Research Topics
| R DringenSummaryCountry: Germany Publications
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Publications
Peroxide detoxification by brain cellsRalf Dringen
Interfakultares Institut fur Biochemie der Universitat Tubingen, Hoppe Seyler Strasse 4, D 72076 Tubingen, Germany
J Neurosci Res 79:157-65. 2005..This article gives an overview on the mechanisms involved in peroxide detoxification in brain cells and on the capacity of the different types of neural cells to dispose of peroxides...
The multidrug resistance protein 1 (Mrp1), but not Mrp5, mediates export of glutathione and glutathione disulfide from brain astrocytesTobias Minich
Institute for Biochemistry, University of Tuebingen, Germany
J Neurochem 97:373-84. 2006..These data demonstrate that in astrocytes Mrp1 mediates 60% of the GSH export, that Mrp1 is exclusively responsible for GSSG export and that Mrp5 does not contribute to these transport processes...
Aminopeptidase N mediates the utilization of the GSH precursor CysGly by cultured neuronsR Dringen
Physiologisch chemisches Institut der Universität, Hoppe Seyler Street, 4, D 72076 Tubingen, Germany
J Neurosci Res 66:1003-8. 2001..The data presented demonstrates that cultured rat neurons express ApN and that this ectopeptidase participates in the utilization of CysGly as precursor for neuronal glutathione...
Metabolism and functions of glutathione in brainR Dringen
Physiologisch chemisches Institut der Universität, Hoppe Seyler Str 4, D 72076 Tubingen, Germany
Prog Neurobiol 62:649-71. 2000..These results also suggest an involvement of a compromised astroglial glutathione system in the oxidative stress reported for neurological disorders...
N-acetylcysteine, but not methionine or 2-oxothiazolidine-4-carboxylate, serves as cysteine donor for the synthesis of glutathione in cultured neurons derived from embryonal rat brainR Dringen
Physiologisch chemisches Institut der Universität, Tubingen, Germany
Neurosci Lett 259:79-82. 1999..In contrast, generation of cysteine from 2-oxothiazolidine-4-carboxylate by the reaction of 5-oxoprolinase or from methionine by the transsulfuration pathway appears not to take place in these cultured neurons...
Glutathione restoration as indicator for cellular metabolism of astroglial cellsR Dringen
Physiologisch chemisches Institut der Universität Tübingen, Deutschland
Dev Neurosci 20:401-7. 1998..The results presented demonstrate that glutathione restoration can be used as an indicator for amino acid as well as energy metabolism of astroglial cells...
Rapid clearance of tertiary butyl hydroperoxide by cultured astroglial cells via oxidation of glutathioneR Dringen
Physiologisch chemisches Institut der Universität, Tubingen, Germany
Glia 23:139-45. 1998..In the presence of 3 mM mercaptosuccinate oxidation of glutathione was almost completely inhibited. These results demonstrate that an exogenous hydroperoxide is detoxified rapidly by astroglial cells via the glutathione system...
Involvement of glutathione peroxidase and catalase in the disposal of exogenous hydrogen peroxide by cultured astroglial cellsR Dringen
Physiologisch Chemisches Institut, Eberhard Karls Universitat Tubingen, Germany
Brain Res 759:67-75. 1997..These results demonstrate that glutathione peroxidase and catalase are involved in the detoxification of H2O2 by astroglial cells and that both enzymes are able to substitute for each other in the detoxification of H2O2...
Anethole dithiolethione, a putative neuroprotectant, increases intracellular and extracellular glutathione levels during starvation of cultured astroglial cellsR Dringen
Physiologisch chemisches Institut der Universität Tübingen, Germany
Naunyn Schmiedebergs Arch Pharmacol 358:616-22. 1998..Considering the lowered glutathione levels in neurodegenerative syndromes, we conclude that further evaluation of the therapeutic potential of the compound is warranted...
The multidrug resistance protein MRP1 mediates the release of glutathione disulfide from rat astrocytes during oxidative stressJ Hirrlinger
Physiologisch chemisches Institut der Universität, Tubingen, Germany
J Neurochem 76:627-36. 2001..Our data identify rat astrocytes as a MRP1-expressin, brain cell type and demonstrate that this transporter participates in the release of glutathione disulfide from astrocytes during oxidative stress...
The gamma-glutamyl transpeptidase inhibitor acivicin preserves glutathione released by astroglial cells in cultureR Dringen
Physiologisch chemisches Institut der Universität, Tubingen
Neurochem Res 22:727-33. 1997..These results suggest that glutathione released from astroglial cells can serve as substrate for the ectoenzyme gamma-glutamyl transpeptidase of these cells...
Glutathione metabolism in brain metabolic interaction between astrocytes and neurons in the defense against reactive oxygen speciesR Dringen
Physiologisch chemisches Institut der Universität, Tubingen, Germany
Eur J Biochem 267:4912-6. 2000..In coculture astrocytes protect neurons against the toxicity of reactive oxygen species. One mechanism of this interaction is the supply by astrocytes of glutathione precursors to neurons...
Glutathione peroxidase 1 and glutathione are required to protect mouse astrocytes from iron-mediated hydrogen peroxide toxicityJeff R Liddell
School of Psychology, Psychiatry and Psychological Medicine, Monash University, Clayton, Victoria, Australia
J Neurosci Res 84:578-86. 2006..These results demonstrate that GPx1 contributes to the rapid clearance of H(2)O(2) by mouse astrocytes and that both GPx1 and a high concentration of glutathione are required to protect these cells from iron-dependent peroxide damage...
Expression of hepatoma-derived growth factor family members in the adult central nervous systemHeba M El-Tahir
Institut fur Physiologische Chemie, Rheinische Friedrich Wilhelms Universitat, Nussallee 11, 53115 Bonn, Germany
BMC Neurosci 7:6. 2006..In addition we performed Western blot analysis of various brain regions as well as neuronal and glial cell cultures...
Multidrug resistance protein 1-mediated export of glutathione and glutathione disulfide from brain astrocytesJohannes Hirrlinger
Max-Planck Institute for Experimental Medicine, Department of Neurogenetics, , Germany
Methods Enzymol 400:395-409. 2005..In addition, our methods could be useful in investigating mechanisms of export of GSH and GSSG from other cell types...
Oxidative and antioxidative potential of brain microglial cellsRalf Dringen
Faculty 2 Biology Chemistry, University of Bremen, Bremen, Germany
Antioxid Redox Signal 7:1223-33. 2005..Their good antioxidative potential protects microglial cells against oxidative damage that could impair important functions of these cells in defense and repair of the brain...
Progressive degeneration of human mesencephalic neuron-derived cells triggered by dopamine-dependent oxidative stress is dependent on the mixed-lineage kinase pathwayJulie Lotharius
Department of Disease Biology, H Lundbeck A S, 2500 Valby, Denmark
J Neurosci 25:6329-42. 2005....
Glucose-6-phosphate dehydrogenase and NADPH-consuming enzymes in the rat olfactory bulbEnrica Biagiotti
Institute of Biological Chemistry G. Fornaini, University of Urbino Carlo Bo, Urbino, Italy
J Neurosci Res 80:434-41. 2005....
Chemotherapy-induced cell death in primary cerebellar granule neurons but not in astrocytes: in vitro paradigm of differential neurotoxicityAntje Wick
Laboratory of Molecular Neurodegeneration, Department of General Neurology and Hertie Institute for Clinical Brain Research, , Germany
J Neurochem 91:1067-74. 2004..zVAD-fmk, a caspase inhibitor and brain-derived neurotrophic factor (BDNF), but not MK-801, a non-competitive NMDA receptor antagonist, significantly reduced vincristine- or topotecan-induced cell death...
Endogenous glutathione and catalase protect cultured rat astrocytes from the iron-mediated toxicity of hydrogen peroxideJeff R Liddell
Department of Psychology, Monash University, Clayton, Vic. 3800, Australia
Neurosci Lett 364:164-7. 2004..These results demonstrate that chelatable iron is involved in the toxicity of H2O2 and that both the glutathione system and catalase protect astrocytes from this toxicity...
Cytosolic and mitochondrial isoforms of NADP+-dependent isocitrate dehydrogenases are expressed in cultured rat neurons, astrocytes, oligodendrocytes and microglial cellsTobias Minich
, , Germany
J Neurochem 86:605-14. 2003..In contrast, in cultures of neurons and oligodendrocytes about 75% of total ICDH activity was present in the cytosolic fractions. Putative functions of ICDHs in cytosol and mitochondria of brain cells are discussed...
Expression of mRNAs of multidrug resistance proteins (Mrps) in cultured rat astrocytes, oligodendrocytes, microglial cells and neuronesJohannes Hirrlinger
, , Germany
J Neurochem 82:716-9. 2002..Putative physiological functions of Mrps in brain cells are discussed...
Oligodendroglial cells in culture effectively dispose of exogenous hydrogen peroxide: comparison with cultured neurones, astroglial and microglial cellsJohannes Hirrlinger
, , Germany
J Neurochem 82:635-44. 2002....
Effects of dopamine on the glutathione metabolism of cultured astroglial cells: implications for Parkinson's diseaseJohannes Hirrlinger
, , Germany
J Neurochem 82:458-67. 2002..These observations are discussed in the context of the brain's GSH metabolism in Parkinson's disease...
Glutathione release from cultured brain cells: multidrug resistance protein 1 mediates the release of GSH from rat astroglial cellsJohannes Hirrlinger
Physiologisch chemisches Institut der Universität, Tubingen, Germany
J Neurosci Res 69:318-26. 2002..In conclusion, the data presented are a strong indication that Mrp1 participates in the release of GSH from astroglial cells...
Zinc stimulates the production of toxic reactive oxygen species (ROS) and inhibits glutathione reductase in astrocytesGlenda M Bishop
School of Psychology, Psychiatry and Psychological Medicine, Monash University, Wellington Rd, Clayton, Victoria, Australia
Free Radic Biol Med 42:1222-30. 2007..Taken together these results indicate that Zn toxicity in astrocytes is primarily associated with the generation of intracellular ROS, rather than the inhibition of GR...
