Flupenthixol and cefotiam: effects on vitamin A metabolism in rats
We examined the alterations in vitamin A metabolism as a result of flupenthixol or cefotiam administration. The impact of these drugs on indices of vitamin A status was evaluated in Brown Norway and Long–Evans rats. Intramuscular drug administration for 28 d resulted in a decline in systemic retinol...
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| Veröffentlicht in: | British journal of nutrition 2004-10, Vol.92 (4), p.597-605 |
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| creator | Schindler, Rainer Fielenbach, Tanja Rave, Gerhard |
| description | We examined the alterations in vitamin A metabolism as a result of flupenthixol or cefotiam administration. The impact of these drugs on indices of vitamin A status was evaluated in Brown Norway and Long–Evans rats. Intramuscular drug administration for 28 d resulted in a decline in systemic retinol. Changes in circulating retinol with time for chronic dosing showed drug treatment (P |
| doi_str_mv | 10.1079/BJN20041236 |
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The impact of these drugs on indices of vitamin A status was evaluated in Brown Norway and Long–Evans rats. Intramuscular drug administration for 28 d resulted in a decline in systemic retinol. Changes in circulating retinol with time for chronic dosing showed drug treatment (P<0·001) and time (P<0·03) to be significant factors, but rat strain (P=0·33) was not a significant factor. Flupenthixol was the most active retinol-lowering compound (P<0·005). At the end of the 28 d period, hepatic retinyl ester hydrolase activity was greater in drug-treated rats than in controls (P<0·05). With regard to effects on liver reserves: (1) flupenthixol treatment resulted in vitamin A depletion (P<0·05); (2) cefotiam treatment stimulated vitamin A accumulation; (3) distinctive patterns of retinol and its esters were seen in response to treatment. It is reasonable to assume that the drugs interfere with vitamin A in at least two ways: (1) lowering of plasma retinol, an early event in the interaction, may be caused by inhibition of hepatic holo-retinol-binding protein secretion or stimulation of clearance, or both; (2) when plasma retinol levels are persistently low, and as the hepatic deposits of the xenobiotics build up, there are changes in the vitamin A pool size and composition of the liver. Candidate enzymes are retinyl ester hydrolase and cytochrome P450. The relationship between these two events will be studied in further detail.</description><identifier>ISSN: 0007-1145</identifier><identifier>EISSN: 1475-2662</identifier><identifier>DOI: 10.1079/BJN20041236</identifier><identifier>PMID: 15522128</identifier><identifier>CODEN: BJNUAV</identifier><language>eng</language><publisher>Cambridge, UK: Cambridge University Press</publisher><subject>Animals ; Anti-Bacterial Agents - pharmacology ; Antibiotics ; Biological and medical sciences ; Carboxylic Ester Hydrolases - metabolism ; Cefotiam - pharmacology ; Cefotiam–vitamin A interaction ; Cytochrome ; Drug Interactions ; Drugs ; Enzymes ; Esters ; Flupenthixol - pharmacology ; Flupenthixol–vitamin A interaction ; Human subjects ; Infections ; Kidney - metabolism ; Liver ; Liver - metabolism ; Male ; Medical sciences ; Metabolism ; Neuropharmacology ; Penicillin ; Peritoneal dialysis ; Pharmacology. Drug treatments ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) ; Psychology. Psychoanalysis. Psychiatry ; Psychopharmacology ; Rats ; Rats, Inbred BN ; Rats, Long-Evans ; Retinyl ester hydrolase ; Vitamin A ; Vitamin A - blood ; Vitamin A - metabolism ; Weight Gain - drug effects ; Xenobiotics</subject><ispartof>British journal of nutrition, 2004-10, Vol.92 (4), p.597-605</ispartof><rights>Copyright © The Nutrition Society 2004</rights><rights>2004 INIST-CNRS</rights><rights>The Nutrition Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-d738651e93fff42de6cd0d144c734f1b936755c1a2ee344538a4f5da2a80f1ef3</citedby><cites>FETCH-LOGICAL-c504t-d738651e93fff42de6cd0d144c734f1b936755c1a2ee344538a4f5da2a80f1ef3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16199922$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15522128$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schindler, Rainer</creatorcontrib><creatorcontrib>Fielenbach, Tanja</creatorcontrib><creatorcontrib>Rave, Gerhard</creatorcontrib><title>Flupenthixol and cefotiam: effects on vitamin A metabolism in rats</title><title>British journal of nutrition</title><addtitle>Br J Nutr</addtitle><description>We examined the alterations in vitamin A metabolism as a result of flupenthixol or cefotiam administration. The impact of these drugs on indices of vitamin A status was evaluated in Brown Norway and Long–Evans rats. Intramuscular drug administration for 28 d resulted in a decline in systemic retinol. Changes in circulating retinol with time for chronic dosing showed drug treatment (P<0·001) and time (P<0·03) to be significant factors, but rat strain (P=0·33) was not a significant factor. Flupenthixol was the most active retinol-lowering compound (P<0·005). At the end of the 28 d period, hepatic retinyl ester hydrolase activity was greater in drug-treated rats than in controls (P<0·05). With regard to effects on liver reserves: (1) flupenthixol treatment resulted in vitamin A depletion (P<0·05); (2) cefotiam treatment stimulated vitamin A accumulation; (3) distinctive patterns of retinol and its esters were seen in response to treatment. It is reasonable to assume that the drugs interfere with vitamin A in at least two ways: (1) lowering of plasma retinol, an early event in the interaction, may be caused by inhibition of hepatic holo-retinol-binding protein secretion or stimulation of clearance, or both; (2) when plasma retinol levels are persistently low, and as the hepatic deposits of the xenobiotics build up, there are changes in the vitamin A pool size and composition of the liver. Candidate enzymes are retinyl ester hydrolase and cytochrome P450. The relationship between these two events will be studied in further detail.</description><subject>Animals</subject><subject>Anti-Bacterial Agents - pharmacology</subject><subject>Antibiotics</subject><subject>Biological and medical sciences</subject><subject>Carboxylic Ester Hydrolases - metabolism</subject><subject>Cefotiam - pharmacology</subject><subject>Cefotiam–vitamin A interaction</subject><subject>Cytochrome</subject><subject>Drug Interactions</subject><subject>Drugs</subject><subject>Enzymes</subject><subject>Esters</subject><subject>Flupenthixol - pharmacology</subject><subject>Flupenthixol–vitamin A interaction</subject><subject>Human subjects</subject><subject>Infections</subject><subject>Kidney - metabolism</subject><subject>Liver</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolism</subject><subject>Neuropharmacology</subject><subject>Penicillin</subject><subject>Peritoneal dialysis</subject><subject>Pharmacology. Drug treatments</subject><subject>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopharmacology</subject><subject>Rats</subject><subject>Rats, Inbred BN</subject><subject>Rats, Long-Evans</subject><subject>Retinyl ester hydrolase</subject><subject>Vitamin A</subject><subject>Vitamin A - blood</subject><subject>Vitamin A - metabolism</subject><subject>Weight Gain - drug effects</subject><subject>Xenobiotics</subject><issn>0007-1145</issn><issn>1475-2662</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</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>eNpt0EtPGzEUBWALtYI07Yp9O0Lqqhrq69fMsANEwktUVWHDxrrx2NR0HsF2Kvj3NUrUdNGNrSt_OtY9hOwDPQRaNV9PLm8YpQIYVztkAqKSJVOKvSETSmlVAgi5R97F-JjHGmizS_ZASsaA1RNyMutWSzukn_557Aoc2sJYNyaP_VFhnbMmxWIcit8-Ye-H4rjobcLF2PnYF3kOmOJ78tZhF-2HzT0ld7Oz29Pz8vrb_OL0-Lo0kopUthWvlQTbcOecYK1VpqUtCGEqLhwsGq4qKQ0gs5YLIXmNwskWGdbUgXV8Sg7WucswPq1sTPpxXIUhf6kZ8JoLlo8p-bJGJowxBuv0Mvgew4sGql_r0v_UlfXHTeRq0dt2azf9ZPB5AzAa7FzAwfi4dQqapmEsu3LtfEz2-e87hl9aVbySWs2_a3V1M7u956Dn2X9ae4ejxoeQM-9-MAqcAmWS1s020WC_CL59sNt1_7fKH-aTln4</recordid><startdate>20041001</startdate><enddate>20041001</enddate><creator>Schindler, Rainer</creator><creator>Fielenbach, Tanja</creator><creator>Rave, Gerhard</creator><general>Cambridge University Press</general><scope>FBQ</scope><scope>BSCLL</scope><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>7QP</scope><scope>7RV</scope><scope>7T5</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope></search><sort><creationdate>20041001</creationdate><title>Flupenthixol and cefotiam: effects on vitamin A metabolism in rats</title><author>Schindler, Rainer ; Fielenbach, Tanja ; Rave, Gerhard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-d738651e93fff42de6cd0d144c734f1b936755c1a2ee344538a4f5da2a80f1ef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Anti-Bacterial Agents - pharmacology</topic><topic>Antibiotics</topic><topic>Biological and medical sciences</topic><topic>Carboxylic Ester Hydrolases - metabolism</topic><topic>Cefotiam - pharmacology</topic><topic>Cefotiam–vitamin A interaction</topic><topic>Cytochrome</topic><topic>Drug Interactions</topic><topic>Drugs</topic><topic>Enzymes</topic><topic>Esters</topic><topic>Flupenthixol - pharmacology</topic><topic>Flupenthixol–vitamin A interaction</topic><topic>Human subjects</topic><topic>Infections</topic><topic>Kidney - metabolism</topic><topic>Liver</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolism</topic><topic>Neuropharmacology</topic><topic>Penicillin</topic><topic>Peritoneal dialysis</topic><topic>Pharmacology. Drug treatments</topic><topic>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopharmacology</topic><topic>Rats</topic><topic>Rats, Inbred BN</topic><topic>Rats, Long-Evans</topic><topic>Retinyl ester hydrolase</topic><topic>Vitamin A</topic><topic>Vitamin A - blood</topic><topic>Vitamin A - metabolism</topic><topic>Weight Gain - drug effects</topic><topic>Xenobiotics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schindler, Rainer</creatorcontrib><creatorcontrib>Fielenbach, Tanja</creatorcontrib><creatorcontrib>Rave, Gerhard</creatorcontrib><collection>AGRIS</collection><collection>Istex</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Agriculture Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest research library</collection><collection>Research Library (Corporate)</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 Basic</collection><jtitle>British journal of nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schindler, Rainer</au><au>Fielenbach, Tanja</au><au>Rave, Gerhard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Flupenthixol and cefotiam: effects on vitamin A metabolism in rats</atitle><jtitle>British journal of nutrition</jtitle><addtitle>Br J Nutr</addtitle><date>2004-10-01</date><risdate>2004</risdate><volume>92</volume><issue>4</issue><spage>597</spage><epage>605</epage><pages>597-605</pages><issn>0007-1145</issn><eissn>1475-2662</eissn><coden>BJNUAV</coden><abstract>We examined the alterations in vitamin A metabolism as a result of flupenthixol or cefotiam administration. The impact of these drugs on indices of vitamin A status was evaluated in Brown Norway and Long–Evans rats. Intramuscular drug administration for 28 d resulted in a decline in systemic retinol. Changes in circulating retinol with time for chronic dosing showed drug treatment (P<0·001) and time (P<0·03) to be significant factors, but rat strain (P=0·33) was not a significant factor. Flupenthixol was the most active retinol-lowering compound (P<0·005). At the end of the 28 d period, hepatic retinyl ester hydrolase activity was greater in drug-treated rats than in controls (P<0·05). With regard to effects on liver reserves: (1) flupenthixol treatment resulted in vitamin A depletion (P<0·05); (2) cefotiam treatment stimulated vitamin A accumulation; (3) distinctive patterns of retinol and its esters were seen in response to treatment. It is reasonable to assume that the drugs interfere with vitamin A in at least two ways: (1) lowering of plasma retinol, an early event in the interaction, may be caused by inhibition of hepatic holo-retinol-binding protein secretion or stimulation of clearance, or both; (2) when plasma retinol levels are persistently low, and as the hepatic deposits of the xenobiotics build up, there are changes in the vitamin A pool size and composition of the liver. Candidate enzymes are retinyl ester hydrolase and cytochrome P450. The relationship between these two events will be studied in further detail.</abstract><cop>Cambridge, UK</cop><pub>Cambridge University Press</pub><pmid>15522128</pmid><doi>10.1079/BJN20041236</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Anti-Bacterial Agents - pharmacology Antibiotics Biological and medical sciences Carboxylic Ester Hydrolases - metabolism Cefotiam - pharmacology Cefotiam–vitamin A interaction Cytochrome Drug Interactions Drugs Enzymes Esters Flupenthixol - pharmacology Flupenthixol–vitamin A interaction Human subjects Infections Kidney - metabolism Liver Liver - metabolism Male Medical sciences Metabolism Neuropharmacology Penicillin Peritoneal dialysis Pharmacology. Drug treatments Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) Psychology. Psychoanalysis. Psychiatry Psychopharmacology Rats Rats, Inbred BN Rats, Long-Evans Retinyl ester hydrolase Vitamin A Vitamin A - blood Vitamin A - metabolism Weight Gain - drug effects Xenobiotics |
| title | Flupenthixol and cefotiam: effects on vitamin A metabolism in rats |
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