-trans-11,14-cis-eikosatetraenoat</term></item><item><term>LTD4</term><term>(S)5-Hydroxy-(R)-6-S-cysteinylglycyl-7,9-trans-11,14-cis-eikosatetraenoat</term></item><item><term>LTE4</term><term>(S)5-Hydroxy-(R)-6-S-cysteinyl-7,9-trans-11,14-cis-eikosatetraenoat</term></item><item><term>LTE4NAc</term><term>N-Acetyl-LTE4</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Biomedicine</head><item><term>Molecular Medicine</term></item><item><term>Internal Medicine</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1988-07-05">Created</change><change when="1988-10-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-2">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/4010E799B631240493F7ABC3C70791AF6458B8FB/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Springer, Publisher found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer-Verlag</PublisherName><PublisherLocation>Berlin/Heidelberg</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>109</JournalID><JournalPrintISSN>0023-2173</JournalPrintISSN><JournalElectronicISSN>1432-1440</JournalElectronicISSN><JournalTitle>Klinische Wochenschrift</JournalTitle><JournalAbbreviatedTitle>Klin Wochenschr</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Biomedicine</JournalSubject><JournalSubject Type="Secondary">Molecular Medicine</JournalSubject><JournalSubject Type="Secondary">Internal Medicine</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>66</VolumeIDStart><VolumeIDEnd>66</VolumeIDEnd><VolumeIssueCount>24</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>20</IssueIDStart><IssueIDEnd>20</IssueIDEnd><IssueArticleCount>20</IssueArticleCount><IssueHistory><CoverDate><DateString>17. Oktober 1988</DateString><Year>1988</Year><Month>10</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1988</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art1"><ArticleInfo Language="De" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF01733441</ArticleID><ArticleDOI>10.1007/BF01733441</ArticleDOI><ArticleSequenceNumber>1</ArticleSequenceNumber><ArticleTitle Language="De">Stoffwechsel und Analyse von Leukotrienen in vivo</ArticleTitle><ArticleTitle Language="En">Metabolism and analysis of leukotrienes in vivo</ArticleTitle><ArticleCategory>Heinrich-Wieland-Preis-Vorlesung</ArticleCategory><ArticleFirstPage>997</ArticleFirstPage><ArticleLastPage>1004</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2005</Year><Month>5</Month><Day>4</Day></RegistrationDate><Received><Year>1988</Year><Month>7</Month><Day>5</Day></Received><Accepted><Year>1988</Year><Month>7</Month><Day>5</Day></Accepted></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1988</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>109</JournalID><VolumeIDStart>66</VolumeIDStart><VolumeIDEnd>66</VolumeIDEnd><IssueIDStart>20</IssueIDStart><IssueIDEnd>20</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>D.</GivenName><FamilyName>Keppler</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Deutsches Krebsforschungszentrum</OrgDivision><OrgName>Abteilung Tumorbiochemie</OrgName><OrgAddress><City>Heidelberg</City></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Leukotrienes are potent mediators of inflammatory and allergic reactions involved, among others, in endotoxin action and shock, tissue trauma, acute liver injury, hepatorenal syndrome, inflammatory bowel disease, acute pancreatitis, and asthma. Studies on metabolism and analysis of these arachidonate metabolites in vivo are a prerequisite for an improved understanding of their role under physiological and pathophysiological conditions and for the development of inhibitors of leukotriene synthesis and of receptor antagonists. Leukotriene C<Subscript>4</Subscript> and its metabolites, collectively termed the cysteinyl leukotrienes, are predominantly inactivated by the liver. Rapid hepatocellular uptake is followed by partial metabolic inactivation, comprising ω-oxidation and N-acetylation of leukotriene E<Subscript>4</Subscript>, and excretion into bile. A minor portion of the cysteinyl leukotrienes undergoes enterohepatic circulation. In all species investigated so far, hepatobiliary elimination of cysteinyl leukotrienes predominates over renal excretion.</Para><Para>Analysis of the systemic production of cysteinyl leukotrienes in vivo has been accomplished by radioimmunological determination of species-characteristic index metabolites in bile after their separation by high-performance liquid chromatography. The mercapturate N-acetyl-leukotriene E<Subscript>4</Subscript> is the index metabolite of choice in the rat. In man, leukotriene E<Subscript>4</Subscript> is the predominant endogenous cysteinyl leukotriene in both bile and urine. The amounts of cysteinyl leukotrienes detected under various pathophysiological conditions may be sufficient to induce known phenomena associated with the respective disease. As shown under experimental conditions, inhibition of leukotriene synthesis or receptor antagonism can serve as therapeutic approaches.</Para></Abstract><KeywordGroup Language="En"><Heading>Key words</Heading><Keyword>Cysteinyl leukotrienes</Keyword><Keyword>Hepatobiliary elimination</Keyword><Keyword>Hepatorenal syndrome</Keyword><Keyword>Leukotriene metabolism</Keyword><Keyword>Leukotriene analysis</Keyword><Keyword>ω-Oxidation of leukotrienes</Keyword><Keyword>Pancreatitis</Keyword></KeywordGroup><AbbreviationGroup><Heading>Abkürzungen</Heading><DefinitionList><DefinitionListEntry><Term>HPLC</Term><Description><Para>High-performance liquid chromatography, Hochleistungsflüssigkeitschromatographie</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>LT</Term><Description><Para>Leukotrien</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>LTC<Subscript>4</Subscript></Term><Description><Para>(<Emphasis Type="Italic">S</Emphasis>)5-Hydroxy-(<Emphasis Type="Italic">R</Emphasis>)-6-<Emphasis Type="Italic">S</Emphasis>-glutathionyl-7,9-<Emphasis Type="Italic">trans</Emphasis>-11,14-<Emphasis Type="Italic">cis</Emphasis>-eikosatetraenoat</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>LTD<Subscript>4</Subscript></Term><Description><Para>(<Emphasis Type="Italic">S</Emphasis>)5-Hydroxy-(<Emphasis Type="Italic">R</Emphasis>)-6-<Emphasis Type="Italic">S</Emphasis>-cysteinylglycyl-7,9-<Emphasis Type="Italic">trans</Emphasis>-11,14-<Emphasis Type="Italic">cis</Emphasis>-eikosatetraenoat</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>LTE<Subscript>4</Subscript></Term><Description><Para>(<Emphasis Type="Italic">S</Emphasis>)5-Hydroxy-(<Emphasis Type="Italic">R</Emphasis>)-6-<Emphasis Type="Italic">S</Emphasis>-cysteinyl-7,9-<Emphasis Type="Italic">trans</Emphasis>-11,14-<Emphasis Type="Italic">cis</Emphasis>-eikosatetraenoat</Para></Description></DefinitionListEntry><DefinitionListEntry><Term>LTE<Subscript>4</Subscript>NAc</Term><Description><Para>N-Acetyl-LTE<Subscript>4</Subscript></Para></Description></DefinitionListEntry></DefinitionList></AbbreviationGroup><ArticleNote Type="Misc"><SimplePara>Vortrag anläßlich der Preis-Verleihung am 30. Oktober 1987</SimplePara></ArticleNote></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="de"><title>Stoffwechsel und Analyse von Leukotrienen in vivo</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="de"><title>Stoffwechsel und Analyse von Leukotrienen in vivo</title></titleInfo><titleInfo lang="en"><title>Metabolism and analysis of leukotrienes in vivo</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Metabolism and analysis of leukotrienes in vivo</title></titleInfo><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Keppler</namePart><affiliation>Deutsches Krebsforschungszentrum, Abteilung Tumorbiochemie, Heidelberg</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Berlin/Heidelberg</placeTerm></place><dateCreated encoding="w3cdtf">1988-07-05</dateCreated><dateIssued encoding="w3cdtf">1988-10-01</dateIssued><copyrightDate encoding="w3cdtf">1988</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">de</languageTerm><languageTerm type="code" authority="iso639-2b">deu</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Summary: Leukotrienes are potent mediators of inflammatory and allergic reactions involved, among others, in endotoxin action and shock, tissue trauma, acute liver injury, hepatorenal syndrome, inflammatory bowel disease, acute pancreatitis, and asthma. Studies on metabolism and analysis of these arachidonate metabolites in vivo are a prerequisite for an improved understanding of their role under physiological and pathophysiological conditions and for the development of inhibitors of leukotriene synthesis and of receptor antagonists. Leukotriene C4 and its metabolites, collectively termed the cysteinyl leukotrienes, are predominantly inactivated by the liver. Rapid hepatocellular uptake is followed by partial metabolic inactivation, comprising ω-oxidation and N-acetylation of leukotriene E4, and excretion into bile. A minor portion of the cysteinyl leukotrienes undergoes enterohepatic circulation. In all species investigated so far, hepatobiliary elimination of cysteinyl leukotrienes predominates over renal excretion. Analysis of the systemic production of cysteinyl leukotrienes in vivo has been accomplished by radioimmunological determination of species-characteristic index metabolites in bile after their separation by high-performance liquid chromatography. The mercapturate N-acetyl-leukotriene E4 is the index metabolite of choice in the rat. In man, leukotriene E4 is the predominant endogenous cysteinyl leukotriene in both bile and urine. The amounts of cysteinyl leukotrienes detected under various pathophysiological conditions may be sufficient to induce known phenomena associated with the respective disease. As shown under experimental conditions, inhibition of leukotriene synthesis or receptor antagonism can serve as therapeutic approaches.</abstract><note>Heinrich-Wieland-Preis-Vorlesung</note><note>Vortrag anläßlich der Preis-Verleihung am 30. Oktober 1987</note><subject><genre>Abkürzungen</genre><topic>HPLC : High-performance liquid chromatography, Hochleistungsflüssigkeitschromatographie</topic><topic>LT : Leukotrien</topic><topic>LTC4 : (S)5-Hydroxy-(R)-6-S-glutathionyl-7,9-trans-11,14-cis-eikosatetraenoat</topic><topic>LTD4 : (S)5-Hydroxy-(R)-6-S-cysteinylglycyl-7,9-trans-11,14-cis-eikosatetraenoat</topic><topic>LTE4 : (S)5-Hydroxy-(R)-6-S-cysteinyl-7,9-trans-11,14-cis-eikosatetraenoat</topic><topic>LTE4NAc : N-Acetyl-LTE4</topic></subject><relatedItem type="host"><titleInfo><title>Klinische Wochenschrift</title></titleInfo><titleInfo type="abbreviated"><title>Klin Wochenschr</title></titleInfo><genre type="Journal" displayLabel="Archive Journal"></genre><originInfo><dateIssued encoding="w3cdtf">1988-10-01</dateIssued><copyrightDate encoding="w3cdtf">1988</copyrightDate></originInfo><subject><genre>Biomedicine</genre><topic>Molecular Medicine</topic><topic>Internal Medicine</topic></subject><identifier type="ISSN">0023-2173</identifier><identifier type="eISSN">1432-1440</identifier><identifier type="JournalID">109</identifier><identifier type="IssueArticleCount">20</identifier><identifier type="VolumeIssueCount">24</identifier><part><date>1988</date><detail type="volume"><number>66</number><caption>vol.</caption></detail><detail type="issue"><number>20</number><caption>no.</caption></detail><extent unit="pages"><start>997</start><end>1004</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 1988</recordOrigin></recordInfo></relatedItem><identifier type="istex">4010E799B631240493F7ABC3C70791AF6458B8FB</identifier><identifier type="DOI">10.1007/BF01733441</identifier><identifier type="ArticleID">Art1</identifier><identifier type="ArticleID">BF01733441</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag</accessCondition><recordInfo><recordContentSource>SPRINGER</recordContentSource><recordOrigin>Springer-Verlag, 1988</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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