Trumbeckaite 2013 Mitochondrion
|Trumbeckaite S, Gizatullina Z, Arandarcikaite O, Röhnert P, Vielhaber S, Malesevic M, Fischer G, Seppet E, Striggow F, Gellerich FN (2013) 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 13:539–47.|
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: Organotypic hippocampal slice cultures; Mitochondria; Cs9; Oxygen/glucose deprivation
Stress:Ischemia-reperfusion Organism: Rat Tissue;cell: Nervous system Preparation: Homogenate Enzyme: Complex I, Complex II;succinate dehydrogenase Regulation: Substrate Coupling state: LEAK, OXPHOS, ET Pathway: N, S HRR: Oxygraph-2k