Effects of ornithine (alpha)-ketoglutarate on circulatory antioxidants and lipid peroxidation products in ammonium acetate treated rats

The effects of ornithine alpha-ketoglutarate (OKG) on ammonium acetate induced hepatotoxicity were studied biochemically in rats. The levels of urea, nonprotein nitrogen, and thiobarbituric acid reactive substances were significantly increased in ammonium acetate treated rats; these levels were sign...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Annals of nutrition and metabolism 2002-05, Vol.46 (3/4), p.93
Hauptverfasser: Dakshayani, K B, Velvizhi, S, Subramanian, P
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page
container_issue 3/4
container_start_page 93
container_title Annals of nutrition and metabolism
container_volume 46
creator Dakshayani, K B
Velvizhi, S
Subramanian, P
description The effects of ornithine alpha-ketoglutarate (OKG) on ammonium acetate induced hepatotoxicity were studied biochemically in rats. The levels of urea, nonprotein nitrogen, and thiobarbituric acid reactive substances were significantly increased in ammonium acetate treated rats; these levels were significantly decreased in rats treated with ammonium acetate and OKG. Similar patterns of alterations were observed in the levels of free fatty acids, triglycerides, and phospholipids. Furthermore, nonenzymatic antioxidants (vitamins C and E) were significantly decreased in ammonium acetate treated rats, when compared with control rats, and increased in OKG and ammonium acetate treated rats. The biochemical alterations during OKG treatment could be (1) by detoxifying excess ammonia; (2) by participating in nonenzymatic oxidative decarboxylation in the hydrogen peroxide decomposition process, and (3) by enhancing the proper metabolism of fats which could suppress oxygen radical generation and thus prevent the lipid peroxidative damages in rats.
format Article
fullrecord <record><control><sourceid>proquest</sourceid><recordid>TN_cdi_proquest_journals_232081119</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>161969321</sourcerecordid><originalsourceid>FETCH-proquest_journals_2320811193</originalsourceid><addsrcrecordid>eNqNjEtOwzAQhi1EJULhDiNWsIhku69kjYo4APtqFE_otI4d7LEEJ-DauIgDsPr0P_RdqcasrWn7bb-7Vo22G91uO727Ubc5n7Q2tltvGvW9H0caJEMcIabAcuRA8Ih-PuJTeyaJ774IJhSCGGDgNBSPEtMXYBCOn-wqcw0OPM_sYKb029YxwJyiKxc9B8BpioHLBDiQXHySqMJBlec7tRjRZ7r_41I9vOzfnl_bavgolOVwiiWFOh3syurOGNOv_nX6AQjVVZM</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>232081119</pqid></control><display><type>article</type><title>Effects of ornithine (alpha)-ketoglutarate on circulatory antioxidants and lipid peroxidation products in ammonium acetate treated rats</title><source>Jstor Complete Legacy</source><source>Karger Journals</source><source>Alma/SFX Local Collection</source><creator>Dakshayani, K B ; Velvizhi, S ; Subramanian, P</creator><creatorcontrib>Dakshayani, K B ; Velvizhi, S ; Subramanian, P</creatorcontrib><description>The effects of ornithine alpha-ketoglutarate (OKG) on ammonium acetate induced hepatotoxicity were studied biochemically in rats. The levels of urea, nonprotein nitrogen, and thiobarbituric acid reactive substances were significantly increased in ammonium acetate treated rats; these levels were significantly decreased in rats treated with ammonium acetate and OKG. Similar patterns of alterations were observed in the levels of free fatty acids, triglycerides, and phospholipids. Furthermore, nonenzymatic antioxidants (vitamins C and E) were significantly decreased in ammonium acetate treated rats, when compared with control rats, and increased in OKG and ammonium acetate treated rats. The biochemical alterations during OKG treatment could be (1) by detoxifying excess ammonia; (2) by participating in nonenzymatic oxidative decarboxylation in the hydrogen peroxide decomposition process, and (3) by enhancing the proper metabolism of fats which could suppress oxygen radical generation and thus prevent the lipid peroxidative damages in rats.</description><identifier>ISSN: 0250-6807</identifier><identifier>EISSN: 1421-9697</identifier><language>eng</language><publisher>Basel: S. Karger AG</publisher><subject>Ammonia ; Ammonium ; Antioxidants ; Fatty acids ; Hepatotoxicity ; Hydrogen peroxide ; Lipid peroxidation ; Lipids ; Nitrogen ; Peroxidation ; Plasma ; Proteins ; Triglycerides ; Urea ; Vitamin C ; Vitamin E ; Vitamins</subject><ispartof>Annals of nutrition and metabolism, 2002-05, Vol.46 (3/4), p.93</ispartof><rights>Copyright S. Karger AG May-Aug 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids></links><search><creatorcontrib>Dakshayani, K B</creatorcontrib><creatorcontrib>Velvizhi, S</creatorcontrib><creatorcontrib>Subramanian, P</creatorcontrib><title>Effects of ornithine (alpha)-ketoglutarate on circulatory antioxidants and lipid peroxidation products in ammonium acetate treated rats</title><title>Annals of nutrition and metabolism</title><description>The effects of ornithine alpha-ketoglutarate (OKG) on ammonium acetate induced hepatotoxicity were studied biochemically in rats. The levels of urea, nonprotein nitrogen, and thiobarbituric acid reactive substances were significantly increased in ammonium acetate treated rats; these levels were significantly decreased in rats treated with ammonium acetate and OKG. Similar patterns of alterations were observed in the levels of free fatty acids, triglycerides, and phospholipids. Furthermore, nonenzymatic antioxidants (vitamins C and E) were significantly decreased in ammonium acetate treated rats, when compared with control rats, and increased in OKG and ammonium acetate treated rats. The biochemical alterations during OKG treatment could be (1) by detoxifying excess ammonia; (2) by participating in nonenzymatic oxidative decarboxylation in the hydrogen peroxide decomposition process, and (3) by enhancing the proper metabolism of fats which could suppress oxygen radical generation and thus prevent the lipid peroxidative damages in rats.</description><subject>Ammonia</subject><subject>Ammonium</subject><subject>Antioxidants</subject><subject>Fatty acids</subject><subject>Hepatotoxicity</subject><subject>Hydrogen peroxide</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Nitrogen</subject><subject>Peroxidation</subject><subject>Plasma</subject><subject>Proteins</subject><subject>Triglycerides</subject><subject>Urea</subject><subject>Vitamin C</subject><subject>Vitamin E</subject><subject>Vitamins</subject><issn>0250-6807</issn><issn>1421-9697</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNjEtOwzAQhi1EJULhDiNWsIhku69kjYo4APtqFE_otI4d7LEEJ-DauIgDsPr0P_RdqcasrWn7bb-7Vo22G91uO727Ubc5n7Q2tltvGvW9H0caJEMcIabAcuRA8Ih-PuJTeyaJ774IJhSCGGDgNBSPEtMXYBCOn-wqcw0OPM_sYKb029YxwJyiKxc9B8BpioHLBDiQXHySqMJBlec7tRjRZ7r_41I9vOzfnl_bavgolOVwiiWFOh3syurOGNOv_nX6AQjVVZM</recordid><startdate>20020501</startdate><enddate>20020501</enddate><creator>Dakshayani, K B</creator><creator>Velvizhi, S</creator><creator>Subramanian, P</creator><general>S. Karger AG</general><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</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>ATCPS</scope><scope>AZQEC</scope><scope>BEC</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>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0K</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope></search><sort><creationdate>20020501</creationdate><title>Effects of ornithine (alpha)-ketoglutarate on circulatory antioxidants and lipid peroxidation products in ammonium acetate treated rats</title><author>Dakshayani, K B ; Velvizhi, S ; Subramanian, P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_journals_2320811193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Ammonia</topic><topic>Ammonium</topic><topic>Antioxidants</topic><topic>Fatty acids</topic><topic>Hepatotoxicity</topic><topic>Hydrogen peroxide</topic><topic>Lipid peroxidation</topic><topic>Lipids</topic><topic>Nitrogen</topic><topic>Peroxidation</topic><topic>Plasma</topic><topic>Proteins</topic><topic>Triglycerides</topic><topic>Urea</topic><topic>Vitamin C</topic><topic>Vitamin E</topic><topic>Vitamins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dakshayani, K B</creatorcontrib><creatorcontrib>Velvizhi, S</creatorcontrib><creatorcontrib>Subramanian, P</creatorcontrib><collection>ProQuest Central (Corporate)</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Nursing &amp; Allied Health Database</collection><collection>Agricultural Science Collection</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>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 Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural &amp; Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>eLibrary</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Nursing &amp; Allied Health Database (Alumni Edition)</collection><collection>Agricultural Science Database</collection><collection>Consumer Health Database</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing &amp; 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>Annals of nutrition and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dakshayani, K B</au><au>Velvizhi, S</au><au>Subramanian, P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of ornithine (alpha)-ketoglutarate on circulatory antioxidants and lipid peroxidation products in ammonium acetate treated rats</atitle><jtitle>Annals of nutrition and metabolism</jtitle><date>2002-05-01</date><risdate>2002</risdate><volume>46</volume><issue>3/4</issue><spage>93</spage><pages>93-</pages><issn>0250-6807</issn><eissn>1421-9697</eissn><abstract>The effects of ornithine alpha-ketoglutarate (OKG) on ammonium acetate induced hepatotoxicity were studied biochemically in rats. The levels of urea, nonprotein nitrogen, and thiobarbituric acid reactive substances were significantly increased in ammonium acetate treated rats; these levels were significantly decreased in rats treated with ammonium acetate and OKG. Similar patterns of alterations were observed in the levels of free fatty acids, triglycerides, and phospholipids. Furthermore, nonenzymatic antioxidants (vitamins C and E) were significantly decreased in ammonium acetate treated rats, when compared with control rats, and increased in OKG and ammonium acetate treated rats. The biochemical alterations during OKG treatment could be (1) by detoxifying excess ammonia; (2) by participating in nonenzymatic oxidative decarboxylation in the hydrogen peroxide decomposition process, and (3) by enhancing the proper metabolism of fats which could suppress oxygen radical generation and thus prevent the lipid peroxidative damages in rats.</abstract><cop>Basel</cop><pub>S. Karger AG</pub></addata></record>
fulltext fulltext
identifier ISSN: 0250-6807
ispartof Annals of nutrition and metabolism, 2002-05, Vol.46 (3/4), p.93
issn 0250-6807
1421-9697
language eng
recordid cdi_proquest_journals_232081119
source Jstor Complete Legacy; Karger Journals; Alma/SFX Local Collection
subjects Ammonia
Ammonium
Antioxidants
Fatty acids
Hepatotoxicity
Hydrogen peroxide
Lipid peroxidation
Lipids
Nitrogen
Peroxidation
Plasma
Proteins
Triglycerides
Urea
Vitamin C
Vitamin E
Vitamins
title Effects of ornithine (alpha)-ketoglutarate on circulatory antioxidants and lipid peroxidation products in ammonium acetate treated rats
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-06T23%3A41%3A28IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Effects%20of%20ornithine%20(alpha)-ketoglutarate%20on%20circulatory%20antioxidants%20and%20lipid%20peroxidation%20products%20in%20ammonium%20acetate%20treated%20rats&rft.jtitle=Annals%20of%20nutrition%20and%20metabolism&rft.au=Dakshayani,%20K%20B&rft.date=2002-05-01&rft.volume=46&rft.issue=3/4&rft.spage=93&rft.pages=93-&rft.issn=0250-6807&rft.eissn=1421-9697&rft_id=info:doi/&rft_dat=%3Cproquest%3E161969321%3C/proquest%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=232081119&rft_id=info:pmid/&rfr_iscdi=true