Alpha-tocopherol downregulates gulonolactone oxidase activity in sturgeon.
Identifieur interne : 000551 ( PubMed/Checkpoint ); précédent : 000550; suivant : 000552Alpha-tocopherol downregulates gulonolactone oxidase activity in sturgeon.
Auteurs : Régis Moreau [États-Unis] ; Konrad DabrowskiSource :
- Free radical biology & medicine [ 0891-5849 ] ; 2003.
English descriptors
- KwdEn :
- Animals, Antioxidants (metabolism), Antioxidants (pharmacology), Ascorbic Acid (pharmacology), Ascorbic Acid Deficiency, Diet, Down-Regulation, Fishes (physiology), Kidney (drug effects), Kidney (enzymology), L-Gulonolactone Oxidase, Liver (drug effects), Liver (enzymology), Sugar Alcohol Dehydrogenases (metabolism), Survival Rate, alpha-Tocopherol (metabolism), alpha-Tocopherol (pharmacology).
- MESH :
- chemical , metabolism : Antioxidants, Sugar Alcohol Dehydrogenases, alpha-Tocopherol.
- chemical , pharmacology : Antioxidants, Ascorbic Acid, alpha-Tocopherol.
- drug effects : Kidney, Liver.
- enzymology : Kidney, Liver.
- physiology : Fishes.
- Animals, Ascorbic Acid Deficiency, Diet, Down-Regulation, L-Gulonolactone Oxidase, Survival Rate.
Abstract
Gulonolactone oxidase (GLO) is the enzyme responsible for the last step of ascorbic acid biosynthesis. The aim of this study was to investigate the effect of dietary alpha-tocopherol and ascorbic acid on GLO activity in a lower vertebrate, the white sturgeon (Acipenser transmontanus). Both alpha-tocopherol and ascorbic acid modulated renal GLO activity. The increase of dietary levels of alpha-tocopherol and/or ascorbic acid significantly raised the liver concentrations of these two antioxidants and concomitantly lowered kidney's GLO activity. The results suggest that the enzyme of ascorbic acid synthetic pathway responded to the animal's antioxidant status and that its activity was downregulated by alpha-tocopherol. This is the first record of alpha-tocopherol being involved in the regulation of ascorbic acid synthesis. This new observation may provide a hypothesis for the evolutionary loss of GLO expression in teleost fishes.
PubMed: 12726920
Affiliations:
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The aim of this study was to investigate the effect of dietary alpha-tocopherol and ascorbic acid on GLO activity in a lower vertebrate, the white sturgeon (Acipenser transmontanus). Both alpha-tocopherol and ascorbic acid modulated renal GLO activity. The increase of dietary levels of alpha-tocopherol and/or ascorbic acid significantly raised the liver concentrations of these two antioxidants and concomitantly lowered kidney's GLO activity. The results suggest that the enzyme of ascorbic acid synthetic pathway responded to the animal's antioxidant status and that its activity was downregulated by alpha-tocopherol. This is the first record of alpha-tocopherol being involved in the regulation of ascorbic acid synthesis. This new observation may provide a hypothesis for the evolutionary loss of GLO expression in teleost fishes.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12726920</PMID><DateCreated><Year>2003</Year><Month>05</Month><Day>02</Day></DateCreated><DateCompleted><Year>2003</Year><Month>07</Month><Day>24</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0891-5849</ISSN><JournalIssue CitedMedium="Print"><Volume>34</Volume><Issue>10</Issue><PubDate><Year>2003</Year><Month>May</Month><Day>15</Day></PubDate></JournalIssue><Title>Free radical biology & medicine</Title><ISOAbbreviation>Free Radic. Biol. Med.</ISOAbbreviation></Journal><ArticleTitle>Alpha-tocopherol downregulates gulonolactone oxidase activity in sturgeon.</ArticleTitle><Pagination><MedlinePgn>1326-32</MedlinePgn></Pagination><Abstract><AbstractText>Gulonolactone oxidase (GLO) is the enzyme responsible for the last step of ascorbic acid biosynthesis. The aim of this study was to investigate the effect of dietary alpha-tocopherol and ascorbic acid on GLO activity in a lower vertebrate, the white sturgeon (Acipenser transmontanus). Both alpha-tocopherol and ascorbic acid modulated renal GLO activity. The increase of dietary levels of alpha-tocopherol and/or ascorbic acid significantly raised the liver concentrations of these two antioxidants and concomitantly lowered kidney's GLO activity. The results suggest that the enzyme of ascorbic acid synthetic pathway responded to the animal's antioxidant status and that its activity was downregulated by alpha-tocopherol. This is the first record of alpha-tocopherol being involved in the regulation of ascorbic acid synthesis. This new observation may provide a hypothesis for the evolutionary loss of GLO expression in teleost fishes.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Moreau</LastName><ForeName>Régis</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>School of Natural Resources, The Ohio State University, Columbus OH, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dabrowski</LastName><ForeName>Konrad</ForeName><Initials>K</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Free Radic Biol Med</MedlineTA><NlmUniqueID>8709159</NlmUniqueID><ISSNLinking>0891-5849</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000975">Antioxidants</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.1.-</RegistryNumber><NameOfSubstance UI="D013401">Sugar Alcohol Dehydrogenases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.1.3.8</RegistryNumber><NameOfSubstance UI="D050544">L-Gulonolactone Oxidase</NameOfSubstance></Chemical><Chemical><RegistryNumber>H4N855PNZ1</RegistryNumber><NameOfSubstance UI="D024502">alpha-Tocopherol</NameOfSubstance></Chemical><Chemical><RegistryNumber>PQ6CK8PD0R</RegistryNumber><NameOfSubstance UI="D001205">Ascorbic Acid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000975" MajorTopicYN="N">Antioxidants</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001205" MajorTopicYN="N">Ascorbic Acid</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001206" MajorTopicYN="N">Ascorbic Acid Deficiency</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004032" MajorTopicYN="N">Diet</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005399" MajorTopicYN="N">Fishes</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007668" MajorTopicYN="N">Kidney</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050544" MajorTopicYN="N">L-Gulonolactone Oxidase</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008099" MajorTopicYN="N">Liver</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013401" MajorTopicYN="N">Sugar Alcohol Dehydrogenases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015996" MajorTopicYN="N">Survival Rate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D024502" MajorTopicYN="N">alpha-Tocopherol</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2003</Year><Month>5</Month><Day>3</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2003</Year><Month>7</Month><Day>25</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2003</Year><Month>5</Month><Day>3</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12726920</ArticleId><ArticleId IdType="pii">S0891584903001485</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Dabrowski, Konrad" sort="Dabrowski, Konrad" uniqKey="Dabrowski K" first="Konrad" last="Dabrowski">Konrad Dabrowski</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Moreau, Regis" sort="Moreau, Regis" uniqKey="Moreau R" first="Régis" last="Moreau">Régis Moreau</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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