The semiconductor elements arsenic and indium induce apoptosis in rat thymocytes.
Identifieur interne : 004006 ( Main/Exploration ); précédent : 004005; suivant : 004007The semiconductor elements arsenic and indium induce apoptosis in rat thymocytes.
Auteurs : RBID : pubmed:9129167English descriptors
- KwdEn :
- Animals, Apoptosis (drug effects), Arsenic Poisoning, Cell Death (drug effects), Cell Survival (drug effects), Cells, Cultured, DNA Fragmentation (drug effects), Dose-Response Relationship, Drug, Electrophoresis, Agar Gel, Flow Cytometry, Indium (toxicity), Male, Necrosis, Propidium (chemistry), Rats, Rats, Sprague-Dawley, Semiconductors, T-Lymphocytes (cytology), T-Lymphocytes (drug effects), Thymus Gland (cytology), Thymus Gland (drug effects).
- MESH :
- chemical , chemistry : Propidium.
- chemical , toxicity : Indium.
- cytology : T-Lymphocytes, Thymus Gland.
- drug effects : Apoptosis, Cell Death, Cell Survival, DNA Fragmentation, T-Lymphocytes, Thymus Gland.
- Animals, Arsenic Poisoning, Cells, Cultured, Dose-Response Relationship, Drug, Electrophoresis, Agar Gel, Flow Cytometry, Male, Necrosis, Rats, Rats, Sprague-Dawley, Semiconductors.
Abstract
Indium arsenide and gallium arsenide are important new materials in the semiconductor industry due to their superior electronic properties in comparison with the older silicon-based materials. Animal experiments have shown that exposure to these compounds induces marked alterations in gene expression and immune response. Toxicity to the immune system has frequently been related to T and B cell apoptosis. In the present study we show that the semiconductor elements indium (In) and arsenic (As) are able to induce apoptosis in rat thymocytes in vitro. The results show that exposure to InCl3 (1, 10, or 100 microM) or Na AsO2 (0.01, 0.1, or 1 microM) induced DNA laddering after 6 h of incubation without compromising cell viability. These results were corroborated by flow cytometry analysis of propidium iodide-loaded cells, showing a typical high hypodiploid DNA peak in apoptotic thymocytes. Higher doses of In (1 mM) or As (10-100 microM) induced cell death by necrosis. These data indicate that In and As can induce apoptosis and necrosis in T lymphocytes in a dose-dependent manner, which may be of relevance for their immunotoxicity.
PubMed: 9129167
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Animal experiments have shown that exposure to these compounds induces marked alterations in gene expression and immune response. Toxicity to the immune system has frequently been related to T and B cell apoptosis. In the present study we show that the semiconductor elements indium (In) and arsenic (As) are able to induce apoptosis in rat thymocytes in vitro. The results show that exposure to InCl3 (1, 10, or 100 microM) or Na AsO2 (0.01, 0.1, or 1 microM) induced DNA laddering after 6 h of incubation without compromising cell viability. These results were corroborated by flow cytometry analysis of propidium iodide-loaded cells, showing a typical high hypodiploid DNA peak in apoptotic thymocytes. Higher doses of In (1 mM) or As (10-100 microM) induced cell death by necrosis. These data indicate that In and As can induce apoptosis and necrosis in T lymphocytes in a dose-dependent manner, which may be of relevance for their immunotoxicity.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">9129167</PMID><DateCreated><Year>1997</Year><Month>05</Month><Day>19</Day></DateCreated><DateCompleted><Year>1997</Year><Month>05</Month><Day>19</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0300-483X</ISSN><JournalIssue CitedMedium="Print"><Volume>118</Volume><Issue>2-3</Issue><PubDate><Year>1997</Year><Month>Mar</Month><Day>28</Day></PubDate></JournalIssue><Title>Toxicology</Title><ISOAbbreviation>Toxicology</ISOAbbreviation></Journal><ArticleTitle>The semiconductor elements arsenic and indium induce apoptosis in rat thymocytes.</ArticleTitle><Pagination><MedlinePgn>129-36</MedlinePgn></Pagination><Abstract><AbstractText>Indium arsenide and gallium arsenide are important new materials in the semiconductor industry due to their superior electronic properties in comparison with the older silicon-based materials. Animal experiments have shown that exposure to these compounds induces marked alterations in gene expression and immune response. Toxicity to the immune system has frequently been related to T and B cell apoptosis. In the present study we show that the semiconductor elements indium (In) and arsenic (As) are able to induce apoptosis in rat thymocytes in vitro. The results show that exposure to InCl3 (1, 10, or 100 microM) or Na AsO2 (0.01, 0.1, or 1 microM) induced DNA laddering after 6 h of incubation without compromising cell viability. These results were corroborated by flow cytometry analysis of propidium iodide-loaded cells, showing a typical high hypodiploid DNA peak in apoptotic thymocytes. Higher doses of In (1 mM) or As (10-100 microM) induced cell death by necrosis. These data indicate that In and As can induce apoptosis and necrosis in T lymphocytes in a dose-dependent manner, which may be of relevance for their immunotoxicity.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bustamante</LastName><ForeName>J</ForeName><Initials>J</Initials><Affiliation>Department of Physical Chemistry, School of Pharmacy and Biochemistry, University of Buenos Aires, Argentina.</Affiliation></Author><Author ValidYN="Y"><LastName>Dock</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Vahter</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Fowler</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Orrenius</LastName><ForeName>S</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType>Journal Article</PublicationType><PublicationType>Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>IRELAND</Country><MedlineTA>Toxicology</MedlineTA><NlmUniqueID>0361055</NlmUniqueID><ISSNLinking>0300-483X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>045A6V3VFX</RegistryNumber><NameOfSubstance>Indium</NameOfSubstance></Chemical><Chemical><RegistryNumber>31JB8MKF8Z</RegistryNumber><NameOfSubstance>indium trichloride</NameOfSubstance></Chemical><Chemical><RegistryNumber>36015-30-2</RegistryNumber><NameOfSubstance>Propidium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y">Arsenic Poisoning</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Cell Death</DescriptorName><QualifierName MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">DNA Fragmentation</DescriptorName><QualifierName MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Electrophoresis, Agar Gel</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Flow Cytometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Indium</DescriptorName><QualifierName MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Necrosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Propidium</DescriptorName><QualifierName MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Semiconductors</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">T-Lymphocytes</DescriptorName><QualifierName MajorTopicYN="N">cytology</QualifierName><QualifierName MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Thymus Gland</DescriptorName><QualifierName MajorTopicYN="N">cytology</QualifierName><QualifierName MajorTopicYN="Y">drug effects</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1997</Year><Month>3</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1997</Year><Month>3</Month><Day>28</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1997</Year><Month>3</Month><Day>28</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9129167</ArticleId><ArticleId IdType="pii">S0300-483X(96)03607-4</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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