Effects of cobalt on membrane ATPases, oxidant, and antioxidant values in the cerebrum and cerebellum of suckling rats.
Identifieur interne : 000029 ( PubMed/Corpus ); précédent : 000028; suivant : 000030Effects of cobalt on membrane ATPases, oxidant, and antioxidant values in the cerebrum and cerebellum of suckling rats.
Auteurs : Elmouldi Garoui ; Ibtissem Ben Amara ; Dorra Driss ; Awatef Elwej ; Semia Ellouze Chaabouni ; Tahia Boudawara ; Najiba ZeghalSource :
- Biological trace element research [ 1559-0720 ] ; 2013.
English descriptors
- KwdEn :
- Acetylcholinesterase (metabolism), Adenosine Triphosphatases (metabolism), Administration, Oral, Advanced Oxidation Protein Products (metabolism), Animals, Animals, Suckling, Antioxidants (metabolism), Butyrylcholinesterase (metabolism), Catalase (metabolism), Cerebellum (drug effects), Cerebellum (metabolism), Cerebellum (pathology), Cerebrum (drug effects), Cerebrum (metabolism), Cerebrum (pathology), Cobalt (administration & dosage), Cobalt (blood), Cobalt (toxicity), DNA Fragmentation (drug effects), Female, GPI-Linked Proteins (metabolism), Glutathione Peroxidase (metabolism), Hydrogen Peroxide (metabolism), Malondialdehyde (metabolism), Oxidants (metabolism), Pregnancy, Prenatal Exposure Delayed Effects (chemically induced), Prenatal Exposure Delayed Effects (metabolism), Protein Carbonylation (drug effects), Random Allocation, Rats, Rats, Wistar, Superoxide Dismutase (metabolism).
- MESH :
- chemical , administration & dosage : Cobalt.
- chemical , blood : Cobalt.
- chemical , metabolism : Acetylcholinesterase, Adenosine Triphosphatases, Advanced Oxidation Protein Products, Antioxidants, Butyrylcholinesterase, Catalase, GPI-Linked Proteins, Glutathione Peroxidase, Hydrogen Peroxide, Malondialdehyde, Oxidants, Superoxide Dismutase.
- chemically induced : Prenatal Exposure Delayed Effects.
- drug effects : Cerebellum, Cerebrum, DNA Fragmentation, Protein Carbonylation.
- metabolism : Cerebellum, Cerebrum, Prenatal Exposure Delayed Effects.
- pathology : Cerebellum, Cerebrum.
- chemical , toxicity : Cobalt.
- Administration, Oral, Animals, Animals, Suckling, Female, Pregnancy, Random Allocation, Rats, Rats, Wistar.
Abstract
Chronic overexposure to cobalt (Co) may result in neurotoxic effects, but the mechanism of Co-induced neurotoxicity is not yet well established. Our study was conducted to determine whether Co is associated to the induction of central nervous system damage in pregnant rats and their progeny. Twelve pregnant female rats were randomly divided into 2 groups: group I served as controls and group II received Co (350 mg/L, orally). Treatments started from the 14th day of pregnancy until day 14 after delivery. Co concentration in plasma was higher in the treated groups than in the controls. Exposure to Co also increased the levels of MDA, PCO, H2O2, and AOPP, while Na(+)K(+)-ATPase and Mg(2+)-ATPase, AChE, and BuChE activities decreased in the cerebrum and cerebellum of suckling pups. A smear without ladder formation on agarose gel was also shown in the cerebrum and cerebellum, indicating random DNA degradation. A reduction in GPx, SOD, CAT, GSH, NPSH, and vitamin C values was observed. The changes were confirmed by histological results. In conclusion, these data showed that the exposure of pregnant and lactating rats to Co resulted in the development of oxidative stress and the impairment of defense systems in the cerebrum and cerebellum of their suckling pups.
DOI: 10.1007/s12011-013-9746-0
PubMed: 23857379
Links to Exploration step
pubmed:23857379Le document en format XML
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rats.</title><author><name sortKey="Garoui, Elmouldi" sort="Garoui, Elmouldi" uniqKey="Garoui E" first="Elmouldi" last="Garoui">Elmouldi Garoui</name><affiliation><nlm:affiliation>Animal Physiology Laboratory, Life Sciences Department, Sfax Faculty of Sciences, University of Sfax, Sfax, Tunisia.</nlm:affiliation></affiliation></author><author><name sortKey="Ben Amara, Ibtissem" sort="Ben Amara, Ibtissem" uniqKey="Ben Amara I" first="Ibtissem" last="Ben Amara">Ibtissem Ben Amara</name></author><author><name sortKey="Driss, Dorra" sort="Driss, Dorra" uniqKey="Driss D" first="Dorra" last="Driss">Dorra Driss</name></author><author><name sortKey="Elwej, Awatef" sort="Elwej, Awatef" uniqKey="Elwej A" first="Awatef" last="Elwej">Awatef Elwej</name></author><author><name sortKey="Chaabouni, Semia Ellouze" sort="Chaabouni, Semia Ellouze" uniqKey="Chaabouni S" first="Semia Ellouze" last="Chaabouni">Semia Ellouze Chaabouni</name></author><author><name sortKey="Boudawara, Tahia" sort="Boudawara, Tahia" uniqKey="Boudawara T" first="Tahia" last="Boudawara">Tahia Boudawara</name></author><author><name sortKey="Zeghal, Najiba" sort="Zeghal, Najiba" uniqKey="Zeghal N" first="Najiba" last="Zeghal">Najiba Zeghal</name></author></analytic><series><title level="j">Biological trace element research</title><idno type="eISSN">1559-0720</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acetylcholinesterase (metabolism)</term><term>Adenosine Triphosphatases (metabolism)</term><term>Administration, Oral</term><term>Advanced Oxidation Protein Products (metabolism)</term><term>Animals</term><term>Animals, Suckling</term><term>Antioxidants (metabolism)</term><term>Butyrylcholinesterase (metabolism)</term><term>Catalase (metabolism)</term><term>Cerebellum (drug effects)</term><term>Cerebellum (metabolism)</term><term>Cerebellum (pathology)</term><term>Cerebrum (drug effects)</term><term>Cerebrum (metabolism)</term><term>Cerebrum (pathology)</term><term>Cobalt (administration & dosage)</term><term>Cobalt (blood)</term><term>Cobalt (toxicity)</term><term>DNA Fragmentation (drug effects)</term><term>Female</term><term>GPI-Linked Proteins (metabolism)</term><term>Glutathione Peroxidase (metabolism)</term><term>Hydrogen Peroxide (metabolism)</term><term>Malondialdehyde (metabolism)</term><term>Oxidants (metabolism)</term><term>Pregnancy</term><term>Prenatal Exposure Delayed Effects (chemically induced)</term><term>Prenatal Exposure Delayed Effects (metabolism)</term><term>Protein Carbonylation (drug effects)</term><term>Random Allocation</term><term>Rats</term><term>Rats, Wistar</term><term>Superoxide Dismutase (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Cobalt</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Cobalt</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Acetylcholinesterase</term><term>Adenosine Triphosphatases</term><term>Advanced Oxidation Protein Products</term><term>Antioxidants</term><term>Butyrylcholinesterase</term><term>Catalase</term><term>GPI-Linked Proteins</term><term>Glutathione Peroxidase</term><term>Hydrogen Peroxide</term><term>Malondialdehyde</term><term>Oxidants</term><term>Superoxide Dismutase</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Prenatal Exposure Delayed Effects</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cerebellum</term><term>Cerebrum</term><term>DNA Fragmentation</term><term>Protein Carbonylation</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cerebellum</term><term>Cerebrum</term><term>Prenatal Exposure Delayed Effects</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cerebellum</term><term>Cerebrum</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Cobalt</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Administration, Oral</term><term>Animals</term><term>Animals, Suckling</term><term>Female</term><term>Pregnancy</term><term>Random Allocation</term><term>Rats</term><term>Rats, Wistar</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Chronic overexposure to cobalt (Co) may result in neurotoxic effects, but the mechanism of Co-induced neurotoxicity is not yet well established. Our study was conducted to determine whether Co is associated to the induction of central nervous system damage in pregnant rats and their progeny. Twelve pregnant female rats were randomly divided into 2 groups: group I served as controls and group II received Co (350 mg/L, orally). Treatments started from the 14th day of pregnancy until day 14 after delivery. Co concentration in plasma was higher in the treated groups than in the controls. Exposure to Co also increased the levels of MDA, PCO, H2O2, and AOPP, while Na(+)K(+)-ATPase and Mg(2+)-ATPase, AChE, and BuChE activities decreased in the cerebrum and cerebellum of suckling pups. A smear without ladder formation on agarose gel was also shown in the cerebrum and cerebellum, indicating random DNA degradation. A reduction in GPx, SOD, CAT, GSH, NPSH, and vitamin C values was observed. The changes were confirmed by histological results. In conclusion, these data showed that the exposure of pregnant and lactating rats to Co resulted in the development of oxidative stress and the impairment of defense systems in the cerebrum and cerebellum of their suckling pups.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23857379</PMID><DateCreated><Year>2013</Year><Month>8</Month><Day>16</Day></DateCreated><DateCompleted><Year>2014</Year><Month>03</Month><Day>14</Day></DateCompleted><DateRevised><Year>2015</Year><Month>4</Month><Day>23</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1559-0720</ISSN><JournalIssue CitedMedium="Internet"><Volume>154</Volume><Issue>3</Issue><PubDate><Year>2013</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Biological trace element research</Title><ISOAbbreviation>Biol Trace Elem Res</ISOAbbreviation></Journal><ArticleTitle>Effects of cobalt on membrane ATPases, oxidant, and antioxidant values in the cerebrum and cerebellum of suckling rats.</ArticleTitle><Pagination><MedlinePgn>387-95</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s12011-013-9746-0</ELocationID><Abstract><AbstractText>Chronic overexposure to cobalt (Co) may result in neurotoxic effects, but the mechanism of Co-induced neurotoxicity is not yet well established. Our study was conducted to determine whether Co is associated to the induction of central nervous system damage in pregnant rats and their progeny. Twelve pregnant female rats were randomly divided into 2 groups: group I served as controls and group II received Co (350 mg/L, orally). Treatments started from the 14th day of pregnancy until day 14 after delivery. Co concentration in plasma was higher in the treated groups than in the controls. Exposure to Co also increased the levels of MDA, PCO, H2O2, and AOPP, while Na(+)K(+)-ATPase and Mg(2+)-ATPase, AChE, and BuChE activities decreased in the cerebrum and cerebellum of suckling pups. A smear without ladder formation on agarose gel was also shown in the cerebrum and cerebellum, indicating random DNA degradation. A reduction in GPx, SOD, CAT, GSH, NPSH, and vitamin C values was observed. The changes were confirmed by histological results. In conclusion, these data showed that the exposure of pregnant and lactating rats to Co resulted in the development of oxidative stress and the impairment of defense systems in the cerebrum and cerebellum of their suckling pups.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Garoui</LastName><ForeName>Elmouldi</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Animal Physiology Laboratory, Life Sciences Department, Sfax Faculty of Sciences, University of Sfax, Sfax, Tunisia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ben Amara</LastName><ForeName>Ibtissem</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Driss</LastName><ForeName>Dorra</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Elwej</LastName><ForeName>Awatef</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Chaabouni</LastName><ForeName>Semia Ellouze</ForeName><Initials>SE</Initials></Author><Author ValidYN="Y"><LastName>Boudawara</LastName><ForeName>Tahia</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Zeghal</LastName><ForeName>Najiba</ForeName><Initials>N</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><ArticleDate DateType="Electronic"><Year>2013</Year><Month>Jul</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biol Trace Elem Res</MedlineTA><NlmUniqueID>7911509</NlmUniqueID><ISSNLinking>0163-4984</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D062107">Advanced Oxidation Protein Products</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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UI="D013482">Superoxide Dismutase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.1.-</RegistryNumber><NameOfSubstance UI="D002091">Butyrylcholinesterase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.1.7</RegistryNumber><NameOfSubstance UI="D000110">Acetylcholinesterase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.1.7</RegistryNumber><NameOfSubstance UI="C548246">Ache protein, rat</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.6.1.-</RegistryNumber><NameOfSubstance UI="D000251">Adenosine Triphosphatases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Eur J Biochem. 2000 Aug;267(16):4912-6</RefSource><PMID Version="1">10931173</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurochem Res. 2009 Dec;34(12):2181-91</RefSource><PMID Version="1">19513830</PMID></CommentsCorrections><CommentsCorrections 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MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017208" MajorTopicYN="N">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013482" MajorTopicYN="N">Superoxide Dismutase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC3744383</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>1</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>6</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>7</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>7</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>3</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23857379</ArticleId><ArticleId IdType="doi">10.1007/s12011-013-9746-0</ArticleId><ArticleId IdType="pmc">PMC3744383</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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