<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Hernadfalvi, Noemi</dc:creator>
  <dc:creator>Langhans, Wolfgang</dc:creator>
  <dc:creator>Meyenburg, Claudia von</dc:creator>
  <dc:creator>Onteniente, Brigitte</dc:creator>
  <dc:creator>Richard, Denis</dc:creator>
  <dc:creator>Arsenijevic, Denis</dc:creator>
  <dc:date>2007</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">To study the role of the redox state regulator glutathione (GSH) in bacterial  lipopolysaccharide (LPS)-induced anorexia we measured GSH in liver, serum and  brain in response to intraperitoneal (ip) lipopolysaccharide (LPS, 4μg/mouse) injection  in LPS-naïve and LPS-pretreated (4 μg/mouse) mice. LPS reduced food intake in  LPS-naïve mice and LPS pretreatment attenuated this effect. LPS reduced total  reduced GSH at 24 hours after injection in LPS-naïve mice. On the other hand, LPS  pretreatment caused an upregulation of GSH levels in brain and liver, and this was  associated with a significant attenuation of LPS-induced anorexia. In addition, LPS  pretreatment increased mitochondrial GSH levels in brain and liver. Pharmacological  GSH depletion with diethylmaleate and L-buthionine sulfoximine in LPS-pretreated  mice ablated the hyposensitivity to the anorexic effect of LPS. Together, these findings  suggest a prominent role for GSH and its intracellular repartition in LPS anorexia.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://folia.unifr.ch/global/documents/300578</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/300578/files/arsenijevic_rgh.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1684/ecn.2007.0090</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>License undefined</dc:rights>
  <dc:source>European Cytokine Network. - 2007, vol. 18, no. 2, p. 39-45</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">reactive oxygen species</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">cytokine</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">food intake</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">liver</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">brain</dc:subject>
  <dc:subject xmlns:ns6="xml" ns6:lang="en">mitochondria</dc:subject>
  <dc:subject>info:eu-repo/classification/udc/57</dc:subject>
  <dc:title xmlns:ns7="xml" ns7:lang="en">Role for glutathione in the hyposensitivity of LPS-pretreated mice to LPS anorexia</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
