Inhibition of carbamoyl phosphate synthetase-I by dietary dehydroepiandrosterone
Dehydroepiandrosterone (DHEA), administered per os, serves to prevent or retard the development of a variety of genetic and induced disorders in mice and rats. This treatment also results in the development of hepatomegaly, a change of liver color from pink to mahogany, peroxisome proliferation in h...
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Veröffentlicht in: | The Journal of steroid biochemistry and molecular biology 1991-05, Vol.38 (5), p.599-609 |
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creator | Marrero, Mario Prough, Russell A. Putnam, Robert S. Bennett, Michael Milewich, Leon |
description | Dehydroepiandrosterone (DHEA), administered
per os, serves to prevent or retard the development of a variety of genetic and induced disorders in mice and rats. This treatment also results in the development of hepatomegaly, a change of liver color from pink to mahogany, peroxisome proliferation in hepatocytes and alterations in hepatocyte mitochondria morphology and respiration. We used one- and two-dimensional polyacrylamide gel electrophoresis (PAGE) to identify changes in the relative levels of liver proteins produced by DHEA treatment of rodents. In mouse liver, there were apparent increases in the levels of 26 proteins and decreases in the levels of 7 proteins. Of the induced proteins the most prominent had
M
r ∼ 72 K; this protein was identified in a previous study as enoyl-CoA hydratase/ 3-hydroxyacyl-CoA dehydrogenase. Another protein of
M
r ∼ 28 K, of unknown nature, also was induced markedly by DHEA treatment of mice and rats. A protein of
M
r ∼ 160 K, which was identified as carbamoyl phosphate synthetase-I (CPS-I), was decreased markedly by DHEA action. This enzyme, which comprises approx. 15–20% of mitochondrial matrix protein, is involved in the entry and rate-limiting step of the urea cycle. The specific activity of CPS-I also was significantly decreased by DHEA, but serum urea levels were normal. To determine whether steroids other than DHEA also induced similar changes, mice were treated with various steroids for 14 days and, thereafter, liver proteins were evaluated by SDS-PAGE: estradiol-17β and isoandrosterone induced both the ∼ 72 and ∼28 kDa proteins, testosterone and androsterone induced the 28 kDa protein only, but etiocholanolone, pregnenolone and progesterone were without effect. The findings of this study serve to demonstrate that: (i) hepatic protein levels are affected by DHEA treatment of mice and rats; (ii) liver CPS-I activity is decreased significantly by DHEA treatment, but serum urea levels remain within the normal range; and (iii) sex steroids and some of their precursors, when administered
per os, also alter liver protein levels. |
doi_str_mv | 10.1016/0960-0760(91)90319-Z |
format | Article |
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per os, serves to prevent or retard the development of a variety of genetic and induced disorders in mice and rats. This treatment also results in the development of hepatomegaly, a change of liver color from pink to mahogany, peroxisome proliferation in hepatocytes and alterations in hepatocyte mitochondria morphology and respiration. We used one- and two-dimensional polyacrylamide gel electrophoresis (PAGE) to identify changes in the relative levels of liver proteins produced by DHEA treatment of rodents. In mouse liver, there were apparent increases in the levels of 26 proteins and decreases in the levels of 7 proteins. Of the induced proteins the most prominent had
M
r ∼ 72 K; this protein was identified in a previous study as enoyl-CoA hydratase/ 3-hydroxyacyl-CoA dehydrogenase. Another protein of
M
r ∼ 28 K, of unknown nature, also was induced markedly by DHEA treatment of mice and rats. A protein of
M
r ∼ 160 K, which was identified as carbamoyl phosphate synthetase-I (CPS-I), was decreased markedly by DHEA action. This enzyme, which comprises approx. 15–20% of mitochondrial matrix protein, is involved in the entry and rate-limiting step of the urea cycle. The specific activity of CPS-I also was significantly decreased by DHEA, but serum urea levels were normal. To determine whether steroids other than DHEA also induced similar changes, mice were treated with various steroids for 14 days and, thereafter, liver proteins were evaluated by SDS-PAGE: estradiol-17β and isoandrosterone induced both the ∼ 72 and ∼28 kDa proteins, testosterone and androsterone induced the 28 kDa protein only, but etiocholanolone, pregnenolone and progesterone were without effect. The findings of this study serve to demonstrate that: (i) hepatic protein levels are affected by DHEA treatment of mice and rats; (ii) liver CPS-I activity is decreased significantly by DHEA treatment, but serum urea levels remain within the normal range; and (iii) sex steroids and some of their precursors, when administered
per os, also alter liver protein levels.</description><identifier>ISSN: 0960-0760</identifier><identifier>EISSN: 1879-1220</identifier><identifier>DOI: 10.1016/0960-0760(91)90319-Z</identifier><identifier>PMID: 1828177</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Analytical, structural and metabolic biochemistry ; Animals ; Biological and medical sciences ; Blood Urea Nitrogen ; Blotting, Western ; Carbamoyl-Phosphate Synthase (Ammonia) - antagonists & inhibitors ; dehydroepiandrosterone ; Dehydroepiandrosterone - pharmacology ; Diet ; Electrophoresis, Gel, Two-Dimensional ; Electrophoresis, Polyacrylamide Gel ; Enzymes and enzyme inhibitors ; Female ; Fundamental and applied biological sciences. Psychology ; Ligases ; Liver - drug effects ; Liver - enzymology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Proteins - drug effects ; Rats ; Rats, Inbred Strains ; Steroids - pharmacology</subject><ispartof>The Journal of steroid biochemistry and molecular biology, 1991-05, Vol.38 (5), p.599-609</ispartof><rights>1991</rights><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c418t-1a3eccfbc9df3600a70c0269a3d08bc8b1b9a97c78b6d1152b369154a77082ea3</citedby><cites>FETCH-LOGICAL-c418t-1a3eccfbc9df3600a70c0269a3d08bc8b1b9a97c78b6d1152b369154a77082ea3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0960-0760(91)90319-Z$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19813301$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1828177$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Marrero, Mario</creatorcontrib><creatorcontrib>Prough, Russell A.</creatorcontrib><creatorcontrib>Putnam, Robert S.</creatorcontrib><creatorcontrib>Bennett, Michael</creatorcontrib><creatorcontrib>Milewich, Leon</creatorcontrib><title>Inhibition of carbamoyl phosphate synthetase-I by dietary dehydroepiandrosterone</title><title>The Journal of steroid biochemistry and molecular biology</title><addtitle>J Steroid Biochem Mol Biol</addtitle><description>Dehydroepiandrosterone (DHEA), administered
per os, serves to prevent or retard the development of a variety of genetic and induced disorders in mice and rats. This treatment also results in the development of hepatomegaly, a change of liver color from pink to mahogany, peroxisome proliferation in hepatocytes and alterations in hepatocyte mitochondria morphology and respiration. We used one- and two-dimensional polyacrylamide gel electrophoresis (PAGE) to identify changes in the relative levels of liver proteins produced by DHEA treatment of rodents. In mouse liver, there were apparent increases in the levels of 26 proteins and decreases in the levels of 7 proteins. Of the induced proteins the most prominent had
M
r ∼ 72 K; this protein was identified in a previous study as enoyl-CoA hydratase/ 3-hydroxyacyl-CoA dehydrogenase. Another protein of
M
r ∼ 28 K, of unknown nature, also was induced markedly by DHEA treatment of mice and rats. A protein of
M
r ∼ 160 K, which was identified as carbamoyl phosphate synthetase-I (CPS-I), was decreased markedly by DHEA action. This enzyme, which comprises approx. 15–20% of mitochondrial matrix protein, is involved in the entry and rate-limiting step of the urea cycle. The specific activity of CPS-I also was significantly decreased by DHEA, but serum urea levels were normal. To determine whether steroids other than DHEA also induced similar changes, mice were treated with various steroids for 14 days and, thereafter, liver proteins were evaluated by SDS-PAGE: estradiol-17β and isoandrosterone induced both the ∼ 72 and ∼28 kDa proteins, testosterone and androsterone induced the 28 kDa protein only, but etiocholanolone, pregnenolone and progesterone were without effect. The findings of this study serve to demonstrate that: (i) hepatic protein levels are affected by DHEA treatment of mice and rats; (ii) liver CPS-I activity is decreased significantly by DHEA treatment, but serum urea levels remain within the normal range; and (iii) sex steroids and some of their precursors, when administered
per os, also alter liver protein levels.</description><subject>Analytical, structural and metabolic biochemistry</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Urea Nitrogen</subject><subject>Blotting, Western</subject><subject>Carbamoyl-Phosphate Synthase (Ammonia) - antagonists & inhibitors</subject><subject>dehydroepiandrosterone</subject><subject>Dehydroepiandrosterone - pharmacology</subject><subject>Diet</subject><subject>Electrophoresis, Gel, Two-Dimensional</subject><subject>Electrophoresis, Polyacrylamide Gel</subject><subject>Enzymes and enzyme inhibitors</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Ligases</subject><subject>Liver - drug effects</subject><subject>Liver - enzymology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C57BL</subject><subject>Proteins - drug effects</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Steroids - pharmacology</subject><issn>0960-0760</issn><issn>1879-1220</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1r3DAQhkVpSTdp_0ELvrSkB6czllcfl0AJ_VgIpIf2kouQ5DFW8Vqu5C3sv6-2uzS35PQyzDPDzMPYG4QrBBQfQQuoQQq41PhBA0dd3z9jK1RS19g08Jyt_iMv2XnOvwCAc5Rn7AxVo1DKFfu-mYbgwhLiVMW-8jY5u437sZqHmOfBLlTl_bQMtNhM9aZy-6oLpUgladh3KdIc7FQyL5TiRK_Yi96OmV6f8oL9_PL5x823-vbu6-bm023tW1RLjZaT973zuuu5ALASPDRCW96Bcl45dNpq6aVyokNcN44LjevWSgmqIcsv2Pvj3jnF3zvKi9mG7Gkc7URxl42CtRKSt0-CKGDdNq0uYHsEfXkmJ-rNnMK2fGoQzMG4Oeg0B51Go_ln3NyXsben_Tu3pe5h6Ki49N-d-jZ7O_bJTj7kB0wr5BywcNdHjoq1P4GSyT7Q5KkLifxiuhgeP-Qvl_qduw</recordid><startdate>19910501</startdate><enddate>19910501</enddate><creator>Marrero, Mario</creator><creator>Prough, Russell A.</creator><creator>Putnam, Robert S.</creator><creator>Bennett, Michael</creator><creator>Milewich, Leon</creator><general>Elsevier Ltd</general><general>Elsevier Science</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>7QL</scope><scope>7TK</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>M81</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>19910501</creationdate><title>Inhibition of carbamoyl phosphate synthetase-I by dietary dehydroepiandrosterone</title><author>Marrero, Mario ; Prough, Russell A. ; Putnam, Robert S. ; Bennett, Michael ; Milewich, Leon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c418t-1a3eccfbc9df3600a70c0269a3d08bc8b1b9a97c78b6d1152b369154a77082ea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>Analytical, structural and metabolic biochemistry</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Urea Nitrogen</topic><topic>Blotting, Western</topic><topic>Carbamoyl-Phosphate Synthase (Ammonia) - antagonists & inhibitors</topic><topic>dehydroepiandrosterone</topic><topic>Dehydroepiandrosterone - pharmacology</topic><topic>Diet</topic><topic>Electrophoresis, Gel, Two-Dimensional</topic><topic>Electrophoresis, Polyacrylamide Gel</topic><topic>Enzymes and enzyme inhibitors</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Ligases</topic><topic>Liver - drug effects</topic><topic>Liver - enzymology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C57BL</topic><topic>Proteins - drug effects</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Steroids - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Marrero, Mario</creatorcontrib><creatorcontrib>Prough, Russell A.</creatorcontrib><creatorcontrib>Putnam, Robert S.</creatorcontrib><creatorcontrib>Bennett, Michael</creatorcontrib><creatorcontrib>Milewich, Leon</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biochemistry Abstracts 3</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of steroid biochemistry and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Marrero, Mario</au><au>Prough, Russell A.</au><au>Putnam, Robert S.</au><au>Bennett, Michael</au><au>Milewich, Leon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of carbamoyl phosphate synthetase-I by dietary dehydroepiandrosterone</atitle><jtitle>The Journal of steroid biochemistry and molecular biology</jtitle><addtitle>J Steroid Biochem Mol Biol</addtitle><date>1991-05-01</date><risdate>1991</risdate><volume>38</volume><issue>5</issue><spage>599</spage><epage>609</epage><pages>599-609</pages><issn>0960-0760</issn><eissn>1879-1220</eissn><abstract>Dehydroepiandrosterone (DHEA), administered
per os, serves to prevent or retard the development of a variety of genetic and induced disorders in mice and rats. This treatment also results in the development of hepatomegaly, a change of liver color from pink to mahogany, peroxisome proliferation in hepatocytes and alterations in hepatocyte mitochondria morphology and respiration. We used one- and two-dimensional polyacrylamide gel electrophoresis (PAGE) to identify changes in the relative levels of liver proteins produced by DHEA treatment of rodents. In mouse liver, there were apparent increases in the levels of 26 proteins and decreases in the levels of 7 proteins. Of the induced proteins the most prominent had
M
r ∼ 72 K; this protein was identified in a previous study as enoyl-CoA hydratase/ 3-hydroxyacyl-CoA dehydrogenase. Another protein of
M
r ∼ 28 K, of unknown nature, also was induced markedly by DHEA treatment of mice and rats. A protein of
M
r ∼ 160 K, which was identified as carbamoyl phosphate synthetase-I (CPS-I), was decreased markedly by DHEA action. This enzyme, which comprises approx. 15–20% of mitochondrial matrix protein, is involved in the entry and rate-limiting step of the urea cycle. The specific activity of CPS-I also was significantly decreased by DHEA, but serum urea levels were normal. To determine whether steroids other than DHEA also induced similar changes, mice were treated with various steroids for 14 days and, thereafter, liver proteins were evaluated by SDS-PAGE: estradiol-17β and isoandrosterone induced both the ∼ 72 and ∼28 kDa proteins, testosterone and androsterone induced the 28 kDa protein only, but etiocholanolone, pregnenolone and progesterone were without effect. The findings of this study serve to demonstrate that: (i) hepatic protein levels are affected by DHEA treatment of mice and rats; (ii) liver CPS-I activity is decreased significantly by DHEA treatment, but serum urea levels remain within the normal range; and (iii) sex steroids and some of their precursors, when administered
per os, also alter liver protein levels.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>1828177</pmid><doi>10.1016/0960-0760(91)90319-Z</doi><tpages>11</tpages></addata></record> |
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subjects | Analytical, structural and metabolic biochemistry Animals Biological and medical sciences Blood Urea Nitrogen Blotting, Western Carbamoyl-Phosphate Synthase (Ammonia) - antagonists & inhibitors dehydroepiandrosterone Dehydroepiandrosterone - pharmacology Diet Electrophoresis, Gel, Two-Dimensional Electrophoresis, Polyacrylamide Gel Enzymes and enzyme inhibitors Female Fundamental and applied biological sciences. Psychology Ligases Liver - drug effects Liver - enzymology Male Mice Mice, Inbred BALB C Mice, Inbred C57BL Proteins - drug effects Rats Rats, Inbred Strains Steroids - pharmacology |
title | Inhibition of carbamoyl phosphate synthetase-I by dietary dehydroepiandrosterone |
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