Trumbeckaite 2013 Mitochondrion: Difference between revisions
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|abstract=We have introduced a sensitive method for studying oxygen/glucose deprivation (OGD)-induced mitochondrial alterations in homogenates of organotypic hippocampal slice cultures (slices) by high-resolution respirometry. Using this approach, we tested the neuroprotective potential of the novel non-immunosuppressive cyclosporin (CsA) derivative Cs9 in comparison with CsA, the immunosuppressive CsA analogue [D-Ser](8)CsA, and MK 801, a N-methyl-D-aspartate (NMDA) receptor antagonist. OGD/reperfusion reduced the glutamate/malate dependent (and protein-related) state 3 respiration to 30% of its value under control conditions. All of the above drugs reversed this effect, with an increase to >88% of the value for control slices not exposed to OGD. We conclude that Cs9, [D-Ser](8)CsA, and MK 801, despite their different modes of action, protect mitochondria from OGD-induced damage. | |abstract=We have introduced a sensitive method for studying oxygen/glucose deprivation (OGD)-induced mitochondrial alterations in homogenates of organotypic hippocampal slice cultures (slices) by high-resolution respirometry. Using this approach, we tested the neuroprotective potential of the novel non-immunosuppressive cyclosporin (CsA) derivative Cs9 in comparison with CsA, the immunosuppressive CsA analogue [D-Ser](8)CsA, and MK 801, a N-methyl-D-aspartate (NMDA) receptor antagonist. OGD/reperfusion reduced the glutamate/malate dependent (and protein-related) state 3 respiration to 30% of its value under control conditions. All of the above drugs reversed this effect, with an increase to >88% of the value for control slices not exposed to OGD. We conclude that Cs9, [D-Ser](8)CsA, and MK 801, despite their different modes of action, protect mitochondria from OGD-induced damage. | ||
|keywords=cyclosporin (CsA) derivative Cs9, CsA analogue [D-Ser](8)CsA, NMDA-receptor antagonist, neuroprotection | |keywords=cyclosporin (CsA) derivative Cs9, CsA analogue [D-Ser](8)CsA, NMDA-receptor antagonist, neuroprotection | ||
|mipnetlab=DE Magdeburg Gellerich FN, EE Tartu Seppet EK, ย | |mipnetlab=DE Magdeburg Gellerich FN, EE Tartu Seppet EK, | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
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|preparations=Homogenate | |preparations=Homogenate | ||
|couplingstates=LEAK, OXPHOS, ETS | |couplingstates=LEAK, OXPHOS, ETS | ||
|substratestates=CI, CII | |substratestates=CI, CII | ||
|enzymes=Complex I, Complex II; Succinate Dehydrogenase | |enzymes=Complex I, Complex II; Succinate Dehydrogenase | ||
|topics=Substrate; Glucose; TCA Cycle | |topics=Substrate; Glucose; TCA Cycle | ||
}} | }} |
Revision as of 18:05, 25 November 2012
Trumbeckaite S, Gizatullina Z, Arandarcikaite O, Roehnert P, Vielhaber S, Malesevic M, Fischer G, Seppet E, Striggow F, Gellerich FN (2012) Oxygen glucose deprivation causes mitochondrial dysfunction in cultivated rat hippocampal slices: Protective effects of CsA, its immunosuppressive congener [D-Ser](8)CsA, the novel non-immunosuppressive cyclosporin derivative Cs9, and the NMDA receptor antagonist MK 801. Mitochondrion [Epub ahead of print]. |
Trumbeckaite S, Gizatullina Z, Arandarcikaite O, Roehnert P, Vielhaber S, Malesevic M, Fischer G, Seppet E, Striggow F, Gellerich FN (2012) Mitochondrion
Abstract: We have introduced a sensitive method for studying oxygen/glucose deprivation (OGD)-induced mitochondrial alterations in homogenates of organotypic hippocampal slice cultures (slices) by high-resolution respirometry. Using this approach, we tested the neuroprotective potential of the novel non-immunosuppressive cyclosporin (CsA) derivative Cs9 in comparison with CsA, the immunosuppressive CsA analogue [D-Ser](8)CsA, and MK 801, a N-methyl-D-aspartate (NMDA) receptor antagonist. OGD/reperfusion reduced the glutamate/malate dependent (and protein-related) state 3 respiration to 30% of its value under control conditions. All of the above drugs reversed this effect, with an increase to >88% of the value for control slices not exposed to OGD. We conclude that Cs9, [D-Ser](8)CsA, and MK 801, despite their different modes of action, protect mitochondria from OGD-induced damage. โข Keywords: cyclosporin (CsA) derivative Cs9, CsA analogue [D-Ser](8)CsA, NMDA-receptor antagonist, neuroprotection
โข O2k-Network Lab: DE Magdeburg Gellerich FN, EE Tartu Seppet EK
Labels:
Stress:Hypoxia, Ischemia-Reperfusion; Preservation"Ischemia-Reperfusion; Preservation" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Rat Tissue;cell: Neurons; Brain"Neurons; Brain" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property. Preparation: Homogenate Enzyme: Complex I, Complex II; Succinate Dehydrogenase"Complex II; Succinate Dehydrogenase" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" property. Regulation: Substrate; Glucose; TCA Cycle"Substrate; Glucose; TCA Cycle" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property. Coupling state: LEAK, OXPHOS, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property.
HRR: Oxygraph-2k