title: Xenon prevents cellular damage in differentiated PC-12 cells exposed to hypoxia.
abstract: BACKGROUND
  The neuroprotective effect of xenon has been demonstrated for glutamatergic neurons. In the present study it is investigated if dopaminergic neurons, i.e. nerve-growth-factor differentiated PC-12 cells, are protected as well against hypoxia-induced cell damage in the presence of xenon.
  
  
  RESULTS
  Pheochromocytoma cells differentiated by addition of nerve growth factor were placed in a N2-saturated atmosphere, a treatment that induced release of dopamine, reaching a maximum after 30 min. By determining extracellular lactate dehydrogenase concentration as marker for concomitant cellular damage, a substantial increase of enzymatic activity was found for N2-treated cells. Replacement of N2 by xenon in such a hypoxic atmosphere resulted in complete protection against cellular damage and prevention of hypoxia-induced dopamine release. Intracellular buffering of Ca2+ using the Ca-chelator 1, 2-bis(2-Aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis(acetoxymethyl) ester (BAPTA) reduced the neuroprotective effect of xenon indicating the essential participation of intracellular Ca2+-ions in the process of xenon-induced neuroprotection.
  
  
  CONCLUSIONS
  The results presented demonstrate the outstanding property of xenon to protect neuron-like cells in a hypoxic situation.
authors.affiliation: University Hospital Charité, Clinic for Anesthesiology and Intensive Care, Experimental Anesthesiology, 14050 Berlin, Germany. christian.Petzelt@charite.de
authors.forename: Christian
authors.initials: C
authors.lastname: Petzelt
authors.forename: Per
authors.initials: P
authors.lastname: Blom
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Schmehl
authors.forename: Jana
authors.initials: J
authors.lastname: Müller
authors.forename: Wolfgang J
authors.initials: WJ
authors.lastname: Kox
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001552:Benzazepines / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D002614:Chelating Agents / Q000494:pharmacology; D004298:Dopamine / Q000009:adverse effects / Q000378:metabolism; D018492:Dopamine Antagonists / Q000494:pharmacology; D018765:Dopamine Uptake Inhibitors / Q000494:pharmacology; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004622:Embryo, Mammalian; D000860:Hypoxia / Q000209:etiology / Q000517:prevention & control*; D007770:L-Lactate Dehydrogenase; D008636:Mesencephalon / Q000166:cytology; D020932:Nerve Growth Factor / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D016716:PC12 Cells / Q000187:drug effects; D010879:Piperazines / Q000494:pharmacology; D051381:Rats; D013469:Sulpiride / Q000494:pharmacology; D014978:Xenon / Q000627:therapeutic use*
chemical_list: D001552:Benzazepines; D002614:Chelating Agents; D018492:Dopamine Antagonists; D018765:Dopamine Uptake Inhibitors; D018696:Neuroprotective Agents; D010879:Piperazines; D014978:Xenon; D004533:Egtazic Acid; D013469:Sulpiride; D020932:Nerve Growth Factor; C043425:vanoxerine; D007770:L-Lactate Dehydrogenase; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D002118:Calcium; D004298:Dopamine