Embryotoxic and teratogenic effects of indium chloride in rats and rabbits.
Identifieur interne : 003A21 ( Main/Exploration ); précédent : 003A20; suivant : 003A22Embryotoxic and teratogenic effects of indium chloride in rats and rabbits.
Auteurs : RBID : pubmed:10681097English descriptors
- KwdEn :
- Abnormalities, Drug-Induced (pathology), Ammonia (metabolism), Animals, Blood Cell Count, Embryo, Mammalian (drug effects), Female, Gestational Age, Hemoglobins (metabolism), Indium (blood), Indium (pharmacokinetics), Indium (toxicity), Placenta (metabolism), Pregnancy, Rabbits, Rats, Rats, Sprague-Dawley, Species Specificity, Teratogens (pharmacokinetics), Teratogens (toxicity).
- MESH :
- chemical , blood : Indium.
- chemical , metabolism : Ammonia, Hemoglobins.
- drug effects : Embryo, Mammalian.
- metabolism : Placenta.
- pathology : Abnormalities, Drug-Induced.
- chemical , pharmacokinetics : Indium, Teratogens.
- chemical , toxicity : Indium, Teratogens.
- Animals, Blood Cell Count, Female, Gestational Age, Pregnancy, Rabbits, Rats, Rats, Sprague-Dawley, Species Specificity.
Abstract
Daily indium chloride doses of control (0), 50, 100, 200, or 400 mg/kg were administered orally to Sprague-Dawley rats by gavage, on d 6-15 of gestation, and daily metal doses of control (0), 50, 100, or 200 mg/kg were administered to New Zealand rabbits on d 6-20 of gestation. Further groups of pregnant rats were treated with control (0) or 400 mg/kg indium chloride orally on one of d 8, 9, 10, 11, 12, 13, 14, or 15 of gestation. The dams and fetuses were examined on d 21 (rats) and 30 (rabbits) of gestation, using standard teratological methods. Indium concentration was determined in the maternal and fetal blood, as well as in the amniotic fluid, by atomic absorption spectrometry. Indium was found to cross the placenta and appeared in fetal blood in proportion to the metal concentration of the maternal blood. In the amniotic fluid, indium concentrations remained below the detection limit. In rats, indium chloride produced dose-dependent maternal toxic effects, with a dose of 400 mg/kg inducing embryotoxicity (embryolethality) and teratogenicity. Doses of 200 and 100 mg/kg were embryotoxic (retarding) and teratogenic, causing skeletal and visceral anomalies in addition to external anomalies (rudimentary or missing tail, syndactylia, clubfoot, exencephalia) in rats. In rabbits, 200 mg/kg indium chloride was lethal for the dams and the embryos (some of the animals died, and the number of abortions and full resorptions increased). This dose was found to be teratogenic (caused gross renal anomalies) and increased the frequency of fetuses with skeletal retardation. In rats, the effects of indium chloride causing fetal retardation was found to be independent of exposure time. The teratogenic effects were the highest on d 11 and 12 of gestation, when indium chloride caused gross external malformations. Data suggest that the teratogenic effects of indium chloride can be attributed primarily to a direct cytotoxic action of indium resulting from placental transfer, but the effect is not a selective one, as it appears only in the presence of maternal toxic effects.
PubMed: 10681097
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Embryotoxic and teratogenic effects of indium chloride in rats and rabbits.</title><author><name sortKey="Ungv Ry, G" uniqKey="Ungv Ry G">G Ungváry</name><affiliation wicri:level="1"><nlm:affiliation>Jözsef Fodor National Center of Public Health, Budapest, Hungary.</nlm:affiliation><country xml:lang="fr">Hongrie</country><wicri:regionArea>Jözsef Fodor National Center of Public Health, Budapest</wicri:regionArea></affiliation></author><author><name sortKey="Szakm Ry, E" uniqKey="Szakm Ry E">E Szakmáry</name></author><author><name sortKey="T Trai, E" uniqKey="T Trai E">E Tátrai</name></author><author><name sortKey="Hud K, A" uniqKey="Hud K A">A Hudák</name></author><author><name sortKey="N Ray, M" uniqKey="N Ray M">M Náray</name></author><author><name sortKey="Morvai, V" uniqKey="Morvai V">V Morvai</name></author></titleStmt><publicationStmt><date when="2000">2000</date><idno type="RBID">pubmed:10681097</idno><idno type="pmid">10681097</idno><idno type="wicri:Area/Main/Corpus">003D35</idno><idno type="wicri:Area/Main/Curation">003D35</idno><idno type="wicri:Area/Main/Exploration">003A21</idno></publicationStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Abnormalities, Drug-Induced (pathology)</term><term>Ammonia (metabolism)</term><term>Animals</term><term>Blood Cell Count</term><term>Embryo, Mammalian (drug effects)</term><term>Female</term><term>Gestational Age</term><term>Hemoglobins (metabolism)</term><term>Indium (blood)</term><term>Indium (pharmacokinetics)</term><term>Indium (toxicity)</term><term>Placenta (metabolism)</term><term>Pregnancy</term><term>Rabbits</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Species Specificity</term><term>Teratogens (pharmacokinetics)</term><term>Teratogens (toxicity)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Indium</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Ammonia</term><term>Hemoglobins</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Embryo, Mammalian</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Placenta</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Abnormalities, Drug-Induced</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Indium</term><term>Teratogens</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Indium</term><term>Teratogens</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Blood Cell Count</term><term>Female</term><term>Gestational Age</term><term>Pregnancy</term><term>Rabbits</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Species Specificity</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Daily indium chloride doses of control (0), 50, 100, 200, or 400 mg/kg were administered orally to Sprague-Dawley rats by gavage, on d 6-15 of gestation, and daily metal doses of control (0), 50, 100, or 200 mg/kg were administered to New Zealand rabbits on d 6-20 of gestation. Further groups of pregnant rats were treated with control (0) or 400 mg/kg indium chloride orally on one of d 8, 9, 10, 11, 12, 13, 14, or 15 of gestation. The dams and fetuses were examined on d 21 (rats) and 30 (rabbits) of gestation, using standard teratological methods. Indium concentration was determined in the maternal and fetal blood, as well as in the amniotic fluid, by atomic absorption spectrometry. Indium was found to cross the placenta and appeared in fetal blood in proportion to the metal concentration of the maternal blood. In the amniotic fluid, indium concentrations remained below the detection limit. In rats, indium chloride produced dose-dependent maternal toxic effects, with a dose of 400 mg/kg inducing embryotoxicity (embryolethality) and teratogenicity. Doses of 200 and 100 mg/kg were embryotoxic (retarding) and teratogenic, causing skeletal and visceral anomalies in addition to external anomalies (rudimentary or missing tail, syndactylia, clubfoot, exencephalia) in rats. In rabbits, 200 mg/kg indium chloride was lethal for the dams and the embryos (some of the animals died, and the number of abortions and full resorptions increased). This dose was found to be teratogenic (caused gross renal anomalies) and increased the frequency of fetuses with skeletal retardation. In rats, the effects of indium chloride causing fetal retardation was found to be independent of exposure time. The teratogenic effects were the highest on d 11 and 12 of gestation, when indium chloride caused gross external malformations. Data suggest that the teratogenic effects of indium chloride can be attributed primarily to a direct cytotoxic action of indium resulting from placental transfer, but the effect is not a selective one, as it appears only in the presence of maternal toxic effects.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">10681097</PMID><DateCreated><Year>2000</Year><Month>02</Month><Day>24</Day></DateCreated><DateCompleted><Year>2000</Year><Month>02</Month><Day>24</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1528-7394</ISSN><JournalIssue CitedMedium="Print"><Volume>59</Volume><Issue>1</Issue><PubDate><Year>2000</Year><Month>Jan</Month><Day>14</Day></PubDate></JournalIssue><Title>Journal of toxicology and environmental health. Part A</Title><ISOAbbreviation>J. Toxicol. Environ. Health Part A</ISOAbbreviation></Journal><ArticleTitle>Embryotoxic and teratogenic effects of indium chloride in rats and rabbits.</ArticleTitle><Pagination><MedlinePgn>27-42</MedlinePgn></Pagination><Abstract><AbstractText>Daily indium chloride doses of control (0), 50, 100, 200, or 400 mg/kg were administered orally to Sprague-Dawley rats by gavage, on d 6-15 of gestation, and daily metal doses of control (0), 50, 100, or 200 mg/kg were administered to New Zealand rabbits on d 6-20 of gestation. Further groups of pregnant rats were treated with control (0) or 400 mg/kg indium chloride orally on one of d 8, 9, 10, 11, 12, 13, 14, or 15 of gestation. The dams and fetuses were examined on d 21 (rats) and 30 (rabbits) of gestation, using standard teratological methods. Indium concentration was determined in the maternal and fetal blood, as well as in the amniotic fluid, by atomic absorption spectrometry. Indium was found to cross the placenta and appeared in fetal blood in proportion to the metal concentration of the maternal blood. In the amniotic fluid, indium concentrations remained below the detection limit. In rats, indium chloride produced dose-dependent maternal toxic effects, with a dose of 400 mg/kg inducing embryotoxicity (embryolethality) and teratogenicity. Doses of 200 and 100 mg/kg were embryotoxic (retarding) and teratogenic, causing skeletal and visceral anomalies in addition to external anomalies (rudimentary or missing tail, syndactylia, clubfoot, exencephalia) in rats. In rabbits, 200 mg/kg indium chloride was lethal for the dams and the embryos (some of the animals died, and the number of abortions and full resorptions increased). This dose was found to be teratogenic (caused gross renal anomalies) and increased the frequency of fetuses with skeletal retardation. In rats, the effects of indium chloride causing fetal retardation was found to be independent of exposure time. The teratogenic effects were the highest on d 11 and 12 of gestation, when indium chloride caused gross external malformations. Data suggest that the teratogenic effects of indium chloride can be attributed primarily to a direct cytotoxic action of indium resulting from placental transfer, but the effect is not a selective one, as it appears only in the presence of maternal toxic effects.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ungváry</LastName><ForeName>G</ForeName><Initials>G</Initials><Affiliation>Jözsef Fodor National Center of Public Health, Budapest, Hungary.</Affiliation></Author><Author ValidYN="Y"><LastName>Szakmáry</LastName><ForeName>E</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Tátrai</LastName><ForeName>E</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Hudák</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Náray</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Morvai</LastName><ForeName>V</ForeName><Initials>V</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType>Comparative Study</PublicationType><PublicationType>Journal Article</PublicationType><PublicationType>Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>J Toxicol Environ Health A</MedlineTA><NlmUniqueID>100960995</NlmUniqueID><ISSNLinking>0098-4108</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance>Hemoglobins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance>Teratogens</NameOfSubstance></Chemical><Chemical><RegistryNumber>045A6V3VFX</RegistryNumber><NameOfSubstance>Indium</NameOfSubstance></Chemical><Chemical><RegistryNumber>31JB8MKF8Z</RegistryNumber><NameOfSubstance>indium trichloride</NameOfSubstance></Chemical><Chemical><RegistryNumber>7664-41-7</RegistryNumber><NameOfSubstance>Ammonia</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N">Abnormalities, Drug-Induced</DescriptorName><QualifierName MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Ammonia</DescriptorName><QualifierName MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Blood Cell Count</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Embryo, Mammalian</DescriptorName><QualifierName MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Gestational Age</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Hemoglobins</DescriptorName><QualifierName MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Indium</DescriptorName><QualifierName MajorTopicYN="N">blood</QualifierName><QualifierName MajorTopicYN="N">pharmacokinetics</QualifierName><QualifierName MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Placenta</DescriptorName><QualifierName MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Rabbits</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Species Specificity</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Teratogens</DescriptorName><QualifierName MajorTopicYN="N">pharmacokinetics</QualifierName><QualifierName MajorTopicYN="Y">toxicity</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2000</Year><Month>2</Month><Day>19</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2000</Year><Month>2</Month><Day>26</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2000</Year><Month>2</Month><Day>19</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10681097</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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