GlutaredoxinV1, Main, Exploration, bibRecord, 000665

Decreased cell proliferation and higher oxidative stress in fibroblasts from Down Syndrome fetuses. Preliminary study.

Identifieur interne : 000665 ( Main/Exploration ); précédent : 000664; suivant : 000666

Decreased cell proliferation and higher oxidative stress in fibroblasts from Down Syndrome fetuses. Preliminary study.

Auteurs : Amparo Gimeno [Espagne] ; José Luis García-Giménez ; Laura Audí ; Nuria Toran ; Pilar Andaluz ; Francisco Dasí ; José Vi A ; Federico V. Pallard

Source :

Biochimica et biophysica acta [ 0006-3002 ] ; 2014.

RBID : pubmed:24184606

Descripteurs français

English descriptors

KwdEn :
- Catalase (genetics), Catalase (metabolism), Cell Proliferation (MeSH), Down Syndrome (genetics), Down Syndrome (metabolism), Down Syndrome (pathology), Female (MeSH), Fetus (MeSH), Fibroblasts (metabolism), Fibroblasts (pathology), Gene Expression Regulation (MeSH), Glutaredoxins (genetics), Glutaredoxins (metabolism), Glutathione (metabolism), Glutathione Peroxidase (genetics), Glutathione Peroxidase (metabolism), Humans (MeSH), Male (MeSH), Oxidative Stress (genetics), Primary Cell Culture (MeSH), Signal Transduction (MeSH), Skin (metabolism), Skin (pathology), Superoxide Dismutase (MeSH), Superoxide Dismutase-1 (MeSH), Telomere (genetics), Telomere (metabolism), Telomere (pathology), Telomere Homeostasis (MeSH), Thioredoxins (genetics), Thioredoxins (metabolism).
MESH :
- chemical , genetics : Catalase, Glutaredoxins, Glutathione Peroxidase, Thioredoxins.
- chemical , metabolism : Catalase, Glutaredoxins, Glutathione, Glutathione Peroxidase, Thioredoxins.
- genetics : Down Syndrome, Oxidative Stress, Telomere.
- metabolism : Down Syndrome, Fibroblasts, Skin, Telomere.
- pathology : Down Syndrome, Fibroblasts, Skin, Telomere.
- Cell Proliferation, Female, Fetus, Gene Expression Regulation, Humans, Male, Primary Cell Culture, Signal Transduction, Superoxide Dismutase, Superoxide Dismutase-1, Telomere Homeostasis.

Abstract

Down Syndrome is the most common chromosomal disease and is also known for its decreased incidence of solid tumors and its progeroid phenotype. Cellular and systemic oxidative stress has been considered as one of the Down Syndrome phenotype causes. We correlated, in a preliminary study, the fibroblast proliferation rate and different cell proliferation key regulators, like Rcan1 and the telomere length from Down Syndrome fetuses, with their oxidative stress profile and the Ribonucleic acid and protein expression of the main antioxidant enzymes together with their activity. Increased oxidized glutathione/glutathione ratio and high peroxide production were found in our cell model. These results correlated with a distorted antioxidant shield. The messenger RNA (SOD1) and protein levels of copper/zinc superoxide dismutase were increased together with a decreased mRNA expression and protein levels of glutathione peroxidase (GPx). As a consequence the [Cu/ZnSOD/(catalase+GPx)] activity ratio increases which explains the oxidative stress generated in the cell model. In addition, the expression of thioredoxin 1 and glutaredoxin 1 is decreased. The results obtained show a decreased antioxidant phenotype that correlates with increased levels of Regulator of calcineurin 1 and attrition of telomeres, both related to oxidative stress and cell cycle impairment. Our preliminary results may explain the proneness to a progeroid phenotype.

DOI: 10.1016/j.bbadis.2013.10.014
PubMed: 24184606

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000694
to stream Main, to step Curation: 000694

Le document en format XML

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<term>Catalase (metabolism)</term>
<term>Cell Proliferation (MeSH)</term>
<term>Down Syndrome (genetics)</term>
<term>Down Syndrome (metabolism)</term>
<term>Down Syndrome (pathology)</term>
<term>Female (MeSH)</term>
<term>Fetus (MeSH)</term>
<term>Fibroblasts (metabolism)</term>
<term>Fibroblasts (pathology)</term>
<term>Gene Expression Regulation (MeSH)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Glutathione (metabolism)</term>
<term>Glutathione Peroxidase (genetics)</term>
<term>Glutathione Peroxidase (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Male (MeSH)</term>
<term>Oxidative Stress (genetics)</term>
<term>Primary Cell Culture (MeSH)</term>
<term>Signal Transduction (MeSH)</term>
<term>Skin (metabolism)</term>
<term>Skin (pathology)</term>
<term>Superoxide Dismutase (MeSH)</term>
<term>Superoxide Dismutase-1 (MeSH)</term>
<term>Telomere (genetics)</term>
<term>Telomere (metabolism)</term>
<term>Telomere (pathology)</term>
<term>Telomere Homeostasis (MeSH)</term>
<term>Thioredoxins (genetics)</term>
<term>Thioredoxins (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Catalase (génétique)</term>
<term>Catalase (métabolisme)</term>
<term>Culture de cellules primaires (MeSH)</term>
<term>Femelle (MeSH)</term>
<term>Fibroblastes (anatomopathologie)</term>
<term>Fibroblastes (métabolisme)</term>
<term>Foetus (MeSH)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Glutathion (métabolisme)</term>
<term>Glutathione peroxidase (génétique)</term>
<term>Glutathione peroxidase (métabolisme)</term>
<term>Homéostasie des télomères (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Peau (anatomopathologie)</term>
<term>Peau (métabolisme)</term>
<term>Prolifération cellulaire (MeSH)</term>
<term>Régulation de l'expression des gènes (MeSH)</term>
<term>Stress oxydatif (génétique)</term>
<term>Superoxide dismutase (MeSH)</term>
<term>Superoxide dismutase-1 (MeSH)</term>
<term>Syndrome de Down (anatomopathologie)</term>
<term>Syndrome de Down (génétique)</term>
<term>Syndrome de Down (métabolisme)</term>
<term>Thiorédoxines (génétique)</term>
<term>Thiorédoxines (métabolisme)</term>
<term>Transduction du signal (MeSH)</term>
<term>Télomère (anatomopathologie)</term>
<term>Télomère (génétique)</term>
<term>Télomère (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Catalase</term>
<term>Glutaredoxins</term>
<term>Glutathione Peroxidase</term>
<term>Thioredoxins</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Catalase</term>
<term>Glutaredoxins</term>
<term>Glutathione</term>
<term>Glutathione Peroxidase</term>
<term>Thioredoxins</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Fibroblastes</term>
<term>Peau</term>
<term>Syndrome de Down</term>
<term>Télomère</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Down Syndrome</term>
<term>Oxidative Stress</term>
<term>Telomere</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Catalase</term>
<term>Glutarédoxines</term>
<term>Glutathione peroxidase</term>
<term>Stress oxydatif</term>
<term>Syndrome de Down</term>
<term>Thiorédoxines</term>
<term>Télomère</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Down Syndrome</term>
<term>Fibroblasts</term>
<term>Skin</term>
<term>Telomere</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Catalase</term>
<term>Fibroblastes</term>
<term>Glutarédoxines</term>
<term>Glutathion</term>
<term>Glutathione peroxidase</term>
<term>Peau</term>
<term>Syndrome de Down</term>
<term>Thiorédoxines</term>
<term>Télomère</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Down Syndrome</term>
<term>Fibroblasts</term>
<term>Skin</term>
<term>Telomere</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Proliferation</term>
<term>Female</term>
<term>Fetus</term>
<term>Gene Expression Regulation</term>
<term>Humans</term>
<term>Male</term>
<term>Primary Cell Culture</term>
<term>Signal Transduction</term>
<term>Superoxide Dismutase</term>
<term>Superoxide Dismutase-1</term>
<term>Telomere Homeostasis</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Culture de cellules primaires</term>
<term>Femelle</term>
<term>Foetus</term>
<term>Homéostasie des télomères</term>
<term>Humains</term>
<term>Mâle</term>
<term>Prolifération cellulaire</term>
<term>Régulation de l'expression des gènes</term>
<term>Superoxide dismutase</term>
<term>Superoxide dismutase-1</term>
<term>Transduction du signal</term>
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<front><div type="abstract" xml:lang="en">Down Syndrome is the most common chromosomal disease and is also known for its decreased incidence of solid tumors and its progeroid phenotype. Cellular and systemic oxidative stress has been considered as one of the Down Syndrome phenotype causes. We correlated, in a preliminary study, the fibroblast proliferation rate and different cell proliferation key regulators, like Rcan1 and the telomere length from Down Syndrome fetuses, with their oxidative stress profile and the Ribonucleic acid and protein expression of the main antioxidant enzymes together with their activity. Increased oxidized glutathione/glutathione ratio and high peroxide production were found in our cell model. These results correlated with a distorted antioxidant shield. The messenger RNA (SOD1) and protein levels of copper/zinc superoxide dismutase were increased together with a decreased mRNA expression and protein levels of glutathione peroxidase (GPx). As a consequence the [Cu/ZnSOD/(catalase+GPx)] activity ratio increases which explains the oxidative stress generated in the cell model. In addition, the expression of thioredoxin 1 and glutaredoxin 1 is decreased. The results obtained show a decreased antioxidant phenotype that correlates with increased levels of Regulator of calcineurin 1 and attrition of telomeres, both related to oxidative stress and cell cycle impairment. Our preliminary results may explain the proneness to a progeroid phenotype. </div>
</front>
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<DateCompleted><Year>2014</Year>
<Month>03</Month>
<Day>27</Day>
</DateCompleted>
<DateRevised><Year>2016</Year>
<Month>11</Month>
<Day>26</Day>
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<Issue>1</Issue>
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<Month>Jan</Month>
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<Title>Biochimica et biophysica acta</Title>
<ISOAbbreviation>Biochim Biophys Acta</ISOAbbreviation>
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<ArticleTitle>Decreased cell proliferation and higher oxidative stress in fibroblasts from Down Syndrome fetuses. Preliminary study.</ArticleTitle>
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<Abstract><AbstractText>Down Syndrome is the most common chromosomal disease and is also known for its decreased incidence of solid tumors and its progeroid phenotype. Cellular and systemic oxidative stress has been considered as one of the Down Syndrome phenotype causes. We correlated, in a preliminary study, the fibroblast proliferation rate and different cell proliferation key regulators, like Rcan1 and the telomere length from Down Syndrome fetuses, with their oxidative stress profile and the Ribonucleic acid and protein expression of the main antioxidant enzymes together with their activity. Increased oxidized glutathione/glutathione ratio and high peroxide production were found in our cell model. These results correlated with a distorted antioxidant shield. The messenger RNA (SOD1) and protein levels of copper/zinc superoxide dismutase were increased together with a decreased mRNA expression and protein levels of glutathione peroxidase (GPx). As a consequence the [Cu/ZnSOD/(catalase+GPx)] activity ratio increases which explains the oxidative stress generated in the cell model. In addition, the expression of thioredoxin 1 and glutaredoxin 1 is decreased. The results obtained show a decreased antioxidant phenotype that correlates with increased levels of Regulator of calcineurin 1 and attrition of telomeres, both related to oxidative stress and cell cycle impairment. Our preliminary results may explain the proneness to a progeroid phenotype. </AbstractText>
<CopyrightInformation>© 2013.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gimeno</LastName>
<ForeName>Amparo</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Anatomy and Human Embryology, Faculty of Medicine, University of Valencia, Av/Blasco Ibáñez, 15, E46010 Valencia, Spain; Fundación Investigación Hospital Clínico Universitario de Valencia, Instituto de Investigación INCLIVA, Avda. Blasco Ibáñez 17, E46010 Valencia, Spain. Electronic address: gimenoa@uv.es.</Affiliation>
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<ForeName>José Luis</ForeName>
<Initials>JL</Initials>
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<Author ValidYN="Y"><LastName>Audí</LastName>
<ForeName>Laura</ForeName>
<Initials>L</Initials>
</Author>
<Author ValidYN="Y"><LastName>Toran</LastName>
<ForeName>Nuria</ForeName>
<Initials>N</Initials>
</Author>
<Author ValidYN="Y"><LastName>Andaluz</LastName>
<ForeName>Pilar</ForeName>
<Initials>P</Initials>
</Author>
<Author ValidYN="Y"><LastName>Dasí</LastName>
<ForeName>Francisco</ForeName>
<Initials>F</Initials>
</Author>
<Author ValidYN="Y"><LastName>Viña</LastName>
<ForeName>José</ForeName>
<Initials>J</Initials>
</Author>
<Author ValidYN="Y"><LastName>Pallardó</LastName>
<ForeName>Federico V</ForeName>
<Initials>FV</Initials>
</Author>
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<Language>eng</Language>
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<ArticleDate DateType="Electronic"><Year>2013</Year>
<Month>10</Month>
<Day>31</Day>
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<MedlineJournalInfo><Country>Netherlands</Country>
<MedlineTA>Biochim Biophys Acta</MedlineTA>
<NlmUniqueID>0217513</NlmUniqueID>
<ISSNLinking>0006-3002</ISSNLinking>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C000606290">SOD1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>52500-60-4</RegistryNumber>
<NameOfSubstance UI="D013879">Thioredoxins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 1.11.1.6</RegistryNumber>
<NameOfSubstance UI="D002374">Catalase</NameOfSubstance>
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<NameOfSubstance UI="D005979">Glutathione Peroxidase</NameOfSubstance>
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<Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber>
<NameOfSubstance UI="D013482">Superoxide Dismutase</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber>
<NameOfSubstance UI="D000072105">Superoxide Dismutase-1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber>
<NameOfSubstance UI="D005978">Glutathione</NameOfSubstance>
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</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D002374" MajorTopicYN="N">Catalase</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
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<MeshHeading><DescriptorName UI="D004314" MajorTopicYN="N">Down Syndrome</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005333" MajorTopicYN="N">Fetus</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005347" MajorTopicYN="N">Fibroblasts</DescriptorName>
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<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
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<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005979" MajorTopicYN="N">Glutathione Peroxidase</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
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<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
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<MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D061251" MajorTopicYN="N">Primary Cell Culture</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
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<MeshHeading><DescriptorName UI="D012867" MajorTopicYN="N">Skin</DescriptorName>
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<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
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<MeshHeading><DescriptorName UI="D000072105" MajorTopicYN="N">Superoxide Dismutase-1</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016615" MajorTopicYN="N">Telomere</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
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<MeshHeading><DescriptorName UI="D059505" MajorTopicYN="N">Telomere Homeostasis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013879" MajorTopicYN="N">Thioredoxins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">BrdU</Keyword>
<Keyword MajorTopicYN="N">Cu/Zn superoxide dismutase</Keyword>
<Keyword MajorTopicYN="N">Cu/ZnSOD</Keyword>
<Keyword MajorTopicYN="N">DHR</Keyword>
<Keyword MajorTopicYN="N">DS</Keyword>
<Keyword MajorTopicYN="N">Down Syndrome</Keyword>
<Keyword MajorTopicYN="N">GAPDH</Keyword>
<Keyword MajorTopicYN="N">GPx</Keyword>
<Keyword MajorTopicYN="N">Glutathione</Keyword>
<Keyword MajorTopicYN="N">Grx1</Keyword>
<Keyword MajorTopicYN="N">Mn superoxide dismutase</Keyword>
<Keyword MajorTopicYN="N">MnSOD</Keyword>
<Keyword MajorTopicYN="N">Progeroid</Keyword>
<Keyword MajorTopicYN="N">ROS</Keyword>
<Keyword MajorTopicYN="N">Rcan1</Keyword>
<Keyword MajorTopicYN="N">Superoxide dismutase</Keyword>
<Keyword MajorTopicYN="N">TL</Keyword>
<Keyword MajorTopicYN="N">Telomere length</Keyword>
<Keyword MajorTopicYN="N">Thioredoxin</Keyword>
<Keyword MajorTopicYN="N">Trx1</Keyword>
<Keyword MajorTopicYN="N">bromodeoxyuridine</Keyword>
<Keyword MajorTopicYN="N">dihydrorhodamine</Keyword>
<Keyword MajorTopicYN="N">glutaredoxin 1</Keyword>
<Keyword MajorTopicYN="N">glutathione peroxidase</Keyword>
<Keyword MajorTopicYN="N">glyceraldehyde-3-phosphate dehydrogenase</Keyword>
<Keyword MajorTopicYN="N">reactive oxygen species</Keyword>
<Keyword MajorTopicYN="N">telomere length</Keyword>
<Keyword MajorTopicYN="N">thioredoxin 1</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year>
<Month>05</Month>
<Day>06</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2013</Year>
<Month>10</Month>
<Day>25</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2013</Year>
<Month>10</Month>
<Day>27</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2013</Year>
<Month>11</Month>
<Day>5</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2013</Year>
<Month>11</Month>
<Day>5</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2014</Year>
<Month>3</Month>
<Day>29</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">24184606</ArticleId>
<ArticleId IdType="pii">S0925-4439(13)00319-0</ArticleId>
<ArticleId IdType="doi">10.1016/j.bbadis.2013.10.014</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>Espagne</li>
</country>
<region><li>Communauté valencienne</li>
</region>
</list>
<tree><noCountry><name sortKey="Andaluz, Pilar" sort="Andaluz, Pilar" uniqKey="Andaluz P" first="Pilar" last="Andaluz">Pilar Andaluz</name>
<name sortKey="Audi, Laura" sort="Audi, Laura" uniqKey="Audi L" first="Laura" last="Audí">Laura Audí</name>
<name sortKey="Dasi, Francisco" sort="Dasi, Francisco" uniqKey="Dasi F" first="Francisco" last="Dasí">Francisco Dasí</name>
<name sortKey="Garcia Gimenez, Jose Luis" sort="Garcia Gimenez, Jose Luis" uniqKey="Garcia Gimenez J" first="José Luis" last="García-Giménez">José Luis García-Giménez</name>
<name sortKey="Pallard, Federico V" sort="Pallard, Federico V" uniqKey="Pallard F" first="Federico V" last="Pallard">Federico V. Pallard</name>
<name sortKey="Toran, Nuria" sort="Toran, Nuria" uniqKey="Toran N" first="Nuria" last="Toran">Nuria Toran</name>
<name sortKey="Vi A, Jose" sort="Vi A, Jose" uniqKey="Vi A J" first="José" last="Vi A">José Vi A</name>
</noCountry>
<country name="Espagne"><region name="Communauté valencienne"><name sortKey="Gimeno, Amparo" sort="Gimeno, Amparo" uniqKey="Gimeno A" first="Amparo" last="Gimeno">Amparo Gimeno</name>
</region>
</country>
</tree>
</affiliations>
</record>

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Decreased cell proliferation and higher oxidative stress in fibroblasts from Down Syndrome fetuses. Preliminary study.

Decreased cell proliferation and higher oxidative stress in fibroblasts from Down Syndrome fetuses. Preliminary study.

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