EXCRETION OF MALONDIALDEHYDE, FORMALDEHYDE, ACETALDEHYDE AND ACETONE IN THE URINE OF RATS FOLLOWING ACUTE AND CHRONIC ADMINISTRATION OF ETHANOL
Identifieur interne : 002673 ( Istex/Corpus ); précédent : 002672; suivant : 002674EXCRETION OF MALONDIALDEHYDE, FORMALDEHYDE, ACETALDEHYDE AND ACETONE IN THE URINE OF RATS FOLLOWING ACUTE AND CHRONIC ADMINISTRATION OF ETHANOL
Auteurs : Sandra E. File ; J. Moser ; D. Bagchi ; P. L. Akubue ; S. J. StohsSource :
- Alcohol and Alcoholism [ 0735-0414 ] ; 1993-05.
Abstract
Recent studies have shown that xenobiotics which induce oxidative Stress result in an increased production and excretion of acetaldehyde (ACT), formaldehyde (FA), acetone (ACON) and malondialdehyde (MDA) in the urine of rats. We have therefore examined the effect of acute and chronic ethanol administration on the excretion of these four lipid metabolites in female Sprague-Dawley rats. Urine samples were collected over dry ice for 6 hr time periods. Aliquots of urine were derivatized with 2,4-dinitrophenylhydrazine HCl, and extracted with n-pentane. High pressure liquid chromatography (HPLC) was used to quantitate and the hydrazones of the four lipid metabolite products. Following a single, oral, acute dose of 5 g ethanol/kg, urinary excretion of ACT increased approximately 5.8-fold from 6 to 12 hr post-treatment, and decreased thereafter. FA excretion decreased by approximately 50% from 0 to 12 hr, returned to control values in the 18–24 hr urine samples, and was 1.3-fold greater than control values at 42–48 hr. ACON increased 3.1-fold over control values from 0 to 30 hr and remained elevated throughout the remaining 18 hr of the study. The excretion of MDA increased approximately 1.5-fold from 18 to 36 hr, then remained constant through the 48 hr time point. In a separate series of experiments, a chronic oral dose of 0.5 g ethanol/kg was administered to rats for 10 consecutive days and the urinary excretion of the lipid metabolites MDA, FA, ACT and ACON was examined for 11 days, beginning with the first day of ethanol administration. During the chronic administration of ethanol, a significant increase in the urinary excretion of ACT began on day 4. An increase in ACON excretion was first observed on day 6, and increases in MDA and FAexcretion were first observed on days 8 and 10, respectively. The results clearly demonstrate that both acute and chronic alcohol consumption markedly afier lipid metabolism and the excretion of lipid metabolites.
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DOI: 10.1093/oxfordjournals.alcalc.a045375
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Creighton University, Omaha, NE 68178, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Moser, J" sort="Moser, J" uniqKey="Moser J" first="J." last="Moser">J. Moser</name><affiliation><mods:affiliation>School of Pharmacy and Allied Health. Creighton University, Omaha, NE 68178, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Bagchi, D" sort="Bagchi, D" uniqKey="Bagchi D" first="D." last="Bagchi">D. Bagchi</name><affiliation><mods:affiliation>School of Pharmacy and Allied Health. Creighton University, Omaha, NE 68178, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Akubue, P L" sort="Akubue, P L" uniqKey="Akubue P" first="P. L." last="Akubue">P. L. Akubue</name><affiliation><mods:affiliation>School of Pharmacy and Allied Health. Creighton University, Omaha, NE 68178, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Stohs, S J" sort="Stohs, S J" uniqKey="Stohs S" first="S. J." last="Stohs">S. J. Stohs</name><affiliation><mods:affiliation>School of Pharmacy and Allied Health. Creighton University, Omaha, NE 68178, U.S.A.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Alcohol and Alcoholism</title><idno type="ISSN">0735-0414</idno><idno type="eISSN">1464-3502</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="1993-05">1993-05</date><biblScope unit="volume">28</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="287">287</biblScope><biblScope unit="page" to="295">295</biblScope></imprint><idno type="ISSN">0735-0414</idno></series><idno type="istex">6B6EB6C9C10BF5A0A704C765180316B4EBF99C18</idno><idno type="DOI">10.1093/oxfordjournals.alcalc.a045375</idno><idno type="ArticleID">28.3.287</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0735-0414</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Recent studies have shown that xenobiotics which induce oxidative Stress result in an increased production and excretion of acetaldehyde (ACT), formaldehyde (FA), acetone (ACON) and malondialdehyde (MDA) in the urine of rats. We have therefore examined the effect of acute and chronic ethanol administration on the excretion of these four lipid metabolites in female Sprague-Dawley rats. Urine samples were collected over dry ice for 6 hr time periods. Aliquots of urine were derivatized with 2,4-dinitrophenylhydrazine HCl, and extracted with n-pentane. High pressure liquid chromatography (HPLC) was used to quantitate and the hydrazones of the four lipid metabolite products. Following a single, oral, acute dose of 5 g ethanol/kg, urinary excretion of ACT increased approximately 5.8-fold from 6 to 12 hr post-treatment, and decreased thereafter. FA excretion decreased by approximately 50% from 0 to 12 hr, returned to control values in the 18–24 hr urine samples, and was 1.3-fold greater than control values at 42–48 hr. ACON increased 3.1-fold over control values from 0 to 30 hr and remained elevated throughout the remaining 18 hr of the study. The excretion of MDA increased approximately 1.5-fold from 18 to 36 hr, then remained constant through the 48 hr time point. In a separate series of experiments, a chronic oral dose of 0.5 g ethanol/kg was administered to rats for 10 consecutive days and the urinary excretion of the lipid metabolites MDA, FA, ACT and ACON was examined for 11 days, beginning with the first day of ethanol administration. During the chronic administration of ethanol, a significant increase in the urinary excretion of ACT began on day 4. An increase in ACON excretion was first observed on day 6, and increases in MDA and FAexcretion were first observed on days 8 and 10, respectively. The results clearly demonstrate that both acute and chronic alcohol consumption markedly afier lipid metabolism and the excretion of lipid metabolites.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>SANDRA E. FILE</name><affiliations><json:string>School of Pharmacy and Allied Health. 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High pressure liquid chromatography (HPLC) was used to quantitate and the hydrazones of the four lipid metabolite products. Following a single, oral, acute dose of 5 g ethanol/kg, urinary excretion of ACT increased approximately 5.8-fold from 6 to 12 hr post-treatment, and decreased thereafter. FA excretion decreased by approximately 50% from 0 to 12 hr, returned to control values in the 18–24 hr urine samples, and was 1.3-fold greater than control values at 42–48 hr. ACON increased 3.1-fold over control values from 0 to 30 hr and remained elevated throughout the remaining 18 hr of the study. The excretion of MDA increased approximately 1.5-fold from 18 to 36 hr, then remained constant through the 48 hr time point. In a separate series of experiments, a chronic oral dose of 0.5 g ethanol/kg was administered to rats for 10 consecutive days and the urinary excretion of the lipid metabolites MDA, FA, ACT and ACON was examined for 11 days, beginning with the first day of ethanol administration. During the chronic administration of ethanol, a significant increase in the urinary excretion of ACT began on day 4. An increase in ACON excretion was first observed on day 6, and increases in MDA and FAexcretion were first observed on days 8 and 10, respectively. 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Creighton University, Omaha, NE 68178, U.S.A.</affiliation></author><author><persName><forename type="first">J.</forename><surname>MOSER</surname></persName><affiliation>School of Pharmacy and Allied Health. Creighton University, Omaha, NE 68178, U.S.A.</affiliation></author><author><persName><forename type="first">D.</forename><surname>BAGCHI</surname></persName><affiliation>School of Pharmacy and Allied Health. Creighton University, Omaha, NE 68178, U.S.A.</affiliation></author><author><persName><forename type="first">P.l.</forename><surname>AKUBUE</surname></persName><affiliation>School of Pharmacy and Allied Health. Creighton University, Omaha, NE 68178, U.S.A.</affiliation></author><author><persName><forename type="first">S. J.</forename><surname>STOHS</surname></persName><affiliation>School of Pharmacy and Allied Health. Creighton University, Omaha, NE 68178, U.S.A.</affiliation></author></analytic><monogr><title level="j">Alcohol and Alcoholism</title><idno type="pISSN">0735-0414</idno><idno type="eISSN">1464-3502</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="1993-05"></date><biblScope unit="volume">28</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="287">287</biblScope><biblScope unit="page" to="295">295</biblScope></imprint></monogr><idno type="istex">6B6EB6C9C10BF5A0A704C765180316B4EBF99C18</idno><idno type="DOI">10.1093/oxfordjournals.alcalc.a045375</idno><idno type="ArticleID">28.3.287</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1993</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Recent studies have shown that xenobiotics which induce oxidative Stress result in an increased production and excretion of acetaldehyde (ACT), formaldehyde (FA), acetone (ACON) and malondialdehyde (MDA) in the urine of rats. We have therefore examined the effect of acute and chronic ethanol administration on the excretion of these four lipid metabolites in female Sprague-Dawley rats. Urine samples were collected over dry ice for 6 hr time periods. Aliquots of urine were derivatized with 2,4-dinitrophenylhydrazine HCl, and extracted with n-pentane. High pressure liquid chromatography (HPLC) was used to quantitate and the hydrazones of the four lipid metabolite products. Following a single, oral, acute dose of 5 g ethanol/kg, urinary excretion of ACT increased approximately 5.8-fold from 6 to 12 hr post-treatment, and decreased thereafter. FA excretion decreased by approximately 50% from 0 to 12 hr, returned to control values in the 18–24 hr urine samples, and was 1.3-fold greater than control values at 42–48 hr. ACON increased 3.1-fold over control values from 0 to 30 hr and remained elevated throughout the remaining 18 hr of the study. The excretion of MDA increased approximately 1.5-fold from 18 to 36 hr, then remained constant through the 48 hr time point. In a separate series of experiments, a chronic oral dose of 0.5 g ethanol/kg was administered to rats for 10 consecutive days and the urinary excretion of the lipid metabolites MDA, FA, ACT and ACON was examined for 11 days, beginning with the first day of ethanol administration. During the chronic administration of ethanol, a significant increase in the urinary excretion of ACT began on day 4. An increase in ACON excretion was first observed on day 6, and increases in MDA and FAexcretion were first observed on days 8 and 10, respectively. The results clearly demonstrate that both acute and chronic alcohol consumption markedly afier lipid metabolism and the excretion of lipid metabolites.</p></abstract><textClass><keywords scheme="keyword"><list><item><term>Articles</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1993-05">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-14">References added</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-21">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/6B6EB6C9C10BF5A0A704C765180316B4EBF99C18/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">alcalc</journal-id><journal-id journal-id-type="publisher-id">alcalc</journal-id><journal-id journal-id-type="pmc">alcalc</journal-id><journal-title>Alcohol and Alcoholism</journal-title><issn pub-type="epub">1464-3502</issn><issn pub-type="ppub">0735-0414</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">28.3.287</article-id><article-id pub-id-type="doi">10.1093/oxfordjournals.alcalc.a045375</article-id><article-categories><subj-group><subject>Articles</subject></subj-group></article-categories><title-group><article-title>EXCRETION OF MALONDIALDEHYDE, FORMALDEHYDE, ACETALDEHYDE AND ACETONE IN THE URINE OF RATS FOLLOWING ACUTE AND CHRONIC ADMINISTRATION OF ETHANOL</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>FILE</surname><given-names>SANDRA E.</given-names></name></contrib><contrib contrib-type="author"><name><surname>MOSER</surname><given-names>J.</given-names></name></contrib><contrib contrib-type="author"><name><surname>BAGCHI</surname><given-names>D.</given-names></name></contrib><contrib contrib-type="author"><name><surname>AKUBUE</surname><given-names>P.l.</given-names></name></contrib><contrib contrib-type="author"><name><surname>STOHS</surname><given-names>S. J.</given-names></name><xref ref-type="corresp" rid="cor1"><sup>*</sup></xref></contrib><aff><institution>School of Pharmacy and Allied Health. Creighton University</institution> <addr-line>Omaha, NE 68178, U.S.A.</addr-line></aff></contrib-group><author-notes><corresp id="cor1"><sup>*</sup>Author to whom correspondence should be addressed</corresp></author-notes><pub-date pub-type="ppub"><month>5</month><year>1993</year></pub-date><volume>28</volume><issue>3</issue><fpage>287</fpage><lpage>295</lpage><history><date date-type="received"><day>03</day><month>8</month><year>1992</year></date><date date-type="rev-recd"><day>17</day><month>11</month><year>1992</year></date><date date-type="accepted"><day>28</day><month>12</month><year>1992</year></date></history><copyright-statement>© 1993 Medical Council on Alcholism</copyright-statement><copyright-year>1993</copyright-year><abstract><p>Recent studies have shown that xenobiotics which induce oxidative Stress result in an increased production and excretion of acetaldehyde (ACT), formaldehyde (FA), acetone (ACON) and malondialdehyde (MDA) in the urine of rats. We have therefore examined the effect of acute and chronic ethanol administration on the excretion of these four lipid metabolites in female Sprague-Dawley rats. Urine samples were collected over dry ice for 6 hr time periods. Aliquots of urine were derivatized with 2,4-dinitrophenylhydrazine HCl, and extracted with <italic>n</italic>-pentane. High pressure liquid chromatography (HPLC) was used to quantitate and the hydrazones of the four lipid metabolite products. Following a single, oral, acute dose of 5 g ethanol/kg, urinary excretion of ACT increased approximately 5.8-fold from 6 to 12 hr post-treatment, and decreased thereafter. FA excretion decreased by approximately 50% from 0 to 12 hr, returned to control values in the 18–24 hr urine samples, and was 1.3-fold greater than control values at 42–48 hr. ACON increased 3.1-fold over control values from 0 to 30 hr and remained elevated throughout the remaining 18 hr of the study. The excretion of MDA increased approximately 1.5-fold from 18 to 36 hr, then remained constant through the 48 hr time point. In a separate series of experiments, a chronic oral dose of 0.5 g ethanol/kg was administered to rats for 10 consecutive days and the urinary excretion of the lipid metabolites MDA, FA, ACT and ACON was examined for 11 days, beginning with the first day of ethanol administration. During the chronic administration of ethanol, a significant increase in the urinary excretion of ACT began on day 4. An increase in ACON excretion was first observed on day 6, and increases in MDA and FAexcretion were first observed on days 8 and 10, respectively. The results clearly demonstrate that both acute and chronic alcohol consumption markedly afier lipid metabolism and the excretion of lipid metabolites.</p></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>EXCRETION OF MALONDIALDEHYDE, FORMALDEHYDE, ACETALDEHYDE AND ACETONE IN THE URINE OF RATS FOLLOWING ACUTE AND CHRONIC ADMINISTRATION OF ETHANOL</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>EXCRETION OF MALONDIALDEHYDE, FORMALDEHYDE, ACETALDEHYDE AND ACETONE IN THE URINE OF RATS FOLLOWING ACUTE AND CHRONIC ADMINISTRATION OF ETHANOL</title></titleInfo><name type="personal"><namePart type="given">SANDRA E.</namePart><namePart type="family">FILE</namePart><affiliation>School of Pharmacy and Allied Health. Creighton University, Omaha, NE 68178, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">MOSER</namePart><affiliation>School of Pharmacy and Allied Health. Creighton University, Omaha, NE 68178, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D.</namePart><namePart type="family">BAGCHI</namePart><affiliation>School of Pharmacy and Allied Health. Creighton University, Omaha, NE 68178, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.l.</namePart><namePart type="family">AKUBUE</namePart><affiliation>School of Pharmacy and Allied Health. Creighton University, Omaha, NE 68178, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S. J.</namePart><namePart type="family">STOHS</namePart><affiliation>School of Pharmacy and Allied Health. Creighton University, Omaha, NE 68178, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><topic>Articles</topic></subject><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">1993-05</dateIssued><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Recent studies have shown that xenobiotics which induce oxidative Stress result in an increased production and excretion of acetaldehyde (ACT), formaldehyde (FA), acetone (ACON) and malondialdehyde (MDA) in the urine of rats. We have therefore examined the effect of acute and chronic ethanol administration on the excretion of these four lipid metabolites in female Sprague-Dawley rats. Urine samples were collected over dry ice for 6 hr time periods. Aliquots of urine were derivatized with 2,4-dinitrophenylhydrazine HCl, and extracted with n-pentane. High pressure liquid chromatography (HPLC) was used to quantitate and the hydrazones of the four lipid metabolite products. Following a single, oral, acute dose of 5 g ethanol/kg, urinary excretion of ACT increased approximately 5.8-fold from 6 to 12 hr post-treatment, and decreased thereafter. FA excretion decreased by approximately 50% from 0 to 12 hr, returned to control values in the 18–24 hr urine samples, and was 1.3-fold greater than control values at 42–48 hr. ACON increased 3.1-fold over control values from 0 to 30 hr and remained elevated throughout the remaining 18 hr of the study. The excretion of MDA increased approximately 1.5-fold from 18 to 36 hr, then remained constant through the 48 hr time point. In a separate series of experiments, a chronic oral dose of 0.5 g ethanol/kg was administered to rats for 10 consecutive days and the urinary excretion of the lipid metabolites MDA, FA, ACT and ACON was examined for 11 days, beginning with the first day of ethanol administration. During the chronic administration of ethanol, a significant increase in the urinary excretion of ACT began on day 4. An increase in ACON excretion was first observed on day 6, and increases in MDA and FAexcretion were first observed on days 8 and 10, respectively. The results clearly demonstrate that both acute and chronic alcohol consumption markedly afier lipid metabolism and the excretion of lipid metabolites.</abstract><note type="author-notes">*Author to whom correspondence should be addressed</note><relatedItem type="host"><titleInfo><title>Alcohol and Alcoholism</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0735-0414</identifier><identifier type="eISSN">1464-3502</identifier><identifier type="PublisherID">alcalc</identifier><identifier type="PublisherID-hwp">alcalc</identifier><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>28</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>287</start><end>295</end></extent></part></relatedItem><identifier type="istex">6B6EB6C9C10BF5A0A704C765180316B4EBF99C18</identifier><identifier type="DOI">10.1093/oxfordjournals.alcalc.a045375</identifier><identifier type="ArticleID">28.3.287</identifier><accessCondition type="use and reproduction" contentType="copyright">© 1993 Medical Council on Alcholism</accessCondition><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><annexes><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/6B6EB6C9C10BF5A0A704C765180316B4EBF99C18/annexes/pdf</uri></json:item></annexes><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/6B6EB6C9C10BF5A0A704C765180316B4EBF99C18/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">SUBSTANCE ABUSE</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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