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@ARTICLE{Grg:10219,
      author       = {Görg, B. and Qvartskhava, N. and Bidmon, H.-J. and
                      Palomero-Gallagher, N. and Kircheis, G. and Zilles, K. and
                      Häussinger, D.},
      title        = {{O}xidative stress markers in the brain of patients with
                      cirrhosis and hepatic encephalopathy},
      journal      = {Hepatology},
      volume       = {52},
      issn         = {0270-9139},
      address      = {New York [u.a.]},
      publisher    = {Wiley Interscience},
      reportid     = {PreJuSER-10219},
      pages        = {256 - 265},
      year         = {2010},
      note         = {This Study was Supported by Deutsche Forschungsgemeinschaft
                      through Sonderforschungsbereich 575 "Experimentelle
                      Hepatologle" (Dusseldorf).},
      abstract     = {Cell culture studies and animal models point to an
                      important role of oxidative/nitrosative stress in the
                      pathogenesis of cerebral ammonia toxicity. However, it is
                      unknown whether oxidative/nitrosative stress in the brain is
                      also characteristic of hepatic encephalopathy (HE) in
                      humans. We therefore analyzed post mortem cortical brain
                      tissue samples from patients with cirrhosis dying with or
                      without HE in comparison with brains from patients without
                      liver disease. Significantly elevated levels of protein
                      tyrosine-nitrated proteins, heat shock protein-27, and
                      8-hydroxyguanosine as a marker for RNA oxidation were found
                      in the cerebral cortex of HE patients, but not of patients
                      with cirrhosis but without HE. Glutamine synthetase (GS)
                      activity was significantly decreased, whereas GS protein
                      expression was not significantly affected. Protein
                      expression of the glutamate/aspartate cotransporter was
                      up-regulated in HE, whereas protein expression of neuronal
                      and inducible nitric oxide synthases, manganese-dependent
                      and copper/zinc-dependent superoxide dismutase, and glial
                      glutamate transporter-1 were not significantly increased.
                      CONCLUSION: These data indicate that HE in patients with
                      cirrhosis is associated with oxidative/nitrosative stress,
                      protein tyrosine nitration, and RNA oxidation, suggesting a
                      role of oxidative stress in the pathogenesis of HE in
                      patients with cirrhosis.},
      keywords     = {Adult / Aged / Amino Acid Transport System X-AG: analysis /
                      Amino Acid Transport System X-AG: metabolism / Biological
                      Markers: analysis / Biological Markers: metabolism /
                      Cerebral Cortex: chemistry / Cerebral Cortex: metabolism /
                      Excitatory Amino Acid Transporter 2: analysis / Excitatory
                      Amino Acid Transporter 2: metabolism / Female /
                      Glutamate-Ammonia Ligase: analysis / Glutamate-Ammonia
                      Ligase: metabolism / Guanosine: analogs $\&$ derivatives /
                      Guanosine: analysis / Guanosine: metabolism / HSP27
                      Heat-Shock Proteins: analysis / HSP27 Heat-Shock Proteins:
                      metabolism / Hepatic Encephalopathy: etiology / Hepatic
                      Encephalopathy: metabolism / Humans / Liver Cirrhosis:
                      complications / Male / Middle Aged / Nitrates: analysis /
                      Nitrates: metabolism / Oxidative Stress / RNA: analysis /
                      RNA: metabolism / Tyrosine: analysis / Tyrosine: metabolism
                      / Amino Acid Transport System X-AG (NLM Chemicals) /
                      Biological Markers (NLM Chemicals) / Excitatory Amino Acid
                      Transporter 2 (NLM Chemicals) / HSP27 Heat-Shock Proteins
                      (NLM Chemicals) / Nitrates (NLM Chemicals) / Guanosine (NLM
                      Chemicals) / 8-hydroxyguanosine (NLM Chemicals) / Tyrosine
                      (NLM Chemicals) / RNA (NLM Chemicals) / Glutamate-Ammonia
                      Ligase (NLM Chemicals) / J (WoSType)},
      cin          = {INM-2 / JARA-BRAIN},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-2-20090406 / $I:(DE-82)080010_20140620$},
      pnm          = {Funktion und Dysfunktion des Nervensystems (FUEK409) /
                      89571 - Connectivity and Activity (POF2-89571)},
      pid          = {G:(DE-Juel1)FUEK409 / G:(DE-HGF)POF2-89571},
      shelfmark    = {Gastroenterology $\&$ Hepatology},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:20583283},
      pmc          = {pmc:PMC3395472},
      UT           = {WOS:000279409200028},
      doi          = {10.1002/hep.23656},
      url          = {https://juser.fz-juelich.de/record/10219},
}