The differential effects of hepatotoxicants on the sulfation pathway in rats

This study characterized the effects of liver damage produced by a variety of hepatotoxicants on several components of the sulfation pathway in rats. Specifically, the concentration of cosubstrate, adenosine 3′-phosphate 5′-phosphosulfate (PAPS), and the hepatic capacity for PAPS synthesis were meas...

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Veröffentlicht in:Toxicology and applied pharmacology 1991-09, Vol.110 (3), p.365-373
Hauptverfasser: Maziasz, T.J., Liu, J., Madhu, C., Klaassen, C.D.
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Liu, J.
Madhu, C.
Klaassen, C.D.
description This study characterized the effects of liver damage produced by a variety of hepatotoxicants on several components of the sulfation pathway in rats. Specifically, the concentration of cosubstrate, adenosine 3′-phosphate 5′-phosphosulfate (PAPS), and the hepatic capacity for PAPS synthesis were measured in livers of rats treated with carbon tetrachloride (CCl 4), 1,1-dichloroethylene (DCE), α-naphthylisothiocyanate (ANIT), aflatoxin B 1 (ATX), allyl alcohol (AA), bromobenzene (BB), cadmium chloride (Cd), or thioacetamide (TA). Liver damage was assessed by measuring serum sorbitol dehydrogenase (SDH) and alanine aminotransferase (ALT) activities as well as by histopathological examination. Hepatic PAPS concentration was generally decreased as a result of treatment with hepatotoxicants (35–80% of control), although BB, AA, and ANIT were without effect. Maximal hepatic capacity for PAPS synthesis, determined as the activities of PAPS synthetic enzymes, ATP sulfurylase, and APS kinase, was selectively decreased by the hepatotoxicants. ATP sulfurylase activity was decreased by Cd and TA (55 and 62% of control, respectively), whereas APS kinase activity was decreased by Cd, TA, BB, and DCE (60–77% of control, respectively). In addition, phenol sulfotransferase (PST) activity was measured toward 1- and 2-naphthol in order to determine whether apparent changes in PST activity in damaged livers are substrate-dependent. Treatment with hepatotoxicants generally decreased 1-naphthol-directed PST activity but not PST activity directed toward 2-naphthol. In conclusion, (1) not all xenobiotic-induced liver injury results in decreased hepatic PAPS concentration, (2) some hepatotoxicants decrease PAPS concentration by a mechanism other than decreased cosubstrate synthesis, and (3) the effect of hepatotoxicants on PST activity is dependent upon the choice of substrate used in the enzymatic assay.
doi_str_mv 10.1016/0041-008X(91)90039-H
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Specifically, the concentration of cosubstrate, adenosine 3′-phosphate 5′-phosphosulfate (PAPS), and the hepatic capacity for PAPS synthesis were measured in livers of rats treated with carbon tetrachloride (CCl 4), 1,1-dichloroethylene (DCE), α-naphthylisothiocyanate (ANIT), aflatoxin B 1 (ATX), allyl alcohol (AA), bromobenzene (BB), cadmium chloride (Cd), or thioacetamide (TA). Liver damage was assessed by measuring serum sorbitol dehydrogenase (SDH) and alanine aminotransferase (ALT) activities as well as by histopathological examination. Hepatic PAPS concentration was generally decreased as a result of treatment with hepatotoxicants (35–80% of control), although BB, AA, and ANIT were without effect. Maximal hepatic capacity for PAPS synthesis, determined as the activities of PAPS synthetic enzymes, ATP sulfurylase, and APS kinase, was selectively decreased by the hepatotoxicants. ATP sulfurylase activity was decreased by Cd and TA (55 and 62% of control, respectively), whereas APS kinase activity was decreased by Cd, TA, BB, and DCE (60–77% of control, respectively). In addition, phenol sulfotransferase (PST) activity was measured toward 1- and 2-naphthol in order to determine whether apparent changes in PST activity in damaged livers are substrate-dependent. Treatment with hepatotoxicants generally decreased 1-naphthol-directed PST activity but not PST activity directed toward 2-naphthol. 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Methods ; L-Iditol 2-Dehydrogenase - blood ; Liver - drug effects ; Liver - enzymology ; Liver - metabolism ; Liver Diseases - enzymology ; Liver Diseases - metabolism ; Male ; Medical sciences ; Phosphoadenosine Phosphosulfate - biosynthesis ; Propanols ; Rats ; Rats, Inbred Strains ; Sulfates - metabolism ; Thioacetamide - adverse effects ; Toxicology</subject><ispartof>Toxicology and applied pharmacology, 1991-09, Vol.110 (3), p.365-373</ispartof><rights>1991</rights><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-92d028ce6511ba0add4c4f814f7cb2f99e867ad51367167901d188a1d76b8e3d3</citedby><cites>FETCH-LOGICAL-c417t-92d028ce6511ba0add4c4f814f7cb2f99e867ad51367167901d188a1d76b8e3d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0041-008X(91)90039-H$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,782,786,3552,27931,27932,46002</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=5045502$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1949007$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Maziasz, T.J.</creatorcontrib><creatorcontrib>Liu, J.</creatorcontrib><creatorcontrib>Madhu, C.</creatorcontrib><creatorcontrib>Klaassen, C.D.</creatorcontrib><title>The differential effects of hepatotoxicants on the sulfation pathway in rats</title><title>Toxicology and applied pharmacology</title><addtitle>Toxicol Appl Pharmacol</addtitle><description>This study characterized the effects of liver damage produced by a variety of hepatotoxicants on several components of the sulfation pathway in rats. Specifically, the concentration of cosubstrate, adenosine 3′-phosphate 5′-phosphosulfate (PAPS), and the hepatic capacity for PAPS synthesis were measured in livers of rats treated with carbon tetrachloride (CCl 4), 1,1-dichloroethylene (DCE), α-naphthylisothiocyanate (ANIT), aflatoxin B 1 (ATX), allyl alcohol (AA), bromobenzene (BB), cadmium chloride (Cd), or thioacetamide (TA). Liver damage was assessed by measuring serum sorbitol dehydrogenase (SDH) and alanine aminotransferase (ALT) activities as well as by histopathological examination. Hepatic PAPS concentration was generally decreased as a result of treatment with hepatotoxicants (35–80% of control), although BB, AA, and ANIT were without effect. Maximal hepatic capacity for PAPS synthesis, determined as the activities of PAPS synthetic enzymes, ATP sulfurylase, and APS kinase, was selectively decreased by the hepatotoxicants. ATP sulfurylase activity was decreased by Cd and TA (55 and 62% of control, respectively), whereas APS kinase activity was decreased by Cd, TA, BB, and DCE (60–77% of control, respectively). In addition, phenol sulfotransferase (PST) activity was measured toward 1- and 2-naphthol in order to determine whether apparent changes in PST activity in damaged livers are substrate-dependent. Treatment with hepatotoxicants generally decreased 1-naphthol-directed PST activity but not PST activity directed toward 2-naphthol. In conclusion, (1) not all xenobiotic-induced liver injury results in decreased hepatic PAPS concentration, (2) some hepatotoxicants decrease PAPS concentration by a mechanism other than decreased cosubstrate synthesis, and (3) the effect of hepatotoxicants on PST activity is dependent upon the choice of substrate used in the enzymatic assay.</description><subject>1-Naphthylisothiocyanate - adverse effects</subject><subject>1-Propanol - adverse effects</subject><subject>Aflatoxin B1 - adverse effects</subject><subject>Alanine Transaminase - blood</subject><subject>Animals</subject><subject>Arylsulfotransferase - drug effects</subject><subject>Arylsulfotransferase - metabolism</subject><subject>Biological and medical sciences</subject><subject>Bromobenzenes - adverse effects</subject><subject>Cadmium - adverse effects</subject><subject>Cadmium Chloride</subject><subject>Carbon Tetrachloride - adverse effects</subject><subject>Chemical and Drug Induced Liver Injury</subject><subject>Cytosol - enzymology</subject><subject>Dichloroethylenes - adverse effects</subject><subject>General aspects. Methods</subject><subject>L-Iditol 2-Dehydrogenase - blood</subject><subject>Liver - drug effects</subject><subject>Liver - enzymology</subject><subject>Liver - metabolism</subject><subject>Liver Diseases - enzymology</subject><subject>Liver Diseases - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Phosphoadenosine Phosphosulfate - biosynthesis</subject><subject>Propanols</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Sulfates - metabolism</subject><subject>Thioacetamide - adverse effects</subject><subject>Toxicology</subject><issn>0041-008X</issn><issn>1096-0333</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1rGzEQhkVpcB03_6CBPZSSHjad2dVqV5dAMUkdMOSSQm5ClkZYYb3rSnLa_PvItUluOenjfd5heBj7gnCJgOIHAMcSoHu4kPhdAtSyXHxgUwQpSqjr-iObviKf2GmMjwAgOccJm6DkudFO2fJ-TYX1zlGgIXndF5TvJsVidMWatjqNafznjR72X0ORMh53vdPJ51eO13_1c-GHIugUP7MTp_tIZ8dzxn7fXN_PF-Xy7tft_OeyNBzbVMrKQtUZEg3iSoO2lhvuOuSuNavKSUmdaLVtsBYtilYCWuw6jbYVq45qW8_Yt8PcbRj_7CgmtfHRUN_rgcZdVCiqpuNSZJAfQBPGGAM5tQ1-o8OzQlB7iWpvSO0NKYnqv0S1yLXz4_zdakP2rXSwlvOvx1xHo3sX9GB8fMUa4E0DVcauDhhlF0-egorG02DI-pAVKzv69_d4AWDQjd4</recordid><startdate>19910915</startdate><enddate>19910915</enddate><creator>Maziasz, T.J.</creator><creator>Liu, J.</creator><creator>Madhu, C.</creator><creator>Klaassen, C.D.</creator><general>Elsevier Inc</general><general>Elsevier</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>7U7</scope><scope>C1K</scope></search><sort><creationdate>19910915</creationdate><title>The differential effects of hepatotoxicants on the sulfation pathway in rats</title><author>Maziasz, T.J. ; Liu, J. ; Madhu, C. ; Klaassen, C.D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-92d028ce6511ba0add4c4f814f7cb2f99e867ad51367167901d188a1d76b8e3d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>1-Naphthylisothiocyanate - adverse effects</topic><topic>1-Propanol - adverse effects</topic><topic>Aflatoxin B1 - adverse effects</topic><topic>Alanine Transaminase - blood</topic><topic>Animals</topic><topic>Arylsulfotransferase - drug effects</topic><topic>Arylsulfotransferase - metabolism</topic><topic>Biological and medical sciences</topic><topic>Bromobenzenes - adverse effects</topic><topic>Cadmium - adverse effects</topic><topic>Cadmium Chloride</topic><topic>Carbon Tetrachloride - adverse effects</topic><topic>Chemical and Drug Induced Liver Injury</topic><topic>Cytosol - enzymology</topic><topic>Dichloroethylenes - adverse effects</topic><topic>General aspects. Methods</topic><topic>L-Iditol 2-Dehydrogenase - blood</topic><topic>Liver - drug effects</topic><topic>Liver - enzymology</topic><topic>Liver - metabolism</topic><topic>Liver Diseases - enzymology</topic><topic>Liver Diseases - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Phosphoadenosine Phosphosulfate - biosynthesis</topic><topic>Propanols</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Sulfates - metabolism</topic><topic>Thioacetamide - adverse effects</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Maziasz, T.J.</creatorcontrib><creatorcontrib>Liu, J.</creatorcontrib><creatorcontrib>Madhu, C.</creatorcontrib><creatorcontrib>Klaassen, C.D.</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>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Maziasz, T.J.</au><au>Liu, J.</au><au>Madhu, C.</au><au>Klaassen, C.D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The differential effects of hepatotoxicants on the sulfation pathway in rats</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>1991-09-15</date><risdate>1991</risdate><volume>110</volume><issue>3</issue><spage>365</spage><epage>373</epage><pages>365-373</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><coden>TXAPA9</coden><abstract>This study characterized the effects of liver damage produced by a variety of hepatotoxicants on several components of the sulfation pathway in rats. Specifically, the concentration of cosubstrate, adenosine 3′-phosphate 5′-phosphosulfate (PAPS), and the hepatic capacity for PAPS synthesis were measured in livers of rats treated with carbon tetrachloride (CCl 4), 1,1-dichloroethylene (DCE), α-naphthylisothiocyanate (ANIT), aflatoxin B 1 (ATX), allyl alcohol (AA), bromobenzene (BB), cadmium chloride (Cd), or thioacetamide (TA). Liver damage was assessed by measuring serum sorbitol dehydrogenase (SDH) and alanine aminotransferase (ALT) activities as well as by histopathological examination. Hepatic PAPS concentration was generally decreased as a result of treatment with hepatotoxicants (35–80% of control), although BB, AA, and ANIT were without effect. Maximal hepatic capacity for PAPS synthesis, determined as the activities of PAPS synthetic enzymes, ATP sulfurylase, and APS kinase, was selectively decreased by the hepatotoxicants. ATP sulfurylase activity was decreased by Cd and TA (55 and 62% of control, respectively), whereas APS kinase activity was decreased by Cd, TA, BB, and DCE (60–77% of control, respectively). In addition, phenol sulfotransferase (PST) activity was measured toward 1- and 2-naphthol in order to determine whether apparent changes in PST activity in damaged livers are substrate-dependent. Treatment with hepatotoxicants generally decreased 1-naphthol-directed PST activity but not PST activity directed toward 2-naphthol. In conclusion, (1) not all xenobiotic-induced liver injury results in decreased hepatic PAPS concentration, (2) some hepatotoxicants decrease PAPS concentration by a mechanism other than decreased cosubstrate synthesis, and (3) the effect of hepatotoxicants on PST activity is dependent upon the choice of substrate used in the enzymatic assay.</abstract><cop>San Diego, CA</cop><pub>Elsevier Inc</pub><pmid>1949007</pmid><doi>10.1016/0041-008X(91)90039-H</doi><tpages>9</tpages></addata></record>
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subjects 1-Naphthylisothiocyanate - adverse effects
1-Propanol - adverse effects
Aflatoxin B1 - adverse effects
Alanine Transaminase - blood
Animals
Arylsulfotransferase - drug effects
Arylsulfotransferase - metabolism
Biological and medical sciences
Bromobenzenes - adverse effects
Cadmium - adverse effects
Cadmium Chloride
Carbon Tetrachloride - adverse effects
Chemical and Drug Induced Liver Injury
Cytosol - enzymology
Dichloroethylenes - adverse effects
General aspects. Methods
L-Iditol 2-Dehydrogenase - blood
Liver - drug effects
Liver - enzymology
Liver - metabolism
Liver Diseases - enzymology
Liver Diseases - metabolism
Male
Medical sciences
Phosphoadenosine Phosphosulfate - biosynthesis
Propanols
Rats
Rats, Inbred Strains
Sulfates - metabolism
Thioacetamide - adverse effects
Toxicology
title The differential effects of hepatotoxicants on the sulfation pathway in rats
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