Ontogenic changes in the nephrotoxicity of chromate correlate with the glutathione oxidoreduction system.
Identifieur interne : 001246 ( Main/Exploration ); précédent : 001245; suivant : 001247Ontogenic changes in the nephrotoxicity of chromate correlate with the glutathione oxidoreduction system.
Auteurs : D. AppenrothSource :
- Journal of trace elements and electrolytes in health and disease [ 0931-2838 ] ; 1994.
Descripteurs français
- KwdFr :
- Acétylcystéine (pharmacologie), Animaux (MeSH), Chromates (administration et posologie), Chromates (toxicité), Composés du sodium (administration et posologie), Composés du sodium (toxicité), Femelle (MeSH), Glutarédoxines (MeSH), Glutathion (métabolisme), Mâle (MeSH), Oxidoreductases (métabolisme), Oxydoréduction (MeSH), Phénobarbital (pharmacologie), Protein-disulfide reductase (glutathione) (MeSH), Protéinurie (urine), Rats (MeSH), Rein (effets des médicaments et des substances chimiques), Rein (enzymologie), Rein (métabolisme), Vieillissement (métabolisme).
- MESH :
- administration et posologie : Chromates, Composés du sodium.
- effets des médicaments et des substances chimiques : Rein.
- enzymologie : Rein.
- métabolisme : Glutathion, Oxidoreductases, Rein, Vieillissement.
- pharmacologie : Acétylcystéine, Phénobarbital.
- toxicité : Chromates, Composés du sodium.
- urine : Animaux, Femelle, Glutarédoxines, Mâle, Oxydoréduction, Protein-disulfide reductase (glutathione), Protéinurie, Rats.
English descriptors
- KwdEn :
- Acetylcysteine (pharmacology), Aging (metabolism), Animals (MeSH), Chromates (administration & dosage), Chromates (toxicity), Female (MeSH), Glutaredoxins (MeSH), Glutathione (metabolism), Kidney (drug effects), Kidney (enzymology), Kidney (metabolism), Male (MeSH), Oxidation-Reduction (MeSH), Oxidoreductases (metabolism), Phenobarbital (pharmacology), Protein Disulfide Reductase (Glutathione) (MeSH), Proteinuria (urine), Rats (MeSH), Sodium Compounds (administration & dosage), Sodium Compounds (toxicity).
- MESH :
- chemical , administration & dosage : Chromates, Sodium Compounds.
- chemical , metabolism : Glutathione, Oxidoreductases.
- chemical , pharmacology : Acetylcysteine, Phenobarbital.
- drug effects : Kidney.
- enzymology : Kidney.
- metabolism : Aging, Kidney.
- chemical , toxicity : Chromates, Sodium Compounds.
- urine : Proteinuria.
- Animals, Female, Glutaredoxins, Male, Oxidation-Reduction, Protein Disulfide Reductase (Glutathione), Rats.
Abstract
The role of GSH concentration and GSSG reductase activity in age differences in chromate nephrotoxicity was investigated. Young and adult rats were injected with 2 and 1 mg sodium chromate/100 g body weight (BW), respectively, which led to equal Cr concentrations in renal tissue. Cr nephrotoxicity was lower in young than in adult rats. It was shown that from 30 minutes after the chromate injection GSSG reductase activity in renal tissue was increased in adult but decreased in young rats by the chromate. GSSG reductase activity was increased in young rats by pretreatment with phenobarbital. The consequence was an enhancement of chromate nephrotoxicity as shown by proteinuria. Renal GSH concentration is lower in young rats and limiting for chromate reduction in vitro in these animals. Therefore, GSH concentration was increased by pretreatment with N-acetylcysteine, which enhanced chromate nephrotoxicity significantly. These results reflect the important role of the GSH oxidoreduction system in chromate nephrotoxicity and its relationship to age differences.
PubMed: 7804027
Affiliations:
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Le document en format XML
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Rep. of Germany.</nlm:affiliation><wicri:noCountry code="subField">Fed</wicri:noCountry></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1994">1994</date><idno type="RBID">pubmed:7804027</idno><idno type="pmid">7804027</idno><idno type="wicri:Area/Main/Corpus">001251</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">001251</idno><idno type="wicri:Area/Main/Curation">001251</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">001251</idno><idno type="wicri:Area/Main/Exploration">001251</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Ontogenic changes in the nephrotoxicity of chromate correlate with the glutathione oxidoreduction system.</title><author><name sortKey="Appenroth, D" sort="Appenroth, D" uniqKey="Appenroth D" first="D" last="Appenroth">D. Appenroth</name><affiliation><nlm:affiliation>Institute of Pharmacology and Toxicology, Friedrich Schiller University, Jena, Fed. Rep. of Germany.</nlm:affiliation><wicri:noCountry code="subField">Fed</wicri:noCountry></affiliation></author></analytic><series><title level="j">Journal of trace elements and electrolytes in health and disease</title><idno type="ISSN">0931-2838</idno><imprint><date when="1994" type="published">1994</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acetylcysteine (pharmacology)</term><term>Aging (metabolism)</term><term>Animals (MeSH)</term><term>Chromates (administration & dosage)</term><term>Chromates (toxicity)</term><term>Female (MeSH)</term><term>Glutaredoxins (MeSH)</term><term>Glutathione (metabolism)</term><term>Kidney (drug effects)</term><term>Kidney (enzymology)</term><term>Kidney (metabolism)</term><term>Male (MeSH)</term><term>Oxidation-Reduction (MeSH)</term><term>Oxidoreductases (metabolism)</term><term>Phenobarbital (pharmacology)</term><term>Protein Disulfide Reductase (Glutathione) (MeSH)</term><term>Proteinuria (urine)</term><term>Rats (MeSH)</term><term>Sodium Compounds (administration & dosage)</term><term>Sodium Compounds (toxicity)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acétylcystéine (pharmacologie)</term><term>Animaux (MeSH)</term><term>Chromates (administration et posologie)</term><term>Chromates (toxicité)</term><term>Composés du sodium (administration et posologie)</term><term>Composés du sodium (toxicité)</term><term>Femelle (MeSH)</term><term>Glutarédoxines (MeSH)</term><term>Glutathion (métabolisme)</term><term>Mâle (MeSH)</term><term>Oxidoreductases (métabolisme)</term><term>Oxydoréduction (MeSH)</term><term>Phénobarbital (pharmacologie)</term><term>Protein-disulfide reductase (glutathione) (MeSH)</term><term>Protéinurie (urine)</term><term>Rats (MeSH)</term><term>Rein (effets des médicaments et des substances chimiques)</term><term>Rein (enzymologie)</term><term>Rein (métabolisme)</term><term>Vieillissement (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Chromates</term><term>Sodium Compounds</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutathione</term><term>Oxidoreductases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Acetylcysteine</term><term>Phenobarbital</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Chromates</term><term>Composés du sodium</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Kidney</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Rein</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Rein</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Kidney</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Aging</term><term>Kidney</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Glutathion</term><term>Oxidoreductases</term><term>Rein</term><term>Vieillissement</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acétylcystéine</term><term>Phénobarbital</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Chromates</term><term>Sodium Compounds</term></keywords><keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Chromates</term><term>Composés du sodium</term></keywords><keywords scheme="MESH" qualifier="urine" xml:lang="en"><term>Proteinuria</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Glutaredoxins</term><term>Male</term><term>Oxidation-Reduction</term><term>Protein Disulfide Reductase (Glutathione)</term><term>Rats</term></keywords><keywords scheme="MESH" qualifier="urine" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Glutarédoxines</term><term>Mâle</term><term>Oxydoréduction</term><term>Protein-disulfide reductase (glutathione)</term><term>Protéinurie</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The role of GSH concentration and GSSG reductase activity in age differences in chromate nephrotoxicity was investigated. Young and adult rats were injected with 2 and 1 mg sodium chromate/100 g body weight (BW), respectively, which led to equal Cr concentrations in renal tissue. Cr nephrotoxicity was lower in young than in adult rats. It was shown that from 30 minutes after the chromate injection GSSG reductase activity in renal tissue was increased in adult but decreased in young rats by the chromate. GSSG reductase activity was increased in young rats by pretreatment with phenobarbital. The consequence was an enhancement of chromate nephrotoxicity as shown by proteinuria. Renal GSH concentration is lower in young rats and limiting for chromate reduction in vitro in these animals. Therefore, GSH concentration was increased by pretreatment with N-acetylcysteine, which enhanced chromate nephrotoxicity significantly. These results reflect the important role of the GSH oxidoreduction system in chromate nephrotoxicity and its relationship to age differences.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">7804027</PMID><DateCompleted><Year>1995</Year><Month>01</Month><Day>30</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>23</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0931-2838</ISSN><JournalIssue CitedMedium="Print"><Volume>8</Volume><Issue>1</Issue><PubDate><Year>1994</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Journal of trace elements and electrolytes in health and disease</Title><ISOAbbreviation>J Trace Elem Electrolytes Health Dis</ISOAbbreviation></Journal><ArticleTitle>Ontogenic changes in the nephrotoxicity of chromate correlate with the glutathione oxidoreduction system.</ArticleTitle><Pagination><MedlinePgn>33-6</MedlinePgn></Pagination><Abstract><AbstractText>The role of GSH concentration and GSSG reductase activity in age differences in chromate nephrotoxicity was investigated. Young and adult rats were injected with 2 and 1 mg sodium chromate/100 g body weight (BW), respectively, which led to equal Cr concentrations in renal tissue. Cr nephrotoxicity was lower in young than in adult rats. It was shown that from 30 minutes after the chromate injection GSSG reductase activity in renal tissue was increased in adult but decreased in young rats by the chromate. GSSG reductase activity was increased in young rats by pretreatment with phenobarbital. The consequence was an enhancement of chromate nephrotoxicity as shown by proteinuria. Renal GSH concentration is lower in young rats and limiting for chromate reduction in vitro in these animals. Therefore, GSH concentration was increased by pretreatment with N-acetylcysteine, which enhanced chromate nephrotoxicity significantly. These results reflect the important role of the GSH oxidoreduction system in chromate nephrotoxicity and its relationship to age differences.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Appenroth</LastName><ForeName>D</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Institute of Pharmacology and Toxicology, Friedrich Schiller University, Jena, Fed. Rep. of Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>J Trace Elem Electrolytes Health Dis</MedlineTA><NlmUniqueID>8807101</NlmUniqueID><ISSNLinking>0931-2838</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002840">Chromates</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017670">Sodium Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>6A49BO6K4M</RegistryNumber><NameOfSubstance UI="C028982">sodium chromate(VI)</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.-</RegistryNumber><NameOfSubstance UI="D010088">Oxidoreductases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.8.4.-</RegistryNumber><NameOfSubstance UI="C020667">glutathione oxidase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.8.4.2</RegistryNumber><NameOfSubstance UI="D011490">Protein Disulfide Reductase (Glutathione)</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical><Chemical><RegistryNumber>WYQ7N0BPYC</RegistryNumber><NameOfSubstance UI="D000111">Acetylcysteine</NameOfSubstance></Chemical><Chemical><RegistryNumber>YQE403BP4D</RegistryNumber><NameOfSubstance UI="D010634">Phenobarbital</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000111" MajorTopicYN="N">Acetylcysteine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000375" MajorTopicYN="N">Aging</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002840" MajorTopicYN="N">Chromates</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</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><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010088" MajorTopicYN="N">Oxidoreductases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010634" MajorTopicYN="N">Phenobarbital</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011490" MajorTopicYN="Y">Protein Disulfide Reductase (Glutathione)</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011507" MajorTopicYN="N">Proteinuria</DescriptorName><QualifierName UI="Q000652" MajorTopicYN="N">urine</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017670" MajorTopicYN="N">Sodium Compounds</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1994</Year><Month>3</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1994</Year><Month>3</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1994</Year><Month>3</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">7804027</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list></list><tree><noCountry><name sortKey="Appenroth, D" sort="Appenroth, D" uniqKey="Appenroth D" first="D" last="Appenroth">D. 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