1 Ocak 2021 Dergi makalesi Açık Erişim

Hogberg, Helena T.; da Silveira E Sa, Rita de Cassia; Kleensang, Andre; Bouhifd, Mounir; Cemiloglu Ulker, Ozge; Smirnova, Lena; Behl, Mamta; Maertens, Alexandra; Zhao, Liang; Hartung, Thomas

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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/3667</identifier>
  <creators>
    <creator>
      <creatorName>Hogberg, Helena T.</creatorName>
      <givenName>Helena T.</givenName>
      <familyName>Hogberg</familyName>
      <affiliation>Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Alternat Anim Testing CAAT, Baltimore, MD 21205 USA</affiliation>
    </creator>
    <creator>
      <creatorName>da Silveira E Sa, Rita de Cassia</creatorName>
      <givenName>Rita de Cassia</givenName>
      <familyName>da Silveira E Sa</familyName>
    </creator>
    <creator>
      <creatorName>Kleensang, Andre</creatorName>
      <givenName>Andre</givenName>
      <familyName>Kleensang</familyName>
      <affiliation>Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Alternat Anim Testing CAAT, Baltimore, MD 21205 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Bouhifd, Mounir</creatorName>
      <givenName>Mounir</givenName>
      <familyName>Bouhifd</familyName>
      <affiliation>Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Alternat Anim Testing CAAT, Baltimore, MD 21205 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Cemiloglu Ulker, Ozge</creatorName>
      <givenName>Ozge</givenName>
      <familyName>Cemiloglu Ulker</familyName>
    </creator>
    <creator>
      <creatorName>Smirnova, Lena</creatorName>
      <givenName>Lena</givenName>
      <familyName>Smirnova</familyName>
      <affiliation>Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Alternat Anim Testing CAAT, Baltimore, MD 21205 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Behl, Mamta</creatorName>
      <givenName>Mamta</givenName>
      <familyName>Behl</familyName>
      <affiliation>NIEHS, Natl Toxicol Program, Durham, NC USA</affiliation>
    </creator>
    <creator>
      <creatorName>Maertens, Alexandra</creatorName>
      <givenName>Alexandra</givenName>
      <familyName>Maertens</familyName>
      <affiliation>Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Alternat Anim Testing CAAT, Baltimore, MD 21205 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Zhao, Liang</creatorName>
      <givenName>Liang</givenName>
      <familyName>Zhao</familyName>
    </creator>
    <creator>
      <creatorName>Hartung, Thomas</creatorName>
      <givenName>Thomas</givenName>
      <familyName>Hartung</familyName>
    </creator>
  </creators>
  <titles>
    <title>Organophosphorus Flame Retardants Are Developmental Neurotoxicants In A Rat Primary Brainsphere In Vitro Model</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2021</publicationYear>
  <dates>
    <date dateType="Issued">2021-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/3667</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1007/s00204-020-02903-2</relatedIdentifier>
  </relatedIdentifiers>
  <rightsList>
    <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
  </rightsList>
  <descriptions>
    <description descriptionType="Abstract">Due to regulatory bans and voluntary substitutions, halogenated polybrominated diphenyl ether (PBDE) flame retardants (FR) are increasingly substituted by mainly organophosphorus FR (OPFR). Leveraging a 3D rat primary neural organotypic in vitro model (rat brainsphere), we compare developmental neurotoxic effects of BDE-47-the most abundant PBDE congener-with four OPFR (isopropylated phenyl phosphate-IPP, triphenyl phosphate-TPHP, isodecyl diphenyl phosphate-IDDP, and tricresyl phosphate (also known as trimethyl phenyl phosphate)-TMPP). Employing mass spectroscopy-based metabolomics and transcriptomics, we observe at similar human-relevant non-cytotoxic concentrations (0.1-5 mu M) stronger developmental neurotoxic effects by OPFR. This includes toxicity to neurons in the low mu M range; all FR decrease the neurotransmitters glutamate and GABA (except BDE-47 and TPHP). Furthermore,n-acetyl aspartate (NAA), considered a neurologic diagnostic molecule, was decreased by all OPFR. At similar concentrations, the FR currently in use decreased plasma membrane dopamine active transporter expression, while BDE-47 did not. Several findings suggest astrogliosis induced by the OPFR, but not BDE-47. At the 5 mu M concentrations, the OPFR more than BDE-47 interfered with myelination. An increase of cytokine gene and receptor expressions suggests that exposure to OPFR may induce an inflammatory response. Pathway/category overrepresentation shows disruption in 1) transmission of action potentials, cell-cell signaling, synaptic transmission, receptor signaling, (2) immune response, inflammation, defense response, (3) cell cycle and (4) lipids metabolism and transportation. Taken together, this appears to be a case of regretful substitution with substances not less developmentally neurotoxic in a primary rat 3D model.</description>
  </descriptions>
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